Lorell B H, Wexler L F, Momomura S, Weinberg E, Apstein C S
Circ Res. 1986 May;58(5):653-63. doi: 10.1161/01.res.58.5.653.
We tested the hypothesis that there is an enhanced susceptibility in hypertrophied cardiac muscle to develop decreased diastolic distensibility of the left ventricle in response to hypoxia. The effects of brief hypoxia (3 minutes) were studied in rats with and without chronic left ventricular pressure overload hypertrophy using an isolated buffer-perfused and isovolumic (balloon-in-left ventricle) heart preparation with excised pericardium and vented right ventricle. We compared hypertrophied hearts from hearts from hypertensive uninephrectomized Wistar-Kyoto rats (n = 12) with normotensive uninephrectomized age-matched controls (n = 13). Coronary flow was held constant and adjusted so that an identical flow per gram left ventricular weight was achieved in both groups. The left ventricular balloon volume was adjusted to produce an initial left ventricular end-diastolic pressure of 10 mm Hg in both groups and was held constant thereafter so that changes in left ventricular end-diastolic pressure during hypoxia represented changes in diastolic chamber distensibility. Under aerobic conditions, left ventricular systolic pressure was 66% higher in the hypertrophied hearts than in the controls, but there was no difference in the rate or extent of left ventricular relaxation as estimated by the exponential time constant of pressure decay and the asymptote to which pressure decayed. In response to hypoxia, left ventricular end-diastolic pressure was significantly higher in the hypertrophied hearts than in the controls (37 +/- 5 vs. 22 +/- 5 mm Hg, P less than 0.001). In response to hypoxia, the rate of left ventricular relaxation was depressed to a comparable degree in both groups, but there was a greater upward shift in the asymptote to which pressure decayed in the hypertrophied hearts. Hypoxia-induced coronary vasodilation as assessed by the change in coronary vascular resistance was similar in the hypertrophied and control hearts (2.9 +/- 0.5 vs. 2.3 +/- 0.9 mm Hg/[(ml/min)/g], NS). The degree of hypoxia-induced anaerobic metabolism as estimated by the coronary arterial-venous lactate concentration difference was also similar in both groups (-0.72 +/- 0.23 vs. -0.73 +/- 0.16 mM/liter, NS). It is concluded that brief hypoxia results in a greater decrease in diastolic distensibility of the left ventricle in the presence of chronic pressure overload hypertrophy than in its absence.
肥厚心肌对缺氧反应时左心室舒张期扩张性降低的易感性增强。使用分离的缓冲液灌注和等容（左心室内置球囊）心脏制备方法，对有或无慢性左心室压力超负荷肥大的大鼠进行短暂缺氧（3分钟）效应的研究，该制备方法切除了心包并使右心室排气。我们将高血压单侧肾切除的Wistar - Kyoto大鼠（n = 12）的肥厚心脏与年龄匹配的正常血压单侧肾切除对照组（n = 13）的心脏进行比较。使两组的冠状动脉血流量保持恒定并进行调整，以使每克左心室重量的血流量相同。两组均将左心室内置球囊的体积调整至产生初始左心室舒张末期压力为10 mmHg，并在此后保持恒定，以便缺氧期间左心室舒张末期压力的变化代表舒张期心室扩张性的变化。在有氧条件下，肥厚心脏的左心室收缩压比对照组高66%，但根据压力衰减的指数时间常数和压力衰减的渐近线估计，左心室舒张速率和程度没有差异。对缺氧的反应中，肥厚心脏的左心室舒张末期压力显著高于对照组（37±5 vs. 22±5 mmHg，P＜0.001）。对缺氧的反应中，两组左心室舒张速率均降低到相当程度，但肥厚心脏中压力衰减的渐近线有更大的上移。通过冠状动脉血管阻力变化评估的缺氧诱导的冠状动脉血管舒张在肥厚心脏和对照心脏中相似（2.9±0.5 vs. 2.3±0.9 mmHg/[(ml/min)/g]，无显著性差异）。通过冠状动脉动静脉乳酸浓度差估计的缺氧诱导的无氧代谢程度在两组中也相似（-0.72±0.23 vs. -0.73±0.16 mM/升，无显著性差异）。结论是，在存在慢性压力超负荷肥大时，短暂缺氧导致左心室舒张期扩张性的降低比不存在时更大。
