The study was supported by the Swiss National Foundation [SNF 310030-149986 to MNG], the University of Fribourg, and Fribourg Hospital.

وتلقى جميع الحيوانات الرعاية الإنسانية في الامتثال للاتفاقية الأوروبية لرعاية الحيوان. تم إجراء العمليات الجراحية وفقا لقانون حماية الحيوان السويسري بعد الحصول على إذن من مكتب الدولة للطب البيطري، فريبورغ، التي وافق عليها المكتب الاتحادي السويسري البيطري، سويسرا. حصاد 1. القلب ملاحظة: تم تنفيذ جميع التدخلات الجراحية تحت التخدير الأيزوفلورين. وقد بذلت جهود لتقليل معاناة الحيوانات. على وجه الخصوص، تلقى جميع الحيوانات الحقن تحت الجلد من 0.1 ملغم / كغم البوبرينورفين قبل التخدير. بروتوكول الجراحية لضمهم احتشاء عضلة القلب وقد وصفت سابقا في أماكن أخرى (13). <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> إجراء القص على حيوان محتشية myocardially تحت التخدير (حيوان تنبيب، 2.5٪ الأيزوفلورين والتخدير المناسبة أكد مخلب قرصة لا ارادي). <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> فتح الحيوان عن طريق قطع الجلد ثم العضلاتمع مقص جراحي. قطع الأضلاع على اليسار واليمين، ثم قم بإزالة الصدر. </li><li style=";text-align:right;direction:rtl"> إزالة التصاقات المتبقية بعد الجراحة السابقة (LAD ربط). قطع الشريان الأورطي وإزالة القلب. وضع الأنسجة في 1 م بوكل (في برنامج تلفزيوني)، ثم يغسل مع برنامج تلفزيوني. </li></ol></li></ol> 2. الأنسجة التحضير <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> وضع القلب محتشية طوليا في الاكريليك مصفوفة قلب فأر. يبقيه عند درجة حرارة -20 درجة مئوية لمدة 1 ساعة. </li><li style=";text-align:right;direction:rtl"> قطع القلب مباشرة في المصفوفة باستخدام شفرة حلاقة مع مستعرضة. ضمان كل شريحة هو 2 مم. قطع ما يقرب من 5-7 شرائح لكل قلب (استنادا إلى مستوى إعادة)؛ وهذا ما يسمى أخذ العينات بطريقة منهجية. </li><li style=";text-align:right;direction:rtl"> في هذه الخطوة، وأداء تلطيخ 2،3،5-triphenyltetrazolium كلوريد (TTC) هو اختياري (الحفاظ على التوجه للشرائح القلب قاعدة للقمة). <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> احتضان في 1٪ عقاري في برنامج تلفزيوني لمدة 50 دقيقة عند 37 درجة مئوية. احتضان في 4٪ بارافورمالدهيد (PFA) لمدة 20 دقيقة إلى 1 ساعة. وضع المقاطع بين هذا وذاكن لوحين من الزجاج مع الفواصل 2 ملم والتقاط الصور مع المجهر stereological إلى جانب وجود كاميرا في 15X التكبير. الحذر! امتصاص العرق هي سامة. </li></ol></li><li style=";text-align:right;direction:rtl"> تجميد الشريحة (1 الخيار الواحد) <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> وضع كل شريحة في قالب من البلاستيك (10 × 10 × 5 مم) مع تصاعد المتوسطة لcryotomy (أفضل درجة حرارة القطع، أكتوبر)، والحفاظ على التوجه (وضع الجانب الموجهة APEX-القسم أسفل على الجزء السفلي من القالب). تجميد الكتل مع الأبخرة 2-methylbutane تحت النيتروجين السائل لتبريد 10-15 دقيقة. وأخيرا، وتخزين الأنسجة عند -80 درجة مئوية. </li></ol></li><li style=";text-align:right;direction:rtl"> Paraffinization (2 الخيار الثاني) <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> وضع كل شريحة في تضمين أشرطة (الحفاظ على التوجه عن طريق وضع الجانب الموجهة للقمة للقسم الأسفل على الجزء السفلي من الكاسيت) ثم في 4٪ PFA لمدة 24 ساعة. وضعها في جهاز معالج الأنسجة بين عشية وضحاها. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> احتضان في الايثانول 70٪ لمدة 2 ساعة. احتضان في إيثانرأ 95٪ لمدة 2 ساعة. احتضان في الإيثانول بنسبة 100٪ لمدة 3 ساعة. احتضان في زايلول لمدة 4 ساعة. احتضان في البارافين (المنصهر في 60 درجة مئوية في الفرن) لمدة 5 ساعة. وأخيرا، وجعل الكتل عن طريق دمج كل شريحة القلب في البارافين. </li></ol></li></ol></li></ol> 3. ماسون-Goldner ثلاثي الألوان تلطيخ <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> جعل أقسام الأنسجة من كتل البارافين مع مشراح اليدوي (سمك: 5 ميكرون) أو من كتل أكتوبر مع ناظم البرد المقرر أن -18 درجة مئوية (سمك: 7 ميكرون). </li><li style=";text-align:right;direction:rtl"> وصمة عار شريحة واحدة من كل جزء القلب لكل الفئران (3-4 أقسام مستعرضة لكل شريحة) مع ماسون-Goldner ثلاثي الألوان تلطيخ (انظر المرفق). ملاحظة: بدء من هذه الخطوة للأقسام البارافين. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> تذوب الشرائح عند 60 درجة مئوية في الفرن. تحت غطاء الدخان، deparaffinize لهم في زايلول مرتين لمدة 10 دقيقة لكل منهما. ترطيب لهم في الإيثانول بنسبة 100٪، و 95٪ من الإيثانول و 70٪ من الإيثانول، والماء المقطر لمدة 3 دقائق لكل منهما. ملاحظة: بدء من هذه الخطوة لcryosectionالصورة. </li><li style=";text-align:right;direction:rtl"> اصلاحها في بوين الحل بين عشية وضحاها. ثم، شطف لهم في ادارة مياه الصنبور ل10-15 دقيقة. شطف في الماء المقطر. احتضان لهم في الهيماتوكسيلين ماير لمدة 3 دقائق. </li><li style=";text-align:right;direction:rtl"> إزالة الشرائح وتركهم في الماء المقطر لمدة 5 دقائق. ثم، احتضان لهم في الحامض بالفوكسين-الشقائقية لمدة 5 دقائق. شطف لهم في حامض الخليك 1٪ لمدة 1 دقيقة. </li><li style=";text-align:right;direction:rtl"> بعد ذلك، احتضان لهم في حمض الفسفومولبديك أورانج G لمدة 1 دقيقة. شطف لهم في حامض الخليك 1٪ لمدة 1 دقيقة، احتضان لهم في صبغ الضوء الأخضر لمدة 10 دقيقة، وشطف لهم في حامض الخليك 1٪ لمدة 1 دقيقة. </li><li style=";text-align:right;direction:rtl"> يذوى منهم في 70٪ من الإيثانول (30 ثانية)، و 95٪ من الإيثانول (30 ثانية)، والإيثانول٪ 100 (5 دقائق). وضع قطرة واحدة من وسط تصاعد راتنجية على أقسام الأنسجة، وغطاء لهم coverslips، والسماح لهم الجافة. </li></ol></li></ol> 4. عائق تحليل الحجم <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> الحصول على صورة واحدة من كل شريحة على مجهر تشريحي (15X التكبير) إلى جانب وجود الكاميرا. تصوير الحاكم مع نفس الإعدادالصورة. </li><li style=";text-align:right;direction:rtl"> استخدام صورة برامج التحليل لقياس سمك ندبة في منتصف احتشاء، وسماكة الحاجز، منطقة تجويف البطين الأيسر (LV)، ومنطقة احتشاء، ومنطقة الأنسجة LV استخدام. <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> تعيين المقياس مع الصورة الحاكم (الشكل 1A). <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> انقر على القياسات ثم حدد مجموعة معامل التحويل. رسم خط على شريط المعايرة. انقر بزر الماوس الأيمن على الصورة وانقر على معايرة النهاية. لاحظ القيمة شريط، ومن ثم انقر فوق موافق. </li></ol></li><li style=";text-align:right;direction:rtl"> حدد LV من الصورة القلب الملون (الشكل 1B). استخدام أداة شريحة متعددة. حدد LV نقطة بنقطة، وانقر ثم انقر بزر الماوس نسخ / لصق في أي مكان. </li><li style=";text-align:right;direction:rtl"> قياس ندبة والحاجز سمك باستخدام أداة قياس قطعة واحدة (الشكل 1C </stرونغ&gt;). </li><li style=";text-align:right;direction:rtl"> كشف تلقائيا LV تجويف، احتشاء، والمناطق LV باستخدام أداة قياس مساحة التلقائي في وضع RGB (1D الشكل). <ol style=";text-align:right;direction:rtl"><li style=";text-align:right;direction:rtl"> انقر على الأداة. تفعيل فقط حدود و متجاورة في وضع RGB. وأخيرا، انقر داخل المنطقة من الفائدة لكشفها. إذا لزم الأمر، واستخدام الأدوات الدقيقة. </li></ol></li></ol></li><li style=";text-align:right;direction:rtl"> حساب حجم احتشاء كنسبة من منطقة احتشاء إلى منطقة LV. </li><li style=";text-align:right;direction:rtl"> حساب مؤشر التوسع على النحو التالي: [LV منطقة تجويف / كامل منطقة LV] / [سمك احتشاء / سماكة الحاجز]، مع منطقة LV بأكملها بما في ذلك كل من تجويف LV ومناطق الأنسجة LV. </li><li style=";text-align:right;direction:rtl"> وأخيرا، وحساب &quot;متوسط&quot; لكل قلب على النحو التالي: [لمتوسط ​​مؤشر توسع من الشرائح محتشية] * [عدد الشرائح محتشية / مجموع عدد من الشرائح]. </li></ol>

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The authors have nothing to disclose.

خطوات حاسمة في إطار بروتوكول الأنسجة التليفية يمكن تقييمها بدقة في نموذج الفئران MI المزمن باستخدام أخذ العينات المنتظمة للقلب حصاد وصورة تحليلات أقسام النسيجية ثلاثي الألوان الملطخة تم الحصول عليها من قاعدة للقمة. خطو...

احتشاء عضلة القلب (MI) هو السبب الرئيسي للوفاة والعجز في جميع أنحاء العالم. أمراض القلب التاجية هي السبب الرئيسي. MI ينتج عن نقص التروية التوالي للأحداث التاجية مثل انسداد. عندما لا يتم تنفيذ ضخه داخل ساعة 6 الأولى، نقص تروية عضلة القلب يدفع نخر لا رجعة فيه. في المرضى، وتوصيف MI يعتمد على أدوات التشخيص المختلفة، بما في ذلك العلامات السريرية، تخطيط القلب الكهربائي، وتقييم مستويات البلازما من المؤشرات الحيوية، وضربات القلب، والتصوير بالرنين المغناطيسي، والنسيجية ويحلل 1. تصنف MI الحادة والمزمنة كما مرحلتين المختلفة للإصابات وفقا لتوقيت نخر عضلة القلب بالنسبة للوقت انسداد الشريان التاجي. المرحلة الحادة، والتي تحدث خلال 7 أيام الأولى، ويرتبط مع فقدان الخلايا العضلية، والتهاب واسعة النطاق، وتجنيد الخلايا الليفية. المرحلة شبه الحادة، التي تتميز شفاء الأنسجة القلبية وتشكيل ندبة، يحدثبين 1 و 4-6 أسابيع. توسيع احتشاء، رقيق البطين الجدار، وتوسع البطين تميز المرحلة المزمنة. إعادة عرض واسعة من البطين الأيسر النتائج تدريجيا في فشل القلب الحاد 2. MI الناجمة عن الدائمين الأمامي الأيسر النازل الشريان (LAD) ربط يمثل نموذج القوارض القياسية من احتشاء عضلة القلب المزمن. يقلد الربطة التاجية وانسداد الشريان التاجي. حجم احتشاء يعتمد على موقع ضمد. يتم إجراء توصيف الإصابة الدماغية عضلة القلب في نموذج القوارض كلاسيكي باستخدام مستويات البلازما العلامات البيولوجية، مثل تروبونين الأول وT 3، تخطيط صدى القلب، التصوير بالرنين المغناطيسي، والأنسجة 4،5. وترتبط مستويات المؤشرات الحيوية مع حد الموت cardiomyocyte. تخطيط صدى القلب يقيم الأيسر ضعف وظيفة البطين الناتجة عن تشوهات جدار الحركة الإقليمية. وبالإضافة إلى ذلك، وتقنيات التصوير غير الغازية، مثل التصوير بالرنين المغناطيسي أو عالية الدقةتخطيط صدى القلب، والسماح للتقييم الانخفاض في حركة الجدار، وحجم منطقة الندبة مع انخفاض التروية وعضلة القلب قابلة للحياة، وترقق الجدار. تسمح أبعاد LV تقييم دقيق لحجم احتشاء. وأخيرا، فإن تقدير حجم عضلة القلب قابلة للحياة ومات لا يمكن أن يؤديها بعد الوفاة باستخدام بقع محددة من المقاطع النسيجية من قلوب حصادها ويسمح التحقق من حجم احتشاء (IS). ميزة أخرى مهمة هي تقييم مؤشر التوسع احتشاء (EI) 6. ويرتبط EI مع احتشاء ويبدأ بطريق ضمن أول 3 أيام. يتميز EI من قبل التخفيض التدريجي في سمك الجدار، وزيادة في حجم تجويف LV، والتغيرات اللاحقة في شكل LV. من أجل تقييم فعالية العلاج من العلاجات الجديدة - على وجه الخصوص، استراتيجيات التجدد على أساس الخلايا، المصفوفات، والجينات التسليم دقيقة تقييم MI في القوارض هو أمر بالغ الأهمية.عندما يقاس على شريحة واحدة حصلت على مستوى العضلات الحليمية، قد يكون متحيزا حجم ويرجع ذلك إلى التنوع الكبير الموجود في تطوير احتشاء التالية ربط الغلام، واحتشاء مهيمنة يمكن بعد ذلك تحجبها. الأهم من ذلك، وقد وصفت منهجيات أكثر دقة لتحديد حجم MI للفئران 7-9 أو الفئران 10. على الرغم من ذلك، هو غير كافية لتحديد بدقة LV إعادة عرض أو أدى إلى انخفاض علاجيا (أو المنع) من التجديد. في الواقع، هو ما يعبر عنه عادة كنسبة مئوية من إجمالي حجم LV المقررة على المقاطع العرضية للقلب. على الرغم من أن هذه الطريقة صالحة لMI الحاد، وترقق الجدار LV التي تحدث خلال إعادة عرض ما زال تحت تقييمها 11،12. تقدير كمي المورفولوجية كاملة من حجم احتشاء والتغيرات الهيكلية يجب تحديد حجم العديد من المعلمات، مثل أطوال شغافية والنخابية وبأقطار، فضلا عن احتشاء والمناطق الصحية. نحن تصف appr المنهجيoach إلى تقييم دقيق MI وإعادة عرض في نموذج الفئران المزمن.

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			<td height="21" style="height:21px;width:247px;">Acrylic rat heart matrix 2mm</td>
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			<td height="41" style="height:41px;width:247px;">INSPIRA ADVANCED VOLUME CONTROLLED VENTILATOR</td>
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			<td height="21" style="height:21px;width:247px;">Acid Fuchsin 
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			<td height="20" style="height:20px;width:247px;">Light green 
			CI 42095</td>
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			<td height="21" style="height:21px;width:247px;">KCl</td>
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			<td style="width:136px;">Sigma Aldrich</td>
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			<td height="21" style="height:21px;width:247px;">Xylol</td>
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			<td style="width:136px;">HoneyWell</td>
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			<td height="21" style="height:21px;width:247px;">2-methylbutane</td>
			<td style="width:119px;">M32631-1L</td>
			<td style="width:136px;">Sigma Aldrich</td>
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			<td height="21" style="height:21px;width:247px;">Stereogical microscope</td>
			<td style="width:119px;">SM2800</td>
			<td style="width:136px;">Nikon</td>
			<td style="width:273px;"></td>
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		<tr height="21">
			<td height="21" style="height:21px;width:247px;">Formaldehyde</td>
			<td style="width:119px;">99340</td>
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		<tr height="21">
			<td height="21" style="height:21px;width:247px;">Embedding cassette</td>
			<td style="width:119px;">K113.1</td>
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			<td style="width:273px;"></td>
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		<tr height="41">
			<td height="41" style="height:41px;width:247px;">Bersoft Image measurement Software</td>
			<td style="width:119px;"></td>
			<td style="width:136px;">Bersoft.com</td>
			<td style="width:273px;">Licensed software</td>
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histological quantification of chronic myocardial infarct in rats

Myocardial infarction is defined as cardiomyocyte death due to prolonged ischemia; an inflammatory response and scar formation (fibrosis) follow the ischemic injury. Following the initial acute phase, chronic remodeling of the left ventricle (LV) modifies the structure and function of the heart. Permanent coronary ligation in small animals has been widely used as a reference model for a chronic model of MI. Thinning of the infarcted wall progressively develops to transmural fibrosis. Histological assessment of infarct size is commonly performed; nevertheless, a standardization of the methods for quantification is missing. Indeed, important methodological aspects, such as the number of sections analyzed and the sampling and quantification methods, are usually not described and therefore preclude comparison across investigations. Too often, quantification is performed on a single section obtained at the level of the papillary muscles. Because novel strategies aimed at reducing infarct expansion and remodeling are under investigation, there is an important need for the standardization of accurate heart sampling protocols. We describe an accurate method to quantify the infarct size using a systematic sampling of harvested rat heart and image analyses of trichromatic stained histological sections obtained from base to apex. We also provide evidence that calculating the expansion index (EI) allowed for infarct size assessment, taking into account changes of the left ventricle throughout the remodeling.

ستة أسابيع بعد LAD ربط، تم حصاد قلوب من الفئران لويس. وقد تم الحصول على أقسام الأنسجة 2 ملم من قمة إلى القاعدة. تم تنفيذ إجراء تلطيخ TTC لتصور منطقة احتشاء، والذي يظهر باللون الأبيض، وعضلة القلب السليم، والذي يظهر باللون الأحمر (الشكل 2). اعتمادا...

Watch this Scientific Journal Video about Histological Quantification of Chronic Myocardial Infarct in Rats at JoVE.com

Histological Quantification of Chronic Myocardial Infarct in Rats

The post-mortem assessment of myocardial infarction (MI) in rodents is based on quantification of the infarct on stained heart sections. We describe an accurate method to quantify the infarct size using systematic sampling of harvested rat hearts from base to apex and image analyses of trichrome-stained histological sections.

الكمي النسيجي المزمن عضلة القلب عائق في الجرذان

Myocardial infarction is defined as cardiomyocyte death due to prolonged ischemia; an inflammatory response and scar formation (fibrosis) follow the ...

histological-quantification-of-chronic-myocardial-infarct-in-rats

Research

JoVE Journal

Medicine

14.4K Views.  University of Fribourg. The post-mortem assessment of myocardial infarction (MI) in rodents is based on quantification of the infarct on stained heart sections. We describe an accurate method to quantify the infarct size using systematic sampling of harvested rat hearts from base to apex and image analyses of trichrome-stained histological sections. 

Video: Histological Quantification of Chronic Myocardial Infarct in Rats

Acute Myocardial Infarction in Rats

With heart failure leading the cause of death in the USA (Hunt), biomedical research is fundamental to advance medical treatments for cardiovascular diseases. Animal models that mimic human cardiac disease, such as myocardial infarction (MI) and ischemia-reperfusion (IR) that induces heart failure as well as pressure-overload (transverse aortic constriction) that induces cardiac hypertrophy and heart failure (Goldman and Tarnavski), are useful models to study cardiovascular disease. In particular, myocardial ischemia (MI) is a leading cause for cardiovascular morbidity and mortality despite controlling certain risk factors such as arteriosclerosis and treatments via surgical intervention (Thygesen). Furthermore, an acute loss of the myocardium following myocardial ischemia (MI) results in increased loading conditions that induces ventricular remodeling of the infarcted border zone and the remote non-infarcted myocardium. Myocyte apoptosis, necrosis and the resultant increased hemodynamic load activate multiple biochemical intracellular signaling that initiates LV dilatation, hypertrophy, ventricular shape distortion, and collagen scar formation. This pathological remodeling and failure to normalize the increased wall stresses results in progressive dilatation, recruitment of the border zone myocardium into the scar, and eventually deterioration in myocardial contractile function (i.e. heart failure). The progression of LV dysfunction and heart failure in rats is similar to that observed in patients who sustain a large myocardial infarction, survive and subsequently develops heart failure (Goldman). The acute myocardial infarction (AMI) model in rats has been used to mimic human cardiovascular disease; specifically used to study cardiac signaling mechanisms associated with heart failure as well as to assess the contribution of therapeutic strategies for the treatment of heart failure. The method described in this report is the rat model of acute myocardial infarction (AMI). This model is also referred to as an acute ischemic cardiomyopathy or ischemia followed by reperfusion (IR); which is induced by an acute 30-minute period of ischemia by ligation of the left anterior descending artery (LAD) followed by reperfusion of the tissue by releasing the LAD ligation (Vasilyev and McConnell). This protocol will focus on assessment of the infarct size and the area-at-risk (AAR) by Evan's blue dye and triphenyl tetrazolium chloride (TTC) following 4-hours of reperfusion; additional comments toward the evaluation of cardiac function and remodeling by modifying the duration of reperfusion, is also presented. Overall, this AMI rat animal model is useful for studying the consequence of a myocardial infarction on cardiac pathophysiological and physiological function.

The rat model of acute myocardial infarction (AMI) is useful to study the consequence of a MI on cardiac pathophysiological and physiological function.

احتشاء عضلة القلب الحاد في الفئران

With heart failure leading the cause of death in the USA (Hunt), biomedical research is fundamental to advance medical treatments for cardiovascular ...

Acute and Chronic Tactile Sensory Testing after Spinal Cord Injury in Rats

Spinal cord injury (SCI) impairs sensory systems causing allodynia1-8. To identify cellular and molecular causes of allodynia, sensitive and valid sensory testing in rat SCI models is needed. However, until recently, no single testing approach had been validated for SCI so that standardized methods have not been implemented across labs. Additionally, available testing methods could not be implemented acutely or when severe motor impairments existed, preventing studies of the development of SCI-induced allodynia3. Here we present two validated sensory testing methods using von Frey Hair (VFH) monofilaments which quantify changes in tactile sensory thresholds after SCI4-5. One test is the well-established Up-Down test which demonstrates high sensitivity and specificity across different SCI severities when tested chronically5. The other test is a newly-developed dorsal VFH test that can be applied acutely after SCI when allodynia develops, prior to motor recovery4-5. Each VFH monofilament applies a calibrated force when touched to the skin of the hind paw until it bends. In the up-down method, alternating VFHs of higher or lower forces are used on the plantar L5 dermatome to delineate flexor withdrawal thresholds. Successively higher forces are applied until withdrawal occurs then lower force VFHs are used until withdrawal ceases. The tactile threshold reflects the force required to elicit withdrawal in 50% of the stimuli. For the new test, each VFH is applied to the dorsal L5 dermatome of the paw while the rat is supported by the examiner. The VFH stimulation occurs in ascending order of force until at least 2 of 3 applications at a given force produces paw withdrawal. Tactile sensory threshold is the lowest force to elicit withdrawal 66% of the time. Acclimation, testing and scoring procedures are described. Aberrant trials that require a retest and typical trials are defined. Animal use was approved by Ohio State University Animal Care and Use Committee.

We describe two tactile sensory testing methods for acute or chronic periods of spinal cord injury in rats. These validated procedures can detect the development and maintenance of allodynia-like sensations.

الحادة والمزمنة الاختبارات الحسية اللمس بعد إصابة الحبل الشوكي في الجرذان

Spinal cord injury (SCI) impairs sensory systems causing allodynia1-8. To identify cellular and molecular causes of allodynia, sensitive and valid sensory ...

Chronic Constriction of the Sciatic Nerve and Pain Hypersensitivity Testing in Rats

Chronic neuropathic pain, resulting from damage to the central or peripheral nervous system, is a prevalent and debilitating condition, affecting 7-18% of the population1,2. Symptoms include spontaneous (tingling, burning, electric-shock like) pain, dysaesthesia, paraesthesia, allodynia (pain resulting from normally non-painful stimuli) and hyperalgesia (an increased response to painful stimuli). The sensory symptoms are co-morbid with behavioural disabilities, such as insomnia and depression. To study chronic neuropathic pain several animal models mimicking peripheral nerve injury have been developed, one of the most widely used is Bennett and Xie's (1988) unilateral sciatic nerve chronic constriction injury (CCI)3 (Figure 1). Here we present a method for performing CCI and testing pain hypersensitivity.
CCI is performed under anaesthesia, with the sciatic nerve on one side exposed by making a skin incision, and cutting through the connective tissue between the gluteus superficialis and biceps femoris muscles. Four chromic gut ligatures are tied loosely around the sciatic nerve at 1 mm intervals, to just occlude but not arrest epineural blood flow. The wound is closed with sutures in the muscle and staples in the skin. The animal is then allowed to recover from surgery for 24 hrs before pain hypersensitivity testing begins.
For behavioural testing, rats are placed into the testing apparatus and are allowed to habituate to the testing procedure. The area tested is the mid-plantar surface of the hindpaw (Figure 2), which falls within the sciatic nerve distribution. Mechanical withdrawal threshold is assessed by mechanically stimulating both injured and uninjured hindpaws using an electronic dynamic plantar von Frey aesthesiometer or manual von Frey hairs4. The mechanical withdrawal threshold is the maximum pressure exerted (in grams) that triggers paw withdrawal. For measurement of thermal withdrawal latency, first described by Hargreaves et al (1988), the hindpaw is exposed to a beam of radiant heat through a transparent glass surface using a plantar analgesia meter5,6. The withdrawal latency to the heat stimulus is recorded as the time for paw withdrawal in both injured and uninjured hindpaws. Following CCI, mechanical withdrawal threshold, as well as thermal withdrawal latency in the injured paw are both significantly reduced, compared to baseline measurements and the uninjured paw (Figure 3). The CCI model of peripheral nerve injury combined with pain hypersensitivity testing provides a model system to investigate the effectiveness of potential therapeutic agents to modify chronic neuropathic pain. In our laboratory, we utilise CCI alongside thermal and mechanical sensitivity of the hindpaws to investigate the role of neuro-immune interactions in the pathogenesis and treatment of neuropathic pain.

Due to the simplicity of surgery and the robust behavioural outcome, chronic constriction of the sciatic nerve is one of the pre-eminent animal models of neuropathic pain. Within 24 hrs following surgery, pain hypersensitivity is established and can be quantitatively measured using a von Frey aesthesiometer (mechanical test) and plantar analgesia meter (thermal test).

مزمن انقباض في العصب الوركي والألم اختبار فرط الحساسية في الفئران

Chronic neuropathic pain, resulting from damage to the central or peripheral nervous system, is a prevalent and debilitating condition, affecting 7-18% of ...

Assessment of Cardiac Function and Myocardial Morphology Using Small Animal Look-locker Inversion Recovery (SALLI) MRI in Rats

Small animal magnetic resonance imaging is an important tool to study cardiac function and changes in myocardial tissue. The high heart rates of small animals (200 to 600 beats/min) have previously limited the role of CMR imaging. Small animal Look-Locker inversion recovery (SALLI) is a T1 mapping sequence for small animals to overcome this problem 1. T1 maps provide quantitative information about tissue alterations and contrast agent kinetics. It is also possible to detect diffuse myocardial processes such as interstitial fibrosis or edema 1-6. Furthermore, from a single set of image data, it is possible to examine heart function and myocardial scarring by generating cine and inversion recovery-prepared late gadolinium enhancement-type MR images 1.
	The presented video shows step-by-step the procedures to perform small animal CMR imaging. Here it is presented with a healthy Sprague-Dawley rat, however naturally it can be extended to different cardiac small animal models.

Assessment of Cardiac Function and Myocardial Morphology Using Small Animal Look-locker Inversion Recovery SALLI MRI in Rats

Contrast enhanced cardiac magnetic resonance (CMR) imaging allows comprehensive in vivo assessment of the heart in small animal models of cardiovascular disease. Here we detail the procedures to perform CMR imaging, reconstruction and analysis using Small Animal Lock-Locker Inversion Recovery (SALLI) in rats.

تقييم وظيفة القلب والصرف عضلة القلب عن طريق الحيوانات الصغيرة نظرة خزانة الاسترداد عكس (صلي) التصوير بالرنين المغناطيسي في الجرذان

Small animal magnetic resonance  imaging is an important tool to study cardiac function and changes in myocardial  tissue. The high heart rates of small ...

MRI and PET in Mouse Models of Myocardial Infarction

Myocardial infarction is one of the leading causes of death in the Western world. The similarity of the mouse heart to the human heart has made it an ideal model for testing novel therapeutic strategies.
In vivo magnetic resonance imaging (MRI) gives excellent views of the heart noninvasively with clear anatomical detail, which can be used for accurate functional assessment. Contrast agents can provide basic measures of tissue viability but these are nonspecific. Positron emission tomography (PET) is a complementary technique that is highly specific for molecular imaging, but lacks the anatomical detail of MRI. Used together, these techniques offer a sensitive, specific and quantitative tool for the assessment of the heart in disease and recovery following treatment.
In this paper we explain how these methods are carried out in mouse models of acute myocardial infarction. The procedures described here were designed for the assessment of putative protective drug treatments. We used MRI to measure systolic function and infarct size with late gadolinium enhancement, and PET with fluorodeoxyglucose (FDG) to assess metabolic function in the infarcted region. The paper focuses on practical aspects such as slice planning, accurate gating, drug delivery, segmentation of images, and multimodal coregistration. The methods presented here achieve good repeatability and accuracy maintaining a high throughput.

We describe how to perform MRI and PET imaging of the mouse heart. The protocol is tailored to assess treatment efficacy in models of myocardial infarction and heart failure.

Myocardial infarction is one of the leading causes of death in the Western world. The similarity of the mouse heart to the human heart has made it an ...

Ultrasonic Assessment of Myocardial Microstructure

Echocardiography is a widely accessible imaging modality that is commonly used to noninvasively characterize and quantify changes in cardiac structure and function. Ultrasonic assessments of cardiac tissue can include analyses of backscatter signal intensity within a given region of interest. Previously established techniques have relied predominantly on the integrated or mean value of backscatter signal intensities, which may be susceptible to variability from aliased data from low frame rates and time delays for algorithms based on cyclic variation. Herein, we describe an ultrasound-based imaging algorithm that extends from previous methods, can be applied to a single image frame&#160;and accounts for the full distribution of signal intensity values derived from a given myocardial sample. When applied to representative mouse and human imaging data, the algorithm distinguishes between subjects with and without exposure to chronic afterload resistance. The algorithm offers an enhanced surrogate measure of myocardial microstructure and can be performed using open-access image analysis software.

Echocardiography is commonly used to noninvasively characterize and quantify changes in cardiac structure and function. We describe an ultrasound-based imaging algorithm that offers an enhanced surrogate measure of myocardial microstructure and can be performed using open-access image analysis software.

تقييم بالموجات فوق الصوتية للهيكل المجهري عضلة القلب

Echocardiography is a widely accessible imaging modality that is commonly used to noninvasively characterize and quantify changes in cardiac structure and ...

Urinary Bladder Distention Evoked Visceromotor Responses as a Model for Bladder Pain in Mice

Approximately 3-8 million people in the United States suffer from interstitial cystitis/bladder pain syndrome (IC/BPS), a debilitating condition characterized by increased urgency and frequency of urination, as well as nocturia and general pelvic pain, especially upon bladder filling or voiding. Despite years of research, the cause of IC/BPS remains elusive and treatment strategies are unable to provide complete relief to patients. In order to study nervous system contributions to the condition, many animal models have been developed to mimic the pain and symptoms associated with IC/BPS. One such murine model is urinary bladder distension (UBD). In this model, compressed air of a specific pressure is delivered to the bladder of a lightly anesthetized animal over a set period of time. Throughout the procedure, wires in the superior oblique abdominal muscles record electrical activity from the muscle. This activity is known as the visceromotor response (VMR) and is a reliable and reproducible measure of nociception. Here, we describe the steps necessary to perform this technique in mice including surgical manipulations, physiological recording, and data analysis. With the use of this model, the coordination between primary sensory neurons, spinal cord secondary afferents, and higher central nervous system areas involved in bladder pain can be unraveled. This basic science knowledge can then be clinically translated to treat patients suffering from IC/BPS.

Approximately 3-8 million people in the United States suffer from interstitial cystitis/bladder pain syndrome (IC/BPS), a debilitating condition characterized in part by pelvic pain. In order to study nervous system contributions to the condition, a physiological model of urinary bladder pain is used in mice and rats.

الردود المثانة البولية انتفاخ مستدعى الحشوي الحركي نموذجا لألم المثانة في الفئران

Approximately 3-8 million people in the United States suffer from interstitial cystitis/bladder pain syndrome (IC/BPS), a debilitating condition ...

Echocardiographic and Histological Examination of Cardiac Morphology in the Mouse

An increasing number of genetically modified mouse models has become available in recent years. Moreover, the number of pharmacological studies performed in mice is high. Phenotypic characterization of these mouse models also requires the examination of cardiac function and morphology. Echocardiography and magnetic resonance imaging (MRI) are commonly used approaches to characterize cardiac function and morphology in mice. Echocardiographic and MRI equipment specialized for use in small rodents is&#160;expensive and requires a dedicated space. This protocol describes cardiac measurements in mice using a clinical echocardiographic system with a 15 MHz human vascular probe. Measurements are performed on anesthetized adult mice. At least three image sequences are recorded and analyzed for each animal in M-mode in the parasternal short-axis view. Afterwards, cardiac histological examination is performed, and cardiomyocyte diameters are determined on hematoxylin-eosin- or wheat germ agglutinin (WGA)-stained paraffin sections. Vessel density is determined morphometrically after Pecam-1 immunostaining. The protocol has been applied successfully to pharmacological studies and different genetic animal models under baseline conditions, as well as after experimental myocardial infarction by the permanent ligation of the left anterior descending coronary artery (LAD). In our experience, echocardiographic investigation is limited to anesthetized animals and is feasible in adult mice weighing at least 25 g.

Echocardiographic examination is frequently used in mice. Expensive high-resolution ultrasound devices have been developed for this purpose. This protocol describes an affordable echocardiographic procedure combined with histological morphometric analyses to determine cardiac morphology.

دراسة مورفولوجيا القلب مشخصين وغذائها في الماوس

An increasing number of genetically modified mouse models has become available in recent years. Moreover, the number of pharmacological studies performed ...

Evaluation of Coronary Flow Reserve After Myocardial Ischemia Reperfusion in Rats

Coronary artery disease is the leading cause of death worldwide. After an acute myocardial infarction, early and successful myocardial intervention via recanalization of the coronary artery is the most effective strategy for reducing the size of ischemic myocardium. The coronary microvasculature cannot be visualized and imaged&#160;in vivo, but there are several invasive and noninvasive techniques that can be used to assess parameters which depend directly on coronary microvascular function. The endothelial function after ischemia reperfusion can be assessed also at the level of the coronary circulation via the coronary flow reserve (CFR).&#160;In this study, peak velocity of left anterior descending (LAD) coronary arteries was measured in rats in vivo via Transthoracic Doppler Echocardiography during resting and stress challenge (induced by Dobutamine). A normal heart can increase its coronary blood flow up to four times above the resting values during stress induction. Following ischemia reperfusion, we found a significantly diminished CFR, which can be used as a marker of coronary microvascular dysfunction. CFR has opened a window on the importance of microvascular dysfunction and has been shown to predict cardiovascular risk independent of whether the severe obstructive disease is present.

Coronary flow reserve (CFR), is defined as the ratio of maximal coronary blood flow to the resting coronary blood flow. We present a protocol for evaluating CFR in rats via ultrasound, which offers the opportunity to predict cardiovascular risk factors in the absence of obstructive coronary disease.

تقييم احتياطي التدفق التاجي بعد إعادة ضخ الإقفارية عضلة القلب في الفئران

Coronary artery disease is the leading cause of death worldwide. After an acute myocardial infarction, early and successful myocardial intervention via ...

Semi-Minimal Invasive Method to Induce Myocardial Infarction in Rats and the Assessment of Cardiac Function by an Isolated Working Heart System

Myocardial infarction (MI) remains the main contributor to morbidity and mortality worldwide. Therefore, research on this topic is mandatory. An easily and highly reproducible MI induction procedure is required to obtain further insight and better understanding of the underlying pathological changes. This procedure can also be used to evaluate the effects or potency of new and promising treatments (as drugs or interventions) in acute MI, subsequent remodeling and heart failure (HF). After intubation and pre-operative preparation of the animal, an anesthetic protocol with isoflurane was performed, and the surgical procedure was conducted&#160;quickly. Using a minimally invasive approach, the left anterior descending artery (LAD) was located and occluded by a ligature. The occlusion can be performed acutely for subsequent reperfusion (ischemia/reperfusion injury). Alternatively, the vessel can be ligated permanently to investigate the development of chronic MI, remodeling or HF. Despite common pitfalls, the drop-out rates are minimal. Various treatments such as remote ischemic conditioning can be examined for their cardioprotective potential pre-, peri- and post-operatively. The post-operative recovery was quick as the anesthesia was precisely controlled and the duration of the operation was short. Post-operative analgesia was administered for three days. The minimally invasive procedure reduces the risk of infection and inflammation. Furthermore, it facilitates rapid recovery. The &#8220;working heart&#8221; measurements were performed ex vivo and enabled precise control of preload, afterload and flow. This procedure requires specific equipment and training for adequate performance. This manuscript provides a detailed step-by-step introduction for conducting these measurements.

This article presents an efficient method to perform myocardial ischemia and subsequent chronic reperfusion in rats using a minimally invasive approach. In addition, left ventricular hemodynamic function of rats is assessed by echocardiography and isolated working heart methods.&#160;

طريقة شبه طفيفة التوغل للحث على احتشاء عضلة القلب في الفئران وتقييم وظيفة القلب من قبل نظام القلب العامل المعزول

Myocardial infarction (MI) remains the main contributor to morbidity and mortality worldwide. Therefore, research on this topic is mandatory. An easily ...