Anderson P G, Bishop S P, Digerness S B
Department of Pathology, University of Alabama at Birmingham 35294.
Am J Pathol. 1987 Oct;129(1):152-67.
The purpose of this study was to compare the functional and morphologic changes that occur during ischemic contracture and reperfusion in the normal and hypertrophied heart. Hearts from Sprague-Dawley, spontaneously hypertensive (SHR), and normotensive Wistar-Kyoto rats were evaluated using a modified Langendorff perfusion apparatus. After obtaining control data, hearts were potassium-arrested, made ischemic, and studied at various time points. Regional coronary flow was assessed with the use of radiolabeled microspheres or Microfil dye infusion, and morphologic changes were evaluated by means of light and electron microscopy. Sarcomere length changes and qualitative morphologic changes during global ischemia demonstrate a transmural progression of ischemic damage starting at the endocardium and extending, with time, epicardially. The progression of ischemic changes in hypertrophied hearts of SHRs was similar to that of normal hearts; however, hypertrophied hearts developed ischemic contracture sooner than normal hearts. In addition, the development of contraction band change after ischemic contracture occurred only when hearts were reperfused and was related to the development of no-reflow.
本研究的目的是比较正常心脏和肥厚心脏在缺血性挛缩和再灌注过程中发生的功能和形态学变化。使用改良的Langendorff灌注装置对来自Sprague-Dawley大鼠、自发性高血压(SHR)大鼠和血压正常的Wistar-Kyoto大鼠的心脏进行评估。在获得对照数据后,使心脏停钾、缺血,并在不同时间点进行研究。使用放射性标记微球或注入Microfil染料评估局部冠状动脉血流,并通过光学显微镜和电子显微镜评估形态学变化。全心缺血期间的肌节长度变化和定性形态学变化表明,缺血损伤呈透壁性进展,始于心内膜,并随时间向外膜延伸。SHR肥厚心脏中缺血变化的进展与正常心脏相似;然而,肥厚心脏比正常心脏更早出现缺血性挛缩。此外,缺血性挛缩后收缩带变化仅在心脏再灌注时发生,且与无复流的发生有关。