Name: a modified two kidney one clip mouse model of renin regulation in renal artery stenosis
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研究得到了NHLBI研究科学家发展补助金（1K01HL135461-01）对JAG的支持。感谢大卫·卡莫纳-贝里奥和伊莎贝尔·阿达尔维-伦吉福的技术援助。

根据美国国立卫生研究院（NIH）指南和美国卫生与公众服务部的范德比尔特大学医学中心（VUMC）动物护理部对小鼠进行饲养和护理。在开始实验之前，所有动物程序都得到了VUMC机构动物护理和使用委员会的批准。
1. 动物准备和解剖
<ol><li>在开始手术前约30分钟打开加热垫的发芽器和水泵。</li>
	<li>用锋利的手术刀切割0.5毫米长的聚氨酯管。取下 0.2 毫米的周长，纵向切开，做成袖口。 注意:这是肾动脉狭窄手术的关键部分，需要极高的精确度，注重细节和耐心。尝试一次切割几块聚氨酯管。在显微镜下执行所有这些程序。</li>
	<li>在继续之前，戴上外科无菌手套和外科口罩。</li>
	<li>使用6-8周的C57BL / 6野生型（WT）小鼠。使用相同数量的雄性和雌性小鼠以避免任何性别偏见。</li>
	<li>在进行手术之前记录小鼠的体重。用聚氨酯管进行肾动脉狭窄的理想重量为18-22克。轻轻地处理小鼠，注射麻醉剂时不要搅拌。给予术前镇痛（酮促，5毫克/ kg身体重量）。 注意:在将小鼠从其住房室转移到手术室时，请非常温和和小心地携带它们，以避免激动。强烈建议将小鼠笼子放在手中而不是手推车中。</li>
	<li>通过腹膜内（I.P.）注射用氯胺酮（100mg / kg BW）和甲苯噻嗪（10mg / kg BW）的混合物麻醉小鼠。</li>
	<li>将鼠标放回笼内，直到完全麻醉。鼠标完全失去知觉大约需要4-5分钟。用镊子捏住尾巴或脚趾，检查鼠标是否完全失去知觉并准备好进行手术。</li>
	<li>将鼠标仰面放在纸巾上。沿着毛发生长的相反方向，使用电动理发器去除外腹部的毛发。剃除手术部位后，用含有碘（或氯己定的）的手术磨砂膏清洁该区域，然后用70%乙醇（或无菌盐水）冲洗。 重复3次。 注意:脱毛手术必须在一定距离上进行，或者最好在与手术手术台不同的工作台上进行，以避免手术过程中的任何头发干扰和头发污染。</li>
	<li>用无菌片盖住加热垫。将鼠标带到手术台上，放在无菌片上，面向小鼠的右侧侧向显微镜。用循环水保持37°C的恒定焊盘温度。</li>
	<li>打开装有所有手术设备的灭菌袋。使用解剖显微镜和无菌利器剪刀，做一个小的侧腹切口（靠近第 13胸肋骨，小鼠的最后一根肋骨），距离椎骨约0.5厘米。沿着腰椎继续，做一个1英寸的切口。</li>
	<li>拉回皮肤和肌肉以暴露肾脏。</li>
	<li>使用无菌棉签清洁并去除周围的脂肪，以隔离肾动脉。使用弯曲的镊子将肾神经与肾动脉隔离开来。</li>
	<li>进行假手术时，应用缝合线以闭合皮肤并将抗生素应用于闭合的伤口，然后进行 术后护理。 如果没有，请继续执行以下部分以切断动脉狭窄。 注意:每个实验都应该有假动物作为外科手术的对照。假动物由经过暴露肾动脉而不在其上放置袖带的外科手术的小鼠组成。</li>
</ol>2. 右肾动脉狭窄
<ol><li>在右肾动脉下方放置两条尼龙缝合线，打出松散的结，然后将袖带放在肾脏和主动脉分叉之间大致等距的肾主动脉周围</li>
	<li>使用尼龙缝合线关闭袖口。每个缝合线打四个结，以避免手术后失去缝合线的可能性。</li>
	<li>通过应用简单的连续缝合线来关闭肌肉中的切口。</li>
	<li>进行简单的断续缝合以闭合皮肤。</li>
	<li>使用IACUC批准的镇痛药。 注意:每次使用前高压灭菌手术工具。如果一次进行多次手术，请用无菌酒精计擦拭所有使用过的工具，并在每次手术后将其放入热发芽器中15-30秒。也为每只老鼠更换无菌手套。</li>
</ol>3. 术后护理
<ol><li>将小鼠放回笼子里，让笼子一半打开，一半关闭，循环水加热垫2-3小时。在笼子内添加凝胶日粮恢复食品。</li>
	<li>第二天腹膜内注射止痛药（酮洛芬）（剂量:5毫克/千克体重）。</li>
	<li>称量接下来两天的小鼠;如果一些小鼠体重减轻超过20%，请咨询兽医，并决定动物是否需要按照适当的IACUC授权程序进行安乐死。</li>
	<li>每天监测小鼠以评估发红，肿胀，疼痛或感染。</li>
	<li>根据机构IACUC政策寻求兽医咨询术后并发症。</li>
</ol>4. 组织采集
<ol><li>手术后3周收获组织。记录每只鼠标的重量。</li>
	<li>用IACUC批准的程序对小鼠实施安乐死。</li>
	<li>将鼠标放在无菌平台上，以仰卧位解剖。</li>
	<li>固定并伸展四肢以限制运动。</li>
	<li>用70%乙醇彻底喷洒小鼠。</li>
	<li>做一个中线切口，用锋利的剪刀打开腹部和胸部区域。</li>
	<li>拉回皮肤和腹膜壁。</li>
	<li>小心地暴露心脏并穿刺右心室并释放小鼠。</li>
	<li>使用镊子取出两个肾脏。肾脏位于小鼠的背部。 注意:不要混合两个肾脏。注意狭窄的肾脏、假肾和对侧肾脏。</li>
	<li>取出肾囊，从任何脂肪中清除它们，并分别记录每个肾脏的重量。</li>
	<li>切开两个肾脏的纵向切片，并在4°C下固定在4%PFA中过夜，以便随后处理石蜡包埋，以进行原位杂交（ISH）和免疫组织化学（IHC）。遵循23，24 报告的 ISH 和 IHC 协议。</li>
	<li>分离剩余肾脏的皮质，并在液氮中快速冷冻以进行蛋白质印迹。将样品储存在-80°C直至分析。</li>
	<li>用蛋白质印迹量化肾素和N-GAL表达，如文献23，24中所述。</li>
</ol>5. 统计
<ol><li>使用单向或双向方差分析进行具有三个或更多条件的实验，然后使用 Bonferroni 事后检验来比较各个组之间的比较。考虑 p 值等于或小于 0.05 的显著性。使用软件（例如，图形键盘棱镜 8.2）执行所有统计分析。</li>
</ol>

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G. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Pressor+responses+to+vasopressin+in+rabbits+with+3-day+renal+artery+stenosis.">Pressor responses to vasopressin in rabbits with 3-day renal artery stenosis.</a> American Journal of Physiology. 240 (6), 862-867 (1981).</li><li>Eirin, A., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Changes+in+glomerular+filtration+rate+after+renal+revascularization+correlate+with+microvascular+hemodynamics+and+inflammation+in+Swine+renal+artery+stenosis.">Changes in glomerular filtration rate after renal revascularization correlate with microvascular hemodynamics and inflammation in Swine renal artery stenosis.</a> Circulation: Cardiovascular Interventions. 5 (5), 720-728 (2012).</li><li>Ma, Z., Jin, X., He, L., Wang, Y. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=CXCL16+regulates+renal+injury+and+fibrosis+in+experimental+renal+artery+stenosis.">CXCL16 regulates renal injury and fibrosis in experimental renal artery stenosis.</a> American Journal of Physiology-Heart and Circulatory. 311 (3), 815-821 (2016).</li><li>Cheng, J., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Temporal+analysis+of+signaling+pathways+activated+in+a+murine+model+of+two-kidney,+one-clip+hypertension.">Temporal analysis of signaling pathways activated in a murine model of two-kidney, one-clip hypertension.</a> American Journal of Physiology-Renal Physiology. 297 (4), 1055-1068 (2009).</li><li>Wiesel, P., Mazzolai, L., Nussberger, J., Pedrazzini, T. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Two-kidney,+one+clip+and+one-kidney,+one+clip+hypertension+in+mice.">Two-kidney, one clip and one-kidney, one clip hypertension in mice.</a> Hypertension. 29 (4), 1025-1030 (1997).</li><li>Johns, C., Gavras, I., Handy, D. E., Salomao, A., Gavras, H. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Models+of+experimental+hypertension+in+mice.">Models of experimental hypertension in mice.</a> Hypertension. 28 (6), 1064-1069 (1996).</li></ol>

作者不申报任何利益冲突，包括财务或其他方面。

肾动脉狭窄是继发性或难治性高血压和肾损伤的重要病因1，29.两个肾脏一夹（2K1C）Goldblatt模型已被用于研究RAS狭窄诱导的肾血管高血压1，17，18，19。以前使用各种动物模型的一些研究表明，肾动脉狭窄是肾素过表达和释放的强大刺激因子，肾损伤<sup class=...

肾动脉狭窄（RAStenosis）是一种棘手的问题，影响约6%的65岁以上人群和高达40%的冠状动脉或外周血管疾病患者1，2。目前对这种疾病的治疗是有限的;因此，迫切需要开发新的疗法来治疗肾血管性高血压或由RAStenosis诱导的抵抗性高血压。肾素血管紧张素醛固酮系统（RAAS）是参与RAS狭窄诱导的高血压或肾血管性高血压发病机制的关键途径3，4。针对 RAAS 的已知疗法（如血管紧张素转换酶抑制剂或血管紧张素受体阻滞剂）可缓解高血压，但需要仔细检查肾衰竭和高钾血症5，6，7。肾素催化RAAS中的速率限制步骤;它将血管紧张素原转化为血管紧张素I。在动脉粥样硬化中，斑块形成导致肾动脉变窄，从而驱动肾素分泌，导致肾血管高血压和肾脏损伤8。许多研究报告了人类肾血管性高血压期间氧化应激水平升高，这与两个肾脏一夹（2K1C）小鼠模型以及其他高血压动物模型2，9，10，11，12，13，14，15，16证实。.RAS狭窄诱发的肾血管性高血压期间肾素表达控制的分子机制尚不清楚，需要进一步研究。
可靠且可重复地概括RAStenosis的实验动物模型对于阐明肾素表达控制的细胞和分子机制以开发新疗法非常重要。2K1C小鼠模型是研究肾血管性高血压发病机制的成熟实验模型17，18，19，20。该模型通过使用夹子17，20，21的肾动脉收缩而生成，因此产生肾动脉阻塞，导致肾素表达增加和高血压17，19，20，21。然而，没有可用的技术报告，其中描述了在动物模型中产生肾动脉狭窄的分步过程。
传统的U形银夹，聚氨酯管和其他夹子已被用于收缩肾动脉以诱导肾动脉狭窄。一些研究表明，夹子的设计和材料对于获得2K1C动物模型的可靠和可重复数据至关重要。根据Lorenz等人的说法，使用传统的U型设计银夹诱导高血压的成功率较低（40-60%）21。由于夹子设计，肾动脉被横向压压，引发一些收缩和更大的概率从肾动脉中移出。银的延展性和延展性可能允许夹子宽度的变化;因此，在小鼠中引起不同的高血压水平。夹子上的二氧化银可引起血管周围炎症、内膜增殖和组织肉芽形成，改变肾动脉直径22。由于用常规U-design银夹获得的高血压水平的可变性，Warner等人和Lorenz等人已经成功地使用圆形设计的聚氨酯管来启动小鼠的肾动脉狭窄，从而产生更可靠和一致的诱导两肾一夹动物模型20，21。
在这份报告中，我们描述了一种手术方案，以在小鼠中产生实验性RAStenosis，使用聚氨酯管来收缩肾动脉。聚氨酯圆形设计袖口是一种更具可重复性，可靠性和低成本的夹子，可在小鼠中产生狭窄。该实验模型的目标是研究和定义肾动脉狭窄期间肾素表达控制的分子和细胞机制。我们通过测量肾素表达和肾损伤标志物中性粒细胞明胶酶相关脂质运载蛋白（N-GAL）来确认RAS狭窄小鼠模型的成功。

<table><tbody><tr><td>Diet Gel</td><td>Clear H&lt;sub&gt;2&lt;/sub&gt;O</td><td>Diet-Gel 76A</td><td>Surgery recovery diet</td></tr><tr><td>EMC Heated Hard pad</td><td>Hallowell</td><td>000A2788B</td><td>Heating pads were used to keep mice warm</td></tr><tr><td>Ethilon Nylon Suture</td><td>Ethicon</td><td>662G</td><td>4-0 (1.5 metric), This suture was used to close the peritoneum, and skin</td></tr><tr><td>Ethilon Nylon Suture</td><td>Ethicon</td><td>2815 G</td><td>8-0 (0.4 metric), This suture was used to close cuff to tie and constrict the artery</td></tr><tr><td>Germinator 500</td><td>Braintree Scientific Inc.</td><td>GER 5287</td><td>Sterilize surgical tools between surgeries</td></tr><tr><td>Ketoprofen</td><td>Zoetis</td><td>Ketofen</td><td>Painkiller</td></tr><tr><td>Polyurethane</td><td>Braintree Scientific Inc.</td><td>MRE-025</td><td>This tube was used to initiate stenosis</td></tr><tr><td>Povidone-iodine antiseptic swabsticks</td><td>Medline</td><td>MDS093901</td><td>It was applied after hair removal and surgery on the skin</td></tr><tr><td>Reflex 7 Clip Applier</td><td>Roboz Surgical Instrument Co</td><td>204-1000</td><td>This clip applier was used to apply clip in case one or more sutures went off</td></tr><tr><td>Sterile towel drapes</td><td>Dynarex</td><td>4410</td><td>It was used as a bedsheet for mice during surgery</td></tr><tr><td>Triple antibiotic ointment</td><td>Medi-First</td><td>22312</td><td></td></tr><tr><td>Water pump</td><td>Stryker</td><td>T/pump Professionals</td><td>Used to warm and circulate water in the heating hard pad to keep mice warm during and post-surgery</td></tr></tbody></table>

a modified two kidney one clip mouse model of renin regulation in renal artery stenosis

肾动脉狭窄是冠状动脉或外周血管疾病患者的常见病症，其中肾素血管紧张素醛固酮系统（RAAS）过度活化。在这种情况下，肾动脉变窄，刺激肾素（RAAS中的限速蛋白酶）表达和释放的增加。由此产生的肾素表达升高是肾血管性高血压的已知驱动因素，通常与肾损伤和终末器官损伤有关。因此，人们对开发针对这种情况的新疗法非常感兴趣。肾动脉狭窄中肾素控制的分子和细胞机制尚不完全清楚，需要进一步研究。为了诱导小鼠肾动脉狭窄，开发了一种修饰的2肾1夹（2K1C）Goldblatt小鼠模型。野生型小鼠右肾被冷冻，假手术小鼠用作对照。肾动脉狭窄后，我们确定了肾素表达和肾损伤。收获肾脏，并使用新鲜皮质来确定肾素的蛋白质和mRNA表达。该动物模型是可重复的，可用于研究参与肾血管性高血压和肾损伤的病理生理学反应，分子和细胞途径。

肾动脉收缩增加狭窄肾中的肾素表达，同时抑制对侧肾的表达。狭窄的两个肾一夹（2K1C）或Goldblatt模型诱导肾素表达增加和肾损伤。这被认为是人类单侧肾动脉狭窄的最佳代表性模型。
使用免疫印迹法测量肾素和原脯素（肾素的前体）的表达。数据显示，与对侧肾和假肾相比，狭窄肾中的肾素和原脯素表达增加，表明袖带收缩肾动脉，导致肾灌注改变（图1</s...

Watch this Scientific Journal Video about A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis at JoVE.com

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

使用聚氨酯管开发改良的2肾1夹（2K1C）Goldblatt小鼠模型以启动肾动脉狭窄，诱导肾素表达增加和肾损伤。在这里，我们描述了准备袖带并将其置于肾动脉上以产生可重复且一致的2K1C小鼠模型的详细程序。

肾动脉狭窄肾素调节的改良双肾单夹小鼠模型

Renal artery stenosis is a common condition in patients with coronary or peripheral vascular disease where the renin angiotensin aldosterone system (RAAS) ...

a-modified-two-kidney-one-clip-mouse-model-renin-regulation-renal

Research

JoVE Journal

Medicine

4.6K 次观看.  Vanderbilt University Medical Center. 使用聚氨酯管开发改良的2肾1夹（2K1C）Goldblatt小鼠模型以启动肾动脉狭窄，诱导肾素表达增加和肾损伤。在这里，我们描述了准备袖带并将其置于肾动脉上以产生可重复且一致的2K1C小鼠模型的详细程序。

视频: A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

Use of a Hanging-weight System for Isolated Renal Artery Occlusion

In hospitalized patients, over 50% of cases of acute kidney injury (AKI) are caused by renal ischemia 1-3. A recent study of hospitalized patients revealed that only a mild increase in serum creatinine levels (0.3 to 0.4 mg/dl) is associated with a 70% greater risk of death than in persons without any increase 1. Along these lines, surgical procedures requiring cross-clamping of the aorta and renal vessels are associated with a renal failure rates of up to 30% 4. Similarly, AKI after cardiac surgery occurs in over 10% of patients under normal circumstances and is associated with dramatic increases in mortality. AKI are also common complications after liver transplantation. At least 8-17% of patients end up requiring renal replacement therapy 5. Moreover, delayed graft function due to tubule cell injury during kidney transplantation is frequently related to ischemia-associated AKI 6. Moreover, AKI occurs in approximately 20% of patients suffering from sepsis 6.The occurrence of AKI is associated with dramatic increases of morbidity and mortality 1. Therapeutic approaches are very limited and the majority of interventional trials in AKI have failed in humans. Therefore, additional therapeutic modalities to prevent renal injury from ischemia are urgently needed 3, 7-9. 
To elucidate mechanisms of renal injury due to ischemia and possible therapeutic strategies murine models are intensively required 7-13. Mouse models provide the possibility of utilizing different genetic models including gene-targeted mice and tissue specific gene-targeted mice (cre-flox system). However, murine renal ischemia is technically challenging and experimental details significantly influence results. We performed a systematic evaluation of a novel model for isolated renal artery occlusion in mice, which specifically avoids the use of clamping or suturing the renal pedicle 14. This model requires a nephrectomy of the right kidney since ischemia can be only performed in one kidney due to the experimental setting. In fact, by using a hanging-weight system, the renal artery is only instrumented once throughout the surgical procedure. In addition, no venous or urethral obstruction occurs with this technique. We could demonstrate time-dose-dependent and highly reproducible renal injury with ischemia by measuring serum creatinine. Moreover, when comparing this new model with conventional clamping of the whole pedicle, renal protection by ischemic preconditioning is more profound and more reliable. Therefore his new technique might be useful for other researchers who are working in the field of acute kidney injury.

A precise murine model for acute kidney injury (AKI) due to ischemia is an important tool to investigate acute kidney injury and possibly find therapeutic tools to treat renal injury. The hanging weight system offers a tool for immediate and reliable renal artery occlusion and reperfusion without causing renal congestion.

一个悬重系统使用隔离肾动脉闭塞

In hospitalized patients, over 50% of cases of acute kidney injury (AKI) are caused by renal ischemia 1-3. A recent study of hospitalized patients ...

科研

医学

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration

Renal ischaemia reperfusion injury (IRI) is a common cause of acute kidney injury (AKI) in patients and occlusion of renal blood flow is unavoidable during renal transplantation. Experimental models that accurately and reproducibly recapitulate renal IRI are crucial in dissecting the pathophysiology of AKI and the development of novel therapeutic agents. Presented here is a mouse model of renal IRI that results in reproducible AKI. This is achieved by a midline laparotomy approach for the surgery with one incision allowing both a right nephrectomy that provides control tissue and clamping of the left renal pedicle to induce ischaemia of the left kidney. By careful monitoring of the clamp position and body temperature during the period of ischaemia this model achieves reproducible functional and structural injury. Mice sacrificed 24 hr&#160;following surgery demonstrate loss of renal function with elevation of the serum or plasma creatinine level as well as structural kidney damage with acute tubular necrosis evident. Renal function improves and the acute tissue injury resolves during the course of 7 days following renal IRI such that this model may be used to study renal regeneration. This model of renal IRI has been utilized to study the molecular and cellular pathophysiology of AKI as well as analysis of the subsequent renal regeneration.

The mouse model of renal ischaemia reperfusion injury described here comprises of a right nephrectomy that provides control tissue and clamping of the left renal pedicle to induce ischaemia that results in acute kidney injury. This model uses a midline laparotomy approach with all steps performed via one incision.

肾缺血再灌注损伤:损伤的小鼠模型和再生

Renal ischaemia reperfusion injury (IRI) is a common cause of acute kidney injury (AKI) in patients and occlusion of renal blood flow is unavoidable ...

Transcutaneous Assessment of Renal Function in Conscious Rodents

Glomerular filtration rate (GFR) is the gold standard to assess overall kidney function. However, traditional methods to evaluate GFR are cumbersome and time-consuming. In addition, serial blood or urine samples are required, with the associated stress for the experimental animals. A recent technique significantly reduces the investment in time and resources, minimizing the invasiveness and the animal stress, but being equally valid as the traditional approaches. The method measures transcutaneously renal function. Using an optical device and the exogenous renal marker fluorescein isothiocyanate (FITC)-sinistrin, this technique is capable of measuring the elimination kinetics of the marker through the skin. With neither blood nor urine samples nor the associated laboratory assays needed, the results of the transcutaneous measurement are almost instantaneously available. The method has been already validated in different species and successfully applied in several models of renal pathology. Moreover, due to its minimally invasive characteristics, it is suitable for sequential measurements within the same animal. Here is provided a detailed protocol to carry out the transcutaneous assessment of renal function in rodents.

Determination of glomerular filtration rate (GFR) is the gold standard to assess overall kidney function. However, traditional procedures to measure this parameter are cumbersome and require a large investment of time. Here we describe a faster and minimally invasive method to determinate GFR transcutaneously.

在鼠害自觉肾功能的评估皮

Glomerular filtration rate (GFR) is the gold standard to assess overall kidney function. However, traditional methods to evaluate GFR are cumbersome and ...

An Effective Mouse Model of Unilateral Renal Ischemia-Reperfusion Injury

Ischemia-reperfusion injury (IRI) is the leading cause of acute renal failure and is a significant contributor to delayed graft function. Animal models are the only available resources that mimic the complexities of the IRI-associated damage encountered in vivo. This paper describes an effective mouse model of unilateral renal IRI that delivers highly reproducible data. Ischemia is induced by occluding the right renal pedicle for 30 min followed by reperfusion. In addition to the surgical procedure, a sequential overview of the expected physiological and histopathological changes following renal IRI will be provided by comparing data from seven different reperfusion times (4 h, 8 h, 16 h, 1 day, 2 days, 4 days, and 7 days). Critical data for planning experiments ahead, such as mean surgical time, average anesthetic consumption, and body weight changes over time, will be shared. This work will help researchers implement a reliable renal IRI model and select the appropriate reperfusion time that aligns with their intended investigative goals.

Renal ischemia-reperfusion injury is associated with high morbidity and mortality in hospitalized patients. Here, we present a simple and effective mouse model of unilateral renal ischemia-reperfusion injury and provide a sequential overview of representative pathological changes observed in the kidney.

单侧肾缺血再灌注损伤的有效小鼠模型

Ischemia-reperfusion injury (IRI) is the leading cause of acute renal failure and is a significant contributor to delayed graft function. Animal models ...

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

The benefits of renal sympathetic denervation (RDN) on blood pressure have been proved in a large number of clinical trials in recent years. However, the regulatory mechanism of RDN on hypertension remains elusive. Thus, it&#39;s essential to establish a simpler RDN model in mice. In this study, osmotic mini pumps filled with Angiotensin II were implanted in 14-week-old C57BL/6 mice. One week after the implantation of the mini-osmotic pump, a modified RDN procedure was performed on bilateral renal arteries of the mice using phenol. Age-sex-matched mice were given saline and served as sham group. Blood pressure was measured at baseline and every week subsequently for 21 days. Then, renal artery, abdominal aorta and heart were collected for histological examination using H&#38;E and Masson staining. In this study, we present a simple, practical, repeatable, and standardized RDN model, which can control hypertension and alleviate cardiac hypertrophy. The technique can denervate peripheral renal sympathetic nerves without renal artery damage. Compared to previous models, the modified RDN facilitates the study of the pathobiology and pathophysiology of hypertension.

Here, we present a protocol for renal sympathetic denervation (RDN) in mice with hypertension induced by Angiotensin II infusion. The procedure is repeatable, convenient and allows to study the regulatory mechanisms of RDN on hypertension and cardiac hypertrophy.

改善肾去神经支配缓解血管紧张素II.诱导的高血压

The benefits of renal sympathetic denervation (RDN) on blood pressure have been proved in a large number of clinical trials in recent years. However, the ...

A Murine Model of Hemodialysis Access-Related Hand Dysfunction

Chronic kidney disease is a major public health problem, and the prevalence of end-stage renal disease (ESRD) requiring chronic renal replacement therapies such as hemodialysis continues to increase. Autogenous arteriovenous fistula (AVF) placement remains a primary vascular access option for ESRD patients. Unfortunately, approximately half of the hemodialysis patients experience dialysis access-related hand dysfunction (ARHD), ranging from subtle paresthesia to digital gangrene. Notably, the underlying biologic drivers responsible for ARHD are poorly understood, and no adequate animal model exists to elucidate the mechanisms and/or develop novel therapeutics for the prevention/treatment of ARHD. Herein, we describe a new mouse model in which an AVF is created between the left common iliac artery and vein, thereby facilitating the assessment of limb pathophysiology. The microsurgery includes vessel isolation, longitudinal venotomy, creation of arteriovenous anastomosis, and venous reconstruction. Sham surgeries include all the critical steps except for AVF creation. Iliac AVF placement results in clinically relevant alterations in central hemodynamics, peripheral ischemia, and impairments in hindlimb neuromotor performance. This novel preclinical AVF model provides a useful platform that recapitulates common neuromotor perturbations reported by hemodialysis patients, allowing researchers to investigate the mechanisms of ARHD pathophysiology and test potential therapeutics.

This protocol details the surgical steps of murine common iliac arteriovenous fistula creation. We developed this model to study hemodialysis access-related limb pathophysiology.

血液透析通路相关手功能障碍的小鼠模型

Chronic kidney disease is a major public health problem, and the prevalence of end-stage renal disease (ESRD) requiring chronic renal replacement ...

The Mouse Isolated Perfused Kidney Technique

The mouse isolated perfused kidney (MIPK) is a technique for keeping a mouse kidney under ex vivo conditions perfused and functional for 1 hr. This is a prerequisite for studying the physiology of the isolated organ and for many innovative applications that may be possible in the future, including perfusion decellularization for kidney bioengineering or the administration of anti-rejection or genome-editing drugs in high doses to prime the kidney for transplantation. During the time of the perfusion, the kidney can be manipulated, renal function can be assessed, and various pharmaceuticals administered. After the procedure, the kidney can be transplanted or processed for molecular biology, biochemical analysis, or microscopy.
This paper describes the perfusate and the surgical technique needed for the ex vivo perfusion of mouse kidneys. Details of the perfusion apparatus are given and data are presented showing the viability of the kidney&#39;s preparation: renal blood flow, vascular resistance, and urine data as functional, transmission electron micrographs of different nephron segments as morphological readouts, and western blots of transport proteins of different nephron segments as molecular readout.

The mouse isolated perfused kidney (MIPK) is a technique for keeping a mouse kidney under ex vivo conditions perfused and functional for 1 hr. The buffers and surgical technique are described in detail.

鼠标离体肾技术

The mouse isolated perfused kidney (MIPK) is a technique for keeping a mouse kidney under ex vivo conditions perfused and functional for 1 hr. This is a ...

生物学

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Chronic kidney disease (CKD) is a great risk factor for cardiovascular disease events and mortality, and progressively develops to the clinical phenotype called "uremic cardiomyopathy". We describe here an experimental CKD mouse model, named 5/6th partial nephrectomy (PNx) with pole ligation, which developed uremic cardiomyopathy at four weeks post-surgery. This PNx model was performed by a two-step surgery. In step-one surgery, both poles of the left kidney were ligated. In step-two surgery, which was performed 7 days after the step-one surgery, the right kidney was removed. For the sham surgery, the same surgery procedures were performed but without pole ligation of the left kidney or removal of the right kidney. The surgical procedures are easier and less time-consuming, compared to other methods. However, the remnant functional renal mass is not as easily controlled as the renal artery ligation. Four weeks after surgery, in comparison with the sham-operated mice, the PNx mice developed impaired renal function, anemia, cardiac hypertrophy, cardiac fibrosis, and decreased heart systolic and diastolic function.

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

This manuscript provides a detailed two-step surgical procedure to perform mouse 5/6th partial nephrectomy (PNx) with pole ligation. Four weeks after surgery, in comparison with sham-operated mice, the PNx mice developed impaired renal function, anemia, cardiac hypertrophy, cardiac fibrosis, and decreased heart systolic and diastolic function.

一种诱导实验性尿毒症心肌病的小鼠 5/6th肾切除模型

Chronic kidney disease (CKD) is a great risk factor for cardiovascular disease events and mortality, and progressively develops to the clinical phenotype ...

<meta charset="utf8"></head><body>大鼠标准化 5/6 肾切除术治疗肾功能不全和灌注不良

5/6 Nephrectomy Using Sharp Bipolectomy Via Midline Laparotomy in Rats

Chronic kidney disease (CKD) affects over 10% of the global population, amounting to more than 800 million individuals worldwide. The advances in the treatment of CKD have had a significant impact on patient outcomes. While in the past, CKD was often considered a death sentence, with many patients succumbing to the complications of end-stage renal disease, it is now increasingly being managed as a chronic condition with the availability of dialysis and kidney transplantation, as well as new pharmaceutical developments such as SGLT2 inhibitors or nonsteroidal mineralocorticoid receptor antagonists. 
Yet, there continues to be a growing demand for further exploration into the pathophysiological processes and potential therapeutic interventions. Reliable biological models play a crucial role in facilitating this research. Given the multifaceted nature of renal disease, which encompasses not only cell biology but also vascular microanatomy and endocrine signaling, an appropriate model must possess a level of biological complexity that only an animal model can offer, rendering rodents an obvious choice.
This manuscript, therefore, provides an intricate, systematic protocol for surgically reducing renal parenchyma through midline laparotomy and combined total and partial nephrectomy in rats for survival as well as non-survival applications. It emphasizes the critical role of precise surgical techniques in ensuring consistent and reliable outcomes. Prime examples of potential applications for this model include biomolecular and pharmaceutical studies as well as the development of innovative intraoperative imaging modalities, such as hyperspectral imaging, to objectively visualize and differentiate renal malperfusion.

<meta charset="utf8"></head><body>5/6 大鼠使用中线剖腹手术进行 Sharp Bipolectomy 的肾切除术

This manuscript introduces a standardized protocol for a 5/6 nephrectomy by sharp bipolectomy via midline laparotomy in a rat model, aiming to induce a state of renal insufficiency via renal parenchyma reduction with a great degree of methodical precision and low risk of technical error.

5/6 大鼠使用中线剖腹手术进行 Sharp Bipolectomy 的肾切除术

Chronic kidney disease (CKD) affects over 10% of the global population, amounting to more than 800 million individuals worldwide. The advances in the ...

肾动脉狭窄肾素调节的改良双肾单夹小鼠模型

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一种诱导实验性尿毒症心肌病的小鼠 5/6^th肾切除模型

5/6 大鼠使用中线剖腹手术进行 Sharp Bipolectomy 的肾切除术

5/6 大鼠使用中线剖腹手术进行 Sharp Bipolectomy 的肾切除术