Holubarsch C, Alpert N R, Goulette R, Mulieri L A
Circ Res. 1982 Dec;51(6):777-86. doi: 10.1161/01.res.51.6.777.
Contracture due to hypoxia, to both oxygen and glucose deficiency, and to potassium chloride was induced in rat left ventricular papillary muscle preparations. Under contracture conditions, the sum of resting heat plus contracture heat was measured using Hill-type, planar vacuum-deposited thermopiles. On the basis of the measured total and initial heat output and the corresponding tension-time integral during single twitches under control conditions (Lmax, 21 degrees C, stimulus frequency 12/min), the expected heat output during contracture was calculated, assuming that the contracture tension is maintained by the same calcium-induced cross-bridge cycling as occurs in the single twitch response. With potassium chloride, the contracture tension was 1.33 +/- 0.27 g/mm2, a value which is similar to those found in hypoxic contracture and in contracture due to both oxygen and glucose deficiency. There was no significant difference between measured and calculated values for resting heat plus contracture heat (8.40 +/- 2.84 mW/g measured, 8.55 +/- 2.50 mW/g calculated); there was a linear correlation (r = 0.99) between predicted and measured values (P less than 0.05). The measured value for resting plus contracture heat in hypoxic contracture was 1.88 +/- 0.37 mW/g, whereas a value of 4.80 +/- 1.09 mW/g (P less than 0.005) was calculated on the basis of the twitch heat per tension-time integral and contracture tension (1.09 +/- 0.31 g/mm2). Contracture tension was 1.80 +/- 0.78 g/mm2 in contracture due to oxygen and glucose deficiency, whereas the value for resting plus contracture eat was 1.61 +/- 0.56 mW/g. The calculated resting plus contracture heat value for this preparation was significantly higher (7.45 +/- 3.75 mW/g; P less than 0.05). There was no significant regression between predicted and measured resting heat plus contracture heat in the hypoxic contracture preparations (slope not different from zero). In contracture due to oxygen and glucose deficiency, the linear regression had a slope of 6.06 (P less than 0.05). The results suggest that the potassium chloride contracture relies on cross-bridge cycling as in a twitch contraction, whereas hypoxic contracture and that due to oxygen and glucose deficiency may be explained by cross-bridge formations with no, or very low, heat production, i.e., contracture tensions due to hypoxia and to oxygen and glucose deficiency are maintained by rigor-like cross-bridge formation or by slowly cycling cross-bridges with a long time of cross-bridge attachment.
在大鼠左心室乳头肌标本中诱导出因缺氧、氧和葡萄糖缺乏以及氯化钾所致的挛缩。在挛缩状态下，使用希尔型平面真空沉积热电堆测量静息热与挛缩热之和。根据在对照条件下（Lmax，21℃，刺激频率12次/分钟）单次抽搐期间测得的总热输出和初始热输出以及相应的张力 - 时间积分，假设挛缩张力由与单次抽搐反应中相同的钙诱导横桥循环维持，计算出挛缩期间的预期热输出。对于氯化钾，挛缩张力为1.33±0.27 g/mm²，该值与在缺氧挛缩以及氧和葡萄糖缺乏所致挛缩中发现的值相似。静息热加挛缩热的测量值与计算值之间无显著差异（测量值为8.40±2.84 mW/g，计算值为8.55±2.50 mW/g）；预测值与测量值之间存在线性相关性（r = 0.99）（P＜0.05）。缺氧挛缩中静息加挛缩热的测量值为1.88±0.37 mW/g，而根据每次抽搐热与张力 - 时间积分以及挛缩张力（1.09±0.31 g/mm²）计算得出的值为4.80±1.09 mW/g（P＜0.005）。氧和葡萄糖缺乏所致挛缩中的挛缩张力为1.80±0.78 g/mm²，而静息加挛缩热的值为1.61±0.56 mW/g。该标本计算出的静息加挛缩热值显著更高（7.45±3.75 mW/g；P＜0.05）。在缺氧挛缩标本中，预测的静息热加挛缩热与测量值之间无显著回归关系（斜率与零无差异）。在氧和葡萄糖缺乏所致挛缩中，线性回归的斜率为6.06（P＜0.05）。结果表明，氯化钾挛缩如同抽搐收缩一样依赖横桥循环，而缺氧挛缩以及氧和葡萄糖缺乏所致挛缩可能由不产生热或产生极少量热的横桥形成来解释，即缺氧以及氧和葡萄糖缺乏所致的挛缩张力由类似强直的横桥形成或由横桥附着时间长的缓慢循环横桥维持。
