Birkeland S, Hexeberg E
Department of Surgery, Haukeland Hospital, University of Bergen, Norway.
Acta Physiol Scand. 1994 Jul;151(3):269-77. doi: 10.1111/j.1748-1716.1994.tb09746.x.
Postsystolic shortening area has been shown to be a sensitive marker of myocardial ischaemia in a one-vessel model. We tested whether postsystolic shortening provoked by interaction between ischaemic and nonischaemic regions is reduced in a two-vessel model, one vessel occluded and one subjected to coronary artery stenosis. Regional function in the left ventricular anterior wall was studied by orthogonal sonomicrometry during left coronary underperfusion in 14 pentobarbital-anaesthetized cats with an acute circumflex coronary artery occlusion. Left coronary underperfusion in two discrete steps decreased subendocardial blood flow in the left ventricular anterior wall to on average 60% (P < 0.001) and 20% (P < 0.001) of control value, while subepicardial flow did not change. End-diastolic lengths of longitudinal segments increased markedly even during mild subendocardial underperfusion, whereas end-diastolic lengths of circumferential segments only increased during severe subendocardial underperfusion with concomitant increase of left ventricular end-diastolic pressure. Systolic shortening, pressure-length loop area and shortening velocity of circumferential segments did not change. In contrast, systolic shortening and total pressure-length loop area of longitudinal segments decreased progressively approaching zero values during severe coronary underperfusion. Shortening velocity of longitudinal segments also decreased progressively during experimental protocol whereas postsystolic shortening area did not change.
postsystolic shortening area is not a marker of subendocardial ischaemia in a two-vessel model which indicates that postsystolic shortening is primarily a phenomenon related to model of ischaemia. End-diastolic lengthening is predominant in the longitudinal axis of the heart during subendocardial ischaemia.
在单支血管模型中，收缩期后缩短面积已被证明是心肌缺血的敏感标志物。我们测试了在双支血管模型（一支血管闭塞，另一支冠状动脉狭窄）中，缺血区域与非缺血区域相互作用引起的收缩期后缩短是否减少。在14只戊巴比妥麻醉的猫中，急性冠状动脉回旋支闭塞，通过正交超声心动图测量法研究左冠状动脉灌注不足时左心室前壁的区域功能。左冠状动脉分两个阶段灌注不足，使左心室前壁心内膜下血流平均降至对照值的60%（P<0.001）和20%（P<0.001），而心外膜下血流未改变。即使在轻度心内膜下灌注不足时，纵向节段的舒张末期长度也显著增加，而圆周节段的舒张末期长度仅在严重心内膜下灌注不足且左心室舒张末期压力同时升高时增加。圆周节段的收缩期缩短、压力-长度环面积和缩短速度未改变。相比之下，在严重冠状动脉灌注不足期间，纵向节段的收缩期缩短和总压力-长度环面积逐渐减小，接近零值。在实验过程中，纵向节段的缩短速度也逐渐降低，而收缩期后缩短面积未改变。
在双支血管模型中，收缩期后缩短面积不是心内膜下缺血的标志物，这表明收缩期后缩短主要是一种与缺血模型相关的现象。在心内膜下缺血期间，心脏纵轴上舒张末期延长占主导。
