Aversano T, Marino P N
Division of Cardiology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
Am J Physiol. 1990 Jun;258(6 Pt 2):H1786-95. doi: 10.1152/ajpheart.1990.258.6.H1786.
To study the influence of ischemic zone size on function in nonischemic regions, wall thickening and the end-systolic pressure-thickness (ESPTR) relationship were measured before and during a 90-s coronary occlusion, which produced either a small or large (24 or 35% of left ventricular mass) area of ischemia. With both size ischemic areas, nonischemic zone isovolumic and ejection phase wall thickening increased during occlusion, primarily because of increased preload and, to a lesser extent, a reduced pressure component of afterload. The nonischemic region ESPTR was unchanged from preocclusion control with small ischemic mass. With larger ischemic mass, the nonischemic region ESPTR was shifted downward and to the left, indicating reduced end-systolic performance. The decline in the nonischemic zone ESPTR with large ischemic zone size was not due to reduced blood flow, shortening deactivation, reflex effects, or "tethering" but rather to the associated decline in coronary perfusion pressure. Thus the increase of nonischemic region wall thickening during acute ischemia is due to a change in ventricular loading conditions and not augmentation of contractile performance. Larger ischemic zone size can impair function in nonischemic myocardium by reducing the erectile component of end-systolic performance.
为研究缺血区域大小对非缺血区域功能的影响，在90秒冠状动脉闭塞前后测量了室壁增厚和收缩末期压力-厚度（ESPTR）关系，冠状动脉闭塞造成了小面积或大面积（分别为左心室质量的24%或35%）的缺血。在两种大小的缺血区域中，闭塞期间非缺血区域等容和射血期室壁增厚均增加，主要是由于前负荷增加，以及在较小程度上后负荷的压力成分降低。小面积缺血时，非缺血区域的ESPTR与闭塞前对照相比无变化。大面积缺血时，非缺血区域的ESPTR向下和向左移动，表明收缩末期功能降低。大面积缺血区域时非缺血区域ESPTR的下降并非由于血流减少、缩短失活、反射效应或“牵拉”，而是由于冠状动脉灌注压的相应下降。因此，急性缺血期间非缺血区域室壁增厚的增加是由于心室负荷条件的改变，而非收缩性能的增强。较大的缺血区域大小可通过降低收缩末期功能的增强成分来损害非缺血心肌的功能。
