Johansson B W
Section of Cardiology, General Hospital, Malmö, Sweden.
Arctic Med Res. 1991;50 Suppl 6:58-62.
During hibernation the animals decrease their body temperature down to a few degrees above 0 degree C. This means that when entering into and arousing from hibernation their body temperature passes the critical level of 20 degrees C, a temperature region where nonhibernating mammals develop circulatory arrest, usually ventricular fibrillation (VF). We found in other experiments that the hibernator heart is resistant to VF, not only induced by hypothermia, but also when induced by local application of aconitine on the epicardium, addition of 0.55 molar CaCl2 to isolated hearts perfused with a potassium free Tyrode solution, addition of procaine to isolated hearts perfused with Tyrode solution after previous administration of adrenaline, ligation of the proximal part of the left anterior descending coronary artery, and electrical stimulation in the vulnerable phase of the heart cycle. Several mechanisms are at work to explain this resistance to VF of the hibernator heart when compared to the nonhibernator heart. The factors of greatest importance seem to be the different adrenergic innervation pattern, different physico-chemical properties with a lower melting point of the lipids in the hibernator, different enzyme temperature activity curves in the hibernator and a different handling of intracellular calcium resulting in a protection against calcium overload in the hibernator heart, when compared with the nonhibernator heart.
在冬眠期间，动物会将体温降至略高于0摄氏度的水平。这意味着在进入和苏醒出冬眠状态时，它们的体温会经过20摄氏度这个关键水平，而非冬眠的哺乳动物在这个温度区域会出现循环骤停，通常是心室颤动（VF）。我们在其他实验中发现，冬眠动物的心脏对VF具有抗性，不仅对低温诱导的VF有抗性，而且对以下情况诱导的VF也有抗性：在心脏外膜局部应用乌头碱、向用无钾台氏液灌注的离体心脏中添加0.55摩尔氯化钙、在先前给予肾上腺素后向用台氏液灌注的离体心脏中添加普鲁卡因、结扎左前降支冠状动脉近端以及在心动周期的易损期进行电刺激。与非冬眠动物的心脏相比，有几种机制在起作用以解释冬眠动物心脏对VF的这种抗性。最重要的因素似乎是不同的肾上腺素能神经支配模式、冬眠动物脂质熔点较低的不同物理化学性质、冬眠动物不同的酶温度活性曲线以及与非冬眠动物心脏相比，冬眠动物对细胞内钙的不同处理方式，从而对冬眠动物心脏的钙超载起到保护作用。
