Abstract

While deep hypothermia is well known to lead to cardiac malfunction up to circulatory arrest, mild hypothermia can prevent hypoxic damage to the heart. Importantly, a large body of research on deep hypothermia was carried out on rats and mice whose myocardium is significantly different from the human. In the present work, we investigated the effect of deep hypothermia on rhythmoinotropic phenomena in the guinea pig (GP) whose myocardium is more alike the human. The force––frequency relationship (FFR), effect of post-rest potentiation, and frequency-dependent acceleration of relaxation (FDAR) were studied in GP right ventricular papillary muscles (PM) within a range of 0.1–3.0 Hz at temperatures of 30, 20 and 10°C. It was shown that a positive FFR, mediated mainly by the inward Ca²⁺ current through the L-type Ca²⁺ channel, persists when cooling to 10°C, suggesting that this mechanism retains its activity even under deep hypothermia. The effect of post-rest potentiation persists down to 20°C, while further cooling replaces potentiation by depression. This may indicate that at 10°C, the functioning of the sarcoplasmic reticulum is impaired, as manifested in the rest-induced inversion of the post-rest potentiation effect. The effect of frequency-dependent acceleration of the kinetics of muscular contraction also persists down to 20°C, supporting the suggestion that this effect in the GP myocardium relies on the sarcoplasmic reticulum. Thus, we found that among the studied frequency-dependent effects, there are those affected by deep hypothermia (post-rest potentiation effect, FDAR) and those resistant to this exposure (FFR), which may reflect the differences in thermal sensitivity of the underlying mechanisms of Ca^{2 +} transport.

中文翻译：

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冷却对豚鼠心肌中力-频率关系、静息增强和频率相关的松弛加速的影响

摘要

众所周知，深低温会导致心脏功能障碍直至循环停止，而轻度低温可以防止心脏缺氧损伤。重要的是，对心肌与人类明显不同的大鼠和小鼠进行了大量关于深低温的研究。在目前的工作中，我们研究了深低温对心肌更像人类的豚鼠 (GP) 的节律性现象的影响。在 GP右心室乳头肌(PM) 中，在 0.1-3.0 Hz 的温度范围内，在 30 , 20 和 10°C。结果表明，主要由内向 Ca ²⁺介导的正 FFR通过 L 型 Ca ^{2+ 的}电流通道，当冷却到 10°C 时仍然存在，这表明即使在深度低温下，这种机制仍能保持其活性。休息后增强的效果持续到 20°C，而进一步冷却会取代抑郁症的增强。这可能表明在 10°C 时，肌浆网的功能受损，表现为休息诱导的休息后增强效应反转。肌肉收缩动力学的频率依赖性加速效应也持续到 20°C，支持 GP 心肌中的这种效应依赖于肌浆网的建议。因此，我们发现在研究的频率依赖效应中，有那些受深度低温影响的（休息后增强效应，FDAR）和那些对这种暴露有抵抗力的（FFR），²⁺运输。