HEMODYNAMIC DETERMINANTS OF TIME-COURSE OF FALL IN CANINE LEFT-VENTRICULAR PRESSURE
HEMODYNAMIC DETERMINANTS OF TIME-COURSE OF FALL IN CANINE LEFT-VENTRICULAR PRESSURE
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DOI：
10.1172/jci108522
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发表时间：
1976-01-01
影响因子：
15.9
通讯作者：
WEISFELDT, ML
中科院分区：
文献类型：
--
作者：
WEISS, JL;FREDERIKSEN, JW;WEISFELDT, ML
在离体犬左心室标本中评估了等容左心室压力下降时程的血流动力学决定因素。在等容搏动或射血后延长的等容舒张期研究了压力下降情况。从最大负dP/dt（压力随时间的变化）时刻起，等容和射血搏动在等容舒张期的压力下降呈指数形式（r≥0.98），因此可用一个时间常数T来表征。较高的心率使T从110次/分钟时的52.6±4.5毫秒略微缩短至160次/分钟时的48.2±6.0毫秒（P<0.01，n = 8）。在等容条件下，较高的心室容积导致较高的左心室峰值压力，但T无显著变化。T从等容搏动时的67.1±5.0毫秒缩短至射血搏动时的45.8±2.9毫秒（P<0.001，n = 14）。在射血搏动中，收缩压峰值较低，收缩末期容积较小。为了区分射血期间收缩期缩短的影响与较低收缩压和较小收缩末期容积的影响，将舒张末期容积大的搏动与舒张末期容积小的搏动进行了比较。舒张末期容积小的搏动缩短较少，但收缩末期容积和收缩压峰值相似。在收缩期缩短更明显的搏动中，T再次更大程度地缩短。氯化钙和毒毛花苷元未导致T发生显著变化，但加速主动舒张的去甲肾上腺素导致T显著缩短（65.6±13.4毫秒对46.3±7.0毫秒，P<0.02）。在缺血恢复期间，与缺血前对照搏动相比，T从59.0±9.6毫秒显著增加至76.8±13.1毫秒（P<0.05）。目前的研究表明，在最大负dP/dt之后等容压力下降的时程是指数形式的，与收缩应力和收缩末期纤维长度无关，且对心率的依赖性极小。T可能是心脏主动舒张系统活动的一个指标，并且似乎取决于收缩期纤维缩短。
The hemodynamic determinants of the time-course of fall in isovolumic left ventricular pressure were assessed in isolated canine left ventricular preparations. Pressure fall was studied in isovolumic beats or during prolonged isovolumic diastole after ejection. Pressure fall from the time of maximum negative dP/dt [change in pressure with time] was exponential during isovolumic relaxation for isovolumic and ejecting beats (r .gtoreq. 0.98) and was therefore characterized by a time constant, T. Higher heart rates shortened T slightly from 52.6 .+-. 4.5 ms at 110/min to 48.2 .+-. 6.0 ms at 160/min (P < 0.01, n = 8). Higher ventricular volumes under isovolumic conditions resulted in higher peak left ventricular pressure but no significant change in T. T did shorten from 67.1 .+-. 5.0 ms in isovolumic beats to 45.8 .+-. 2.9 ms in the ejecting beats (P < 0.001, n = 14). In the ejecting beats, peak systolic pressure was lower, and end-systolic volume smaller. To differentiate the effects of systolic shortening during ejection from those of lower systolic pressure and smaller end-systolic volume, beats with large end-diastolic volumes were compared to beats with smaller end-diastolic volumes. The beats with smaller end-diastolic volumes exhibited less shortening but similar end-systolic volumes and peak systolic pressure. T again shortened to a greater extent in the beats with greater systolic shortening. CaCl2 and acetylstrophanthidin resulted in no significant change in T, but norepinephrine, which accelerates active relaxation, resulted in a significant shortening of T (65.6 .+-. 13.4 vs. 46.3 .+-. 7.0 ms, P < 0.02). During recovery from ischemia, T increased significantly from 59.0 .+-. 9.6 to 76.8 .+-. 13.1 ms when compared with the preischemic control beat (P < 0.05). The present studies show that the time-course of isovolumic pressure fall subsequent to maximum negative dP/dt is exponential, independent of systolic stress and end-systolic fiber length, and minimally dependent on heart rate. T may be an index of the activity of the active cardiac relaxing system and appears dependent on systolic fiber shortening.