Johansson B W
Section of Cardiology, General Hospital, Malmö, Sweden.
Cardiovasc Res. 1996 May;31(5):826-32. doi: 10.1016/0008-6363(95)00192-1.
During hibernation animals decrease their body temperature down to a few degrees above 0 degrees C. This means that when entering into and arousing from hibernation their body temperature passes through the critical level of 20 degrees C, a temperature region where nonhibernating mammals develop circulatory arrest, usually ventricular fibrillation (VF). The hibernator heart is resistant to VF, not only induced by hypothermia, but also when induced by local application of aconitine on the epicardium, and other ways of inducing VF in nonhibernators. Several mechanisms may explain this resistance to VF of the hibernator heart. The factors of greatest importance seem to be the different adrenergic innervation pattern, the different physico-chemical properties with a lower melting point of the lipids in the hibernator, the different enzyme temperature activity curves in the hibernator and the different handling of intracellular calcium, which results in 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。这意味着在进入冬眠和从冬眠中苏醒时，它们的体温会经过20摄氏度这个关键水平，在这个温度区域，非冬眠哺乳动物会出现循环骤停，通常是心室颤动（VF）。冬眠动物的心脏对VF具有抵抗力，不仅对低温诱导的VF有抵抗力，而且对在心脏外膜局部应用乌头碱诱导的VF以及其他在非冬眠动物中诱导VF的方式也有抵抗力。有几种机制可以解释冬眠动物心脏对VF的这种抵抗力。最重要的因素似乎是不同的肾上腺素能神经支配模式、冬眠动物中熔点较低的脂质具有不同的物理化学性质、冬眠动物中不同的酶温度活性曲线以及对细胞内钙的不同处理方式，与非冬眠动物的心脏相比，这导致冬眠动物的心脏能够防止钙超载。
