The influence of pressure overload left ventricular hypertrophy on diastolic properties during hypoxia in isovolumically contracting rat hearts.
The influence of pressure overload left ventricular hypertrophy on diastolic properties during hypoxia in isovolumically contracting rat hearts.
复制标题
压力超负荷左心室肥厚对等容收缩大鼠心脏缺氧期间舒张特性的影响。
DOI：
10.1161/01.res.58.5.653
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发表时间：
1986
影响因子：
20.1
通讯作者：
Apstein,CS
中科院分区：
文献类型：
--
作者：
Lorell,BH;Wexler,LF;Momomura,S;Weinberg,E;Apstein,CS
我们检验了这样一个假设，即肥厚心肌对缺氧反应时左心室舒张期扩张性降低的敏感性增强。使用离体缓冲液灌注和等容（左心室球囊）心脏制备物（切除心包和通气右心室），在有和无慢性左心室压力超负荷肥大的大鼠中研究短暂缺氧（3分钟）的影响。我们比较了来自高血压单侧肾切除Wistar-Kyoto大鼠（n = 12）和血压正常单侧肾切除年龄匹配对照组（n = 13）的心脏肥大。冠状动脉血流保持恒定并进行调整，使两组中每克左心室重量的血流相同。调整左心室球囊容积，使两组的初始左心室舒张末期压均为10 mm Hg，此后保持恒定，以便缺氧期间左心室舒张末期压的变化代表舒张室扩张性的变化。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，左心室舒张的速率或程度没有差异。在对缺氧的反应中，肥厚心脏的左心室舒张末期压显著高于对照组（37 +/- 5 vs. 22 +/- 5 mm Hg，P <0.001）。在缺氧反应中，两组的左心室舒张率降低到相当的程度，但在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的变化评估的缺氧诱导的冠状动脉血管舒张在肥大心脏和对照心脏中相似（2.9 +/- 0.5 vs. 2.3 +/- 0.9 mm Hg/[（ml/min）/g]，NS）。通过冠状动脉-静脉乳酸盐浓度差异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/L，NS）。它的结论是短暂的缺氧的结果在更大的左心室舒张扩张性的慢性压力超负荷性肥厚的存在下，比在其缺席的减少。
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.