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저자는 이익에 대한 재무 충돌이 없습니다.

여기에 설명 된 모델은 인간에서 발견 된 것과 유사한 부상을 제공, 심장 마비와 심폐 소생술의 결과로 발생할 수있는 뇌에 허혈성 모욕을 생산하고 있습니다. 세계적인 뇌 허혈을 생산하는이 방법은 여러 프로토콜 중 하나입니다. 우리는 그것의 비교적 낮은 사망률, 빠른 복구 및 재현성 결과를 제일이 프로토콜을 사용합니다. 심장 마비 / 소생 모델 그러나 기술적으로, 틀림없이 지속적으로 재?...

심장 마비와 뇌졸중의 결과로 뇌 손상 죽음 및 장기 장애의 주요 원인이다. 심장 마비의 피해자를위한 심폐 소생술은 환자의 60 % 이후에 병원에서 사망 적어도 광범위한 뇌 손상의 결과로 미국의 7,8에서 연간 약 70,000 환자의 자발 순환 회복에 성공하면서 만 3-10% 소생 환자의 9,10은 그들의 이전 생활을 다시 시작할 수 있습니다. 분명히, 글로벌 뇌 허혈 다음과 신경 외상을 최소화하기 위해 치료 개입을 설계 뇌 손상으로 이어질 메커니즘을 이해하는 것은 매우 중요합니다. 뇌 허혈 여러 방법을 이용하여 모델링 할 수 있습니다. 가장 일반적으로, 뇌 허혈 따라서 초점 허혈성 뇌졸중 11,12 생산, 두뇌, 중대 뇌동맥의 주요 혈관을 폐색하여 설치류에서 생산된다. 임상 적으로 중요한 반면,국소 뇌 허혈은 심장 마비 / 소생술 의해 뇌 손상을 연구하는 정확한 방법이 아닙니다. 이 임상 패러다임을 모델링하기 위해 전체 뇌 허혈성 혈액 흐름의 재 도입에 선행되어야한다. 밀접하게이 임상 프레 젠 테이션을 모방하기 위해 수사관들이 실험적으로 심폐 소생술 및 제세동 13,14와 심폐 소생술 다음 심장 마비를 유도. 이 모델은 임상 적으로 관련이 있지만 예측할 수없는 심폐 소생술 시간은 변동성을 증가시킬 수하고 해석하는 데이터 분석을 어렵게 만들 수 있습니다. 또한이 모델은 더 이상 가설을 테스트하기 위해 필요한 동물의 수를 증가 높은 사망률과 연관됩니다. 더 재현성, 일관성 있고, 존속 모욕의 허혈 및 / 또는 재관류에 대한 뇌 반응을 조사하는 것이 바람직 할 수있다. 체계적 일부 혈액의 흐름을 유지하면서 허혈은 뇌에 유도 할 수 있습니다. investigatio을 허용하면서이 사망률을 감소N 뇌 2 조직 손상의 메커니즘. 세계적인 뇌 허혈을 생산하기 위해, 중단 또는 크게 뇌, 내부 경동맥 동맥과 척추 동맥을 공급하는 모든 네 개의 혈관의 흐름을 제한 할 필요가있다. 이러한 혈관 문합 루프를 형성 윌리스의 원이라는 혈관 구조를 통해 혈액의 흐름과 뇌를 제공합니다. 이 혈관 구조는 뇌가 근위부 혈관 폐색의 경우에 관류를 유지 할 수 있습니다. 따라서 모든 기여 혈관을 통해 뇌 혈류의 완전한 허혈을 유도하는 것은 발생해야합니다. 경동맥 폐색이 원하는 기간 동안 동맥류 클립의 최소 침습 복부 목 컷 아래로 응용 프로그램을 사용하여 수행 할 수 있습니다. 그들은 척추의 가로 foramina에 incased대로 척추 동맥을 통해 혈액의 흐름 중단이 어려울 수 있습니다. 연구자들은 경동맥 이전에 척추 동맥에게 24-48 시간을 electrocauterizing하여이를 해결했다폐색 및 뇌 허혈 (4VO 모델) 15. 이 방법과는 대조적으로, 스미스 등은. 줄임으로써 글로벌 뇌 허혈을 유도하는 혈액의 흐름이 2 손실 또는 크게 감소 점에 척추 동맥을 통해 혈류를 줄이기 위해 40 mmHg로에 체계적 동맥 혈압 (MAP)을 의미하는 방법을 개발 . 경동맥 폐색과 함께 사용할 경우,이 메소드는 밀접하게 심장 마비 생존자의를 모방 뇌 손상의 패턴의 결과로, 전뇌에 걸쳐 국소 빈혈을 생산하고 있습니다. 이 방법의 추가 정제에, 우리가 여기에 존재하는 모델은 30 mmHg로에 꽉 MAP 규제 ± 1mHg 허혈의 전체 8 분 동안 필요합니다. 우리는 스미스 등에 의해 설계된 독자적인 기술의 낮은 사망률을 유지하면서이 변경이 모델에 의해 유도 된 뇌 손상의 재현성을 향상하였습니다. 세포의 죽음과 조직 손상의 전체 범위의 정확한 표현형에 의한여기에 제시된 모델은 허혈성 기간 16 직접 따라 달라집니다. CA1 뉴런은 재관류 단계 15,17 동안 치료 적 개입에 대한 시간적 창 있다는 것을 제안, 세포 죽음을 지연 허혈 8 분을 나타내는 다음. 재관류의 발병, 신경 신속하게 기능을 회복하고 직접적인 세포의 죽음은 18 감지되지 않습니다. 그러나이 모욕 원인이 세포 죽음 계곡의 유도 (세포 사멸)는 재관류 3,19 ~ 6 시간 사이의 시토크롬 C를 포함한 미토콘드리아에서 apoptogenic 단백질의 방출에 절정에 달하다.에게 재관류 시간 6 사이 24 CA1 해마의 신경 세포 죽음에 최선을 다하고 있고, 사멸 세포 죽음 프로그램은 19 실행됩니다. 그것은 허혈성 손상에 대한 책임이 세포 사멸 표현형은 매우 논쟁 주목해야한다. 다른 사람이 apopt을보고하면서 초기 연구는 괴사는 기본 세포 사멸 표현형 20,21입니다 제안주요 메커니즘 22,23으로 OSIS. 전체에서 현재의 증거는 셀 고전 고사에서 괴사에 이르기까지 셀 죽음 표현형의 스펙트럼 죽을 것이 좋습니다. 세포 죽음의 특정 모드는 각 표현형의 기여의 정도가 다른 요인 24,25 사이, 모욕의 정도에 따라서, 여러 요인에 따라 달라집니다. 재관류 24 시간으로 죽어가는 세포 pyknotic 핵, 집계 세포 내용의 명확한 증거 응축 세포질 및 기능 미토콘드리아 형태의 손실을 가지고있다. 죽은 세포는 더욱 세분화 식세포 및 / 또는 미세 아교 세포와 같은 면역 세포에 의해 침몰하고, CA1 해마 영역에서 삭제됩니다. 재관류 4-7 일까지, 죽은 세포를 제거하고, 모든 남아 염증 세포이며, glial 세포에게 17,26을 활성화됩니다. 따라서 재관류 7 일 CA1 해마 신경 세포의 죽음에 간단한, 비 특​​정 세포 얼룩을 사용하여 정량화 할 수있는 최적의 시간을 나타냅니다크레 실 바이올렛 hemotoxylin - 에오신을 CLUDING 및 형태 학적 포함 기준에 따라 계산. 이 말 재관류 간격으로 나머지 세포는 따라서 뇌 손상의 인덱스를 제공, 생존 세포로 간주 될 수 있습니다. 이 모델은 치료 개입을 테스트하기 위해 활용 될 경우, 실험 설계는 계단 기준 (행정 치료 학술 산업 원탁 회의) 27를 따라하는 것이 좋습니다. 설계 및 연구를 수행 할 때 다음 지침을 준수해야한다 그러나 여기에서 설명하지 않습니다.

<table border="1">
 <tbody>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Material Name</td>
 </tr>
 <tr>
 <td>5-0 VICRYL suture, reverse cutting </td>
 <td>Ethicon</td>
 <td>J391H</td>
 <td></td>
 </tr>
 <tr>
 <td>Scalpel, No.10</td>
 <td>Swann-Morton</td>
 <td>6601</td>
 <td></td>
 </tr>
 <tr>
 <td>Gauze Sponges</td>
 <td>Fisher</td>
 <td>22-362-178</td>
 <td></td>
 </tr>
 <tr>
 <td>18G x 1 &frac12; in needle</td>
 <td>BD</td>
 <td>305201</td>
 <td></td>
 </tr>
 <tr>
 <td>23G x 1 in needle</td>
 <td>BD</td>
 <td>305145</td>
 <td></td>
 </tr>
 <tr>
 <td>26 G x 3/8 in needle</td>
 <td>BD</td>
 <td>305110</td>
 <td></td>
 </tr>
 <tr>
 <td>18 G x 1 &frac14; catheter</td>
 <td>EXEL</td>
 <td>26735</td>
 <td></td>
 </tr>
 <tr>
 <td>1 ml syringe</td>
 <td>BD</td>
 <td>309659</td>
 <td></td>
 </tr>
 <tr>
 <td>10 ml syringe</td>
 <td>BD</td>
 <td>309604</td>
 <td></td>
 </tr>
 <tr>
 <td>60 ml syringe</td>
 <td>BD</td>
 <td>309653</td>
 <td></td>
 </tr>
 <tr>
 <td>Surgilube</td>
 <td>Henry Schein</td>
 <td>1152666</td>
 <td></td>
 </tr>
 <tr>
 <td>.9% Saline, plastic IV bag</td>
 <td>Henry Schein</td>
 <td>1537468</td>
 <td></td>
 </tr>
 <tr>
 <td>Suture 3-0 Silk</td>
 <td>Henry Schein</td>
 <td>1007842</td>
 <td></td>
 </tr>
 <tr>
 <td>Puralube Ophthalmic Ointment</td>
 <td>Henry Schein</td>
 <td>3390017</td>
 <td></td>
 </tr>
 <tr>
 <td>Betadine</td>
 <td>Henry Schein</td>
 <td>6903564</td>
 <td></td>
 </tr>
 <tr>
 <td>Sterile Towel Drape</td>
 <td>Moore Medical</td>
 <td>14170</td>
 <td></td>
 </tr>
 <tr>
 <td>Polyethylene Tubing, 50</td>
 <td>Intramedic</td>
 <td>427411</td>
 <td></td>
 </tr>
 <tr>
 <td>Stopcock, 3 way</td>
 <td>Smiths medical</td>
 <td>MX9311L</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Drug Name</td>
 </tr>
 <tr>
 <td>AERRANE (isoflurane)</td>
 <td>Henry Schein</td>
 <td>2091966</td>
 <td></td>
 </tr>
 <tr>
 <td>Mapap Liquid (Tylenol)</td>
 <td>Major Pharmaceuticals</td>
 <td>1556</td>
 <td></td>
 </tr>
 <tr>
 <td>Kedavet (ketamine)</td>
 <td>Ketathesia Butney</td>
 <td>NDC 50989-996-06</td>
 <td></td>
 </tr>
 <tr>
 <td>Butorphic (butorphanol)</td>
 <td>Lloyd Labs</td>
 <td>4881</td>
 <td></td>
 </tr>
 <tr>
 <td>Heparin</td>
 <td>APP Pharmaceuticals</td>
 <td>504011</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Chemical Name </td>
 </tr>
 <tr>
 <td>Paraformaldehyde prills</td>
 <td>Elecron Microscopy Sci.</td>
 <td>19202</td>
 <td></td>
 </tr>
 <tr>
 <td>2-methylbutane</td>
 <td>Sigma</td>
 <td>270342</td>
 <td></td>
 </tr>
 <tr>
 <td>Cresyl Violet Acetate</td>
 <td>Sigma</td>
 <td>C5042</td>
 <td></td>
 </tr>
 <tr>
 <td>Sucrose</td>
 <td>Sigma</td>
 <td>S9378</td>
 <td></td>
 </tr>
 <tr>
 <td></td>
 <td></td>
 <td></td>
 <td>Software</td>
 </tr>
 <tr>
 <td>ImageJ</td>
 <td>NIH</td>
 <td></td>
 <td></td>
 </tr>
 </tbody>
</table>

2-vessel occlusion/hypotension: a rat model of global brain ischemia

소생 뒤에 심장 마비는 종종 허혈 뇌의 후속 재관류에 의한 극적인 뇌 손상 발생합니다. 글로벌 두뇌 국소 빈혈 빈혈 1에 매우 민감한 것으로 나타 특정 뇌 영역에 손상을 생산하고 있습니다. 해마의 뉴런은 특히 다른 세포 집단과 비교하여 허혈성 모욕 높은 감도를 가지고 해마의 CA1 지역은 허혈 / 재관류 2에 특히 취약합니다. 치료 개입, 또는 뇌 손상에 관련된 메커니즘 연구의 설계는 임상 상태와 유사한 재현 방식으로 손상을 생산하는 모델을 필요로한다. 저혈압과의 양자 경동맥 혈관 폐색 (2VOH) 심장 마비와 심폐 소생술 중에 발생할 수있는 대뇌 이벤트를 에뮬레이트 가역 전뇌 허혈을 생산하는 모델입니다. 우리는 스미스 등의 수정 모델에 대해 설명합니다. (1984) 2같은 첫 번째 샌더슨 등. (2008) 3, 선택적으로 취약한 뇌 영역 3-6 재현성 부상을 생산하고있는 현재의 형태로 제시. 이 모델의 신뢰성은 적용 성 저혈압, 허혈 기간, 주변 온도 제어, 특정 마취 요법, 그리고 근면 수술 후 치료 기간 동안 전신 혈압의 정밀 제어에 의해 결정됩니다. 덜 취약 뇌 영역이 절약되는 동안 8 분 허혈성 모욕, 재관류 6 ~ 24 시간의 과정을 통해 진행 CA1 해마 신경 세포의 죽음을 생산하고 있습니다. 이 진보적 인 세포의 죽음은 쉽게 CA1 뉴런의 가까운 완전한 손실이 시점에서 분명로서, 재관류 7-14일 후 계량입니다. 이 뇌 손상 모델 이외에, 우리는 간단하면서도 철저한 방법론을 사용 CA1 손상을 정량화하기위한 방법을 제시한다. 중요한 것은, 정량화는 간단한 카메라 장착 현미경을 사용하여 수행 할 수 있습니다다 무료 ImageJ에 (NIH) 소프트웨어 플러그인, 엄청난 비용 stereology 소프트웨어 프로그램의 필요성 및 손상 평가를위한 전동 현미경 스테이지를 미연에 방지.

세계적인 뇌 허혈 / 재관류 2VOH 모델은 해마의 CA1 영역에서 신경 세포의 죽음의 원인이됩니다. 그림 2이 14 일 재관류 후 처리 세계적인 뇌 허혈 8 분에 의해 생성 부상을 나타냅니다. 그림 2A와 2B는 가짜의 해마를 비교하고 크레 실 바이올렛으로 염색 후 허혈성 뇌. 그림 2A는 그대로 CA1 등 정상적인 형태를 전시 가짜로 작동하는 쥐의 해마를 보여줍니다. ?...

Watch this Scientific Journal Video about 2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia at JoVE.com

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

전신 저혈압과 함께 양측 경동맥 폐색 재현 심각도 해마에 손​​상 쥐 세계적인 뇌 허혈을 생산하고 있습니다. 동물의 주제는 뇌 손상의 예측 패턴 장애인, 그들은 적당하게 복구하고, 사망률은 상대적으로 낮다.

2 혈관 폐색 / 저혈압 : 세계적인 두뇌 국소 빈혈의 쥐 모델

Cardiac arrest followed by resuscitation often results in dramatic brain damage caused by ischemia and subsequent reperfusion of the brain. Global brain ...

2-vessel-occlusionhypotension-a-rat-model-of-global-brain-ischemia

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JoVE Journal

Medicine

19.8K 조회수.  Wayne State University School of Medicine. 전신 저혈압과 함께 양측 경동맥 폐색 재현 심각도 해마에 손​​상 쥐 세계적인 뇌 허혈을 생산하고 있습니다. 동물의 주제는 뇌 손상의 예측 패턴 장애인, 그들은 적당하게 복구하고, 사망률은 상대적으로 낮다.

비디오: 2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

MRI-guided Disruption of the Blood-brain Barrier using Transcranial Focused Ultrasound in a Rat Model

Focused ultrasound (FUS) disruption of the blood-brain barrier (BBB) is an increasingly investigated technique for circumventing the BBB1-5. The BBB is a significant obstacle to pharmaceutical treatments of brain disorders as it limits the passage of molecules from the vasculature into the brain tissue to molecules less than approximately 500 Da in size6. FUS induced BBB disruption (BBBD) is temporary and reversible4 and has an advantage over chemical means of inducing BBBD by being highly localized. FUS induced BBBD provides a means for investigating the effects of a wide range of therapeutic agents on the brain, which would not otherwise be deliverable to the tissue in sufficient concentration. While a wide range of ultrasound parameters have proven successful at disrupting the BBB2,5,7, there are several critical steps in the experimental procedure to ensure successful disruption with accurate targeting. This protocol outlines how to achieve MRI-guided FUS induced BBBD in a rat model, with a focus on the critical animal preparation and microbubble handling steps of the experiment.

Microbubble-mediated focused ultrasound disruption of the blood-brain barrier (BBB) is a promising technique for non-invasive targeted drug delivery in the brain1-3. This protocol outlines the experimental procedure for MRI-guided transcranial BBB disruption in a rat model.

쥐 모델에서 Transcranial 집중 초음파를 사용하여 혈액 - 뇌 장벽의 MRI를 유도 장애

Focused ultrasound (FUS) disruption of the blood-brain barrier (BBB) is an increasingly investigated technique for circumventing the BBB1-5. The BBB is a ...

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A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion

Surgical trauma by thoracotomy in open-chest models of coronary ligation induces an immune response which modifies different mechanisms involved in ischemia and reperfusion. Immune response includes cytokine expression and release or secretion of endogenous ligands of innate immune receptors. Activation of innate immunity can potentially modulate infarct size. We have modified an existing murine closed-chest model using hanging weights which could be useful for studying myocardial pre- and postconditioning and the role of innate immunity in myocardial ischemia and reperfusion. This model allows animals to recover from surgical trauma before onset of myocardial ischemia.
Volatile anesthetics have been intensely studied and their preconditioning effect for the ischemic heart is well known. However, this protective effect precludes its use in open chest models of coronary artery ligation. Thus, another advantage could be the use of the well controllable volatile anesthetics for instrumentation in a chronic closed-chest model, since their preconditioning effect lasts up to 72 hours. Chronic heart diseases with intermittent ischemia and multiple hit models are other possible applications of this model.
For the chronic closed-chest model, intubated and ventilated mice undergo a lateral blunt thoracotomy via the 4th intercostal space. Following identification of the left anterior descending a ligature is passed underneath the vessel and both suture ends are threaded through an occluder. Then, both suture ends are passed through the chest wall, knotted to form a loop and left in the subcutaneous tissue. After chest closure and recovery for 5 days, mice are anesthetized again, chest skin is reopened and hanging weights are hooked up to the loop under ECG control.
At the end of the ischemia/reperfusion protocol, hearts can be stained with TTC for infarct size assessment or undergo perfusion fixation to allow morphometric studies in addition to histology and immunohistochemistry.

Surgical trauma induces an inflammatory response. Cytokines and endogenous ligands are known to modulate myocardial infarct size following ischemia and reperfusion. We present a modified closed-chest model of murine ischemia and reperfusion using hanging weights to minimize effects of thoracotomy.

심근 국소 빈혈 및 Reperfusion의 Murine 폐쇄 가슴 모델

Surgical trauma by thoracotomy in open-chest models of coronary ligation induces an immune response which modifies different mechanisms involved in ...

Rat Model of Blood-brain Barrier Disruption to Allow Targeted Neurovascular Therapeutics

Endothelial cells with tight junctions along with the basement membrane and astrocyte end feet surround cerebral blood vessels to form the blood-brain barrier1. The barrier selectively excludes molecules from crossing between the blood and the brain based upon their size and charge. This function can impede the delivery of therapeutics for neurological disorders. A number of chemotherapeutic drugs, for example, will not effectively cross the blood-brain barrier to reach tumor cells2. Thus, improving the delivery of drugs across the blood-brain barrier is an area of interest.
The most prevalent methods for enhancing the delivery of drugs to the brain are direct cerebral infusion and blood-brain barrier disruption3. Direct intracerebral infusion guarantees that therapies reach the brain; however, this method has a limited ability to disperse the drug4. Blood-brain barrier disruption (BBBD) allows drugs to flow directly from the circulatory system into the brain and thus more effectively reach dispersed tumor cells. Three methods of barrier disruption include osmotic barrier disruption, pharmacological barrier disruption, and focused ultrasound with microbubbles. Osmotic disruption, pioneered by Neuwelt, uses a hypertonic solution of 25% mannitol that dehydrates the cells of the blood-brain barrier causing them to shrink and disrupt their tight junctions. Barrier disruption can also be accomplished pharmacologically with vasoactive compounds such as histamine5 and bradykinin6. This method, however, is selective primarily for the brain-tumor barrier7. Additionally, RMP-7, an analog of the peptide bradykinin, was found to be inferior when compared head-to-head with osmotic BBBD with 25% mannitol8. Another method, focused ultrasound (FUS) in conjunction with microbubble ultrasound contrast agents, has also been shown to reversibly open the blood-brain barrier9. In comparison to FUS, though, 25% mannitol has a longer history of safety in human patients that makes it a proven tool for translational research10-12.
In order to accomplish BBBD, mannitol must be delivered at a high rate directly into the brain's arterial circulation. In humans, an endovascular catheter is guided to the brain where rapid, direct flow can be accomplished. This protocol models human BBBD as closely as possible. Following a cut-down to the bifurcation of the common carotid artery, a catheter is inserted retrograde into the ECA and used to deliver mannitol directly into the internal carotid artery (ICA) circulation. Propofol and N2O anesthesia are used for their ability to maximize the effectiveness of barrier disruption13. If executed properly, this procedure has the ability to safely, effectively, and reversibly open the blood-brain barrier and improve the delivery of drugs that do not ordinarily reach the brain 8,13,14.

Blood-brain barrier disruption aids the delivery of certain drugs to the brain. Mannitol delivered intra-arterially shrinks cells surrounding blood vessels in order to physically disrupt the barrier.

혈액 - 뇌 장벽 장애의 쥐 모델 Neurovascular 치료학 타겟이 분명한 허용하려면

Endothelial cells with tight junctions along with the basement membrane and astrocyte end feet surround cerebral blood vessels to form the blood-brain ...

In situ Transverse Rectus Abdominis Myocutaneous Flap: A Rat Model of Myocutaneous Ischemia Reperfusion Injury

Free tissue transfer is the gold standard of reconstructive surgery to repair complex defects not amenable to local options or those requiring composite tissue. Ischemia reperfusion injury (IRI) is a known cause of partial free flap failure and has no effective treatment. Establishing a laboratory model of this injury can prove costly both financially as larger mammals are conventionally used and in the expertise required by the technical difficulty of these procedures typically requires employing an experienced microsurgeon. This publication and video demonstrate the effective use of a model of IRI in rats which does not require microsurgical expertise. This procedure is an in situ model of a transverse abdominis myocutaneous (TRAM) flap where atraumatic clamps are utilized to reproduce the ischemia-reperfusion injury associated with this surgery. A laser Doppler Imaging (LDI) scanner is employed to assess flap perfusion and the image processing software, Image J to assess percentage area skin survival as a primary outcome measure of injury.

In situ Transverse Rectus Abdominis Myocutaneous Flap: A Rat Model of Myocutaneous Ischemia Reperfusion Injury

Free tissue transfer is widely employed in reconstructive surgery to restore form and function following oncological resection and trauma. Preconditioning this tissue prior to surgery may improve outcome. This article describes an in situ transverse rectus abdominis myocutaneous flap (TRAM) in rats as a means for testing preconditioning strategies.

Myocutaneous 국소 빈혈 reperfusion 상해의 쥐 모델 : 현장 가로 직근 abdominis의 Myocutaneous 플랩의

Free tissue transfer is the gold standard of reconstructive surgery to repair complex defects not amenable to local options or those requiring composite ...

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Ischemia-Reperfusion (IR) injury is known to contribute significantly to the morbidity and mortality associated with ischemic strokes. Ischemic cerebrovascular accidents account for 80% of all strokes. A common cause of IR injury is the rapid inflow of fluids following an acute/chronic occlusion of blood, nutrients, oxygen to the tissue triggering the formation of free radicals.
Ischemic stroke is followed by blood-brain barrier (BBB) dysfunction and vasogenic brain edema. Structurally, tight junctions (TJs) between the endothelial cells play an important role in maintaining the integrity of the blood-brain barrier (BBB). IR injury is an early secondary injury leading to a non-specific, inflammatory response. Oxidative and metabolic stress following inflammation triggers secondary brain damage including BBB permeability and disruption of tight junction (TJ) integrity.
Our protocol presents an in vitro example of oxygen-glucose deprivation and reoxygenation (OGD-R) on rat brain endothelial cell TJ integrity and stress fiber formation. Currently, several experimental in vivo models are used to study the effects of IR injury; however they have several limitations, such as the technical challenges in performing surgeries, gene dependent molecular influences and difficulty in studying mechanistic relationships. However, in vitro models may aid in overcoming many of those limitations. The presented protocol can be used to study the various molecular mechanisms and mechanistic relationships to provide potential therapeutic strategies. However, the results of in vitro studies may differ from standard in vivo studies and should be interpreted with caution.

Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction

Ischemia-Reperfusion (IR) injury is associated with a high rate of morbidity and mortality. The goal of the in vitro model of oxygen-glucose deprivation and reoxygenation (OGD-R) described here is to assess the effects of ischemia reperfusion injury on a variety of cells, particularly in blood-brain barrier (BBB) endothelial cells.

같은 산소 포도당 박탈과 재산 소화<em&gt; 체외</em&gt; 허혈 - 재관류 손상 모델 공부 뇌 혈관 장벽 부전

Ischemia-Reperfusion (IR) injury is known to contribute significantly to the morbidity and mortality associated with ischemic strokes. Ischemic ...

A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia

Stroke research has endured many setbacks in translating neuroprotective therapies into clinical practice. In contrast, the real-world therapy (tPA thrombolysis) rarely produces benefits in mechanical occlusion-based experimental models, which dominate preclinical stroke research. This split between the bench and bedside suggests the need to employ tPA-responsive models in preclinical stroke research. To this end, a simple and tPA-reactive thrombotic stroke model is invented and described here. This model consists of transient occlusion of the unilateral common carotid artery and delivery of 7.5% oxygen through a face mask in adult mice for 30 min, while maintaining the animal rectal temperature at 37.5 &#177; 0.5 &#176;C. Although reversible ligation of the unilateral carotid artery or hypoxia each suppressed cerebral blood flow only transiently, the combination of both insults caused lasting reperfusion deficits, fibrin and platelet deposition, and large infarct in the middle cerebral artery-supplied territory. Importantly, tail-vein injection of recombinant tPA at 0.5, 1, or 4 hr post-tHI (10 mg/kg) provided time-dependent reduction of the mortality rate and infarct size. This new stroke model is simple and can be standardized across laboratories to compare experimental results. Further, it induces thrombosis without craniectomy or introducing pre-formed emboli. Given these unique merits, the tHI model is a useful addition to the repertoire of preclinical stroke research.

Thromboembolic stroke models are vital tools for optimizing the recanalization therapy. Here we report a murine thrombotic stroke model based on transient cerebral hypoxic-ischemic (tHI) insult, which triggers thrombosis and infarction, and responds favorably to tissue plasminogen activator (tPA)-mediated fibrinolysis in a therapeutic window similar to those in stroke patients.

과도 대뇌 저산소증 - 허혈을 기반으로 혈전 성 뇌졸중 모델

Stroke research has endured many setbacks in translating neuroprotective therapies into clinical practice. In contrast, the real-world therapy (tPA ...

Reproducible Motor Deficit Following Aortic Occlusion in a Rat Model Of Spinal Cord Ischemia

Spinal cord ischemia is a fatal complication following thoracoabdominal aortic aneurysm surgery. Researchers can investigate the strategies for preventing and treating this complication using experimental models of spinal cord ischemia. The model described here demonstrates varying degrees of paraplegia that relate to the length of occlusion following thoracic aortic occlusion in a rat spinal cord ischemia model.
A 2-Fr. balloon-tipped catheter was advanced through the femoral artery into the descending thoracic aorta until the catheter tip was placed at the left subclavian artery in anesthetized male Sprague-Dawley rats. Spinal cord ischemia was induced by inflating the catheter balloon. After a set period of occlusion (9, 10, or 11 min), the balloon was deflated. Neurologic assessment was performed using the motor deficit index at 24 h after surgery, and the spinal cord was harvested for histopathological examination.
Rats that underwent 9 min of aortic occlusion showed mild and reversible motor impairment in the hind limb. Rats subjected to 10 min of aortic occlusion presented with moderate but reversible motor impairment. Rats subjected to 11 min of aortic occlusion displayed complete and persistent paralysis. The motor neurons in the spinal cord sections were more preserved in rats subjected to shorter duration of aortic occlusion.
Researchers can achieve a reproducible hind limb motor deficit following thoracic aortic occlusion using this spinal cord ischemia model.

This study demonstrates the technique to make a minimally invasive and easily reproducible model of spinal cord ischemia in rats. Various degrees of hind limb motor deficit can be produced by controlling the aortic occlusion time.

척수 쇄 허혈 모델에서 대동맥 폐쇄 후 재현성 운동 부족

Spinal cord ischemia is a fatal complication following thoracoabdominal aortic aneurysm surgery. Researchers can investigate the strategies for preventing ...

Assessing Therapeutic Angiogenesis in a Murine Model of Hindlimb Ischemia

Critical limb ischemia (CLI) is a serious condition that entails a high risk of lower limb amputation. Despite revascularization being the gold-standard therapy, a considerable number of CLI patients are not suited for either surgical or endovascular revascularization. Angiogenic therapies are emerging as an option for these patients but are currently still under investigation. Before application in humans, those therapies must be tested in animal models and its mechanisms must be clearly understood. An animal model of hindlimb ischemia (HLI) has been developed by the ligation and excision of the distal external iliac and femoral arteries and veins in mice. A comprehensive panel of tests was assembled to assess the effects of ischemia and putative angiogenic therapies at functional, histologic and molecular levels. Laser Doppler was used for the flow measurement and functional assessment of perfusion. Tissue response was evaluated by the analysis of capillary density after staining with the anti-CD31 antibody on histological sections of gastrocnemius muscle and by measurement of collateral vessel density after diaphonization. Expression of angiogenic genes was quantified by RT-PCR targeting selected angiogenic factors exclusively in endothelial cells (ECs) after laser capture microdissection from mice gastrocnemius muscles. These methods were sensitive in identifying differences between ischemic and non-ischemic limbs and between treated and non-treated limbs. This protocol provides a reproducible model of CLI and a framework for testing angiogenic therapies.

Here, a critical hindlimb ischemia experimental model is presented followed by a battery of functional, histologic and molecular tests&#160;to assess the effectiveness of angiogenic therapies.&#8203;

힌들보 리 허 혈의 뮤린 모델에서 치료 혈관 신생 평가

Critical limb ischemia (CLI) is a serious condition that entails a high risk of lower limb amputation. Despite revascularization being the gold-standard ...

A Pre-clinical Rat Model for the Study of Ischemia-reperfusion Injury in Reconstructive Microsurgery

Ischemia-reperfusion injury is the main cause of flap failure in reconstructive microsurgery. The rat is the preferred preclinical animal model in many areas of biomedical research due to its cost-effectiveness and its translation to humans. This protocol describes a method to create a preclinical free skin flap model in rats with ischemia-reperfusion injury. The described 3 cm x 6 cm rat free skin flap model is easily obtained after the placement of several vascular ligatures and the section of the vascular pedicle. Then, 8 h after the ischemic insult and completion of the microsurgical anastomosis, the free skin flap develops the tissue damage. These ischemia-reperfusion injury-related damages can be studied in this model, making it a suitable model for evaluating therapeutic agents to address this pathophysiological process. Furthermore, two main monitoring techniques are described in the protocol for the assessment of this animal model: transit-time ultrasound technology and laser speckle contrast analysis.

Here, we describe a pre-clinical animal model for studying the pathophysiology of ischemia-reperfusion injury in reconstructive microsurgery. This free skin flap model based on the superficial caudal epigastric vessels in the rat may also allow for the evaluation of different therapies and compounds to counteract ischemia-reperfusion injury-related damage.

재건 미세 수술에서 허혈 재관류 손상의 연구를위한 전 임상 쥐 모델

Ischemia-reperfusion injury is the main cause of flap failure in reconstructive microsurgery. The rat is the preferred preclinical animal model in many ...

Acupuncture in a Rat Model of Asthma

A high platform can fix rats without restriction and completely expose the acupoints on the back during acupuncture manipulation. This article describes methods for the fabrication of the high platform, establishes a rat model of asthma and measures changes in respiratory function using a noninvasive and real-time whole-body plethysmography (WBP) system.

천식의 쥐 모형에 있는 침술

A high platform can fix rats without restriction and completely expose the acupoints on the back during acupuncture manipulation. This article describes ...