Johansson B W
Hjärt-lungkliniken, sektionen för kardiologi, Universitetssjukhuset MAS, Malmö.
Lakartidningen. 2001 Mar 28;98(13):1502-6.
During hibernation, animals lower their body temperature to a few degrees above 0 degree C. This means that when entering and emerging from hibernation their body temperature passes through the critical level of +20 degrees C, a temperature region at which non-hibernating mammals develop circulatory arrest, usually due to ventricular fibrillation (VF). The hibernator heart is resistant to VF, not only that caused by hypothermia, but also VF as induced by local application of aconitine on the epicardium, and also by other factors which ordinarily cause VF in non-hibernators. Several mechanisms may explain the resistance to VF observed in the hibernator heart. The factors of greatest importance seem to be contrasting patterns of adrenergic innervation, divergent physico-chemical properties with a lower solidification point of lipids in the hibernator, distinct enzyme temperature activity curves seen in the hibernator, and differences in the handling of intracellular calcium, resulting in protection against calcium overload in the hibernator heart as compared with the non-hibernator heart.
在冬眠期间，动物会将体温降至略高于0摄氏度的水平。这意味着在进入和退出冬眠时，它们的体温会经过+20摄氏度这一关键水平，在这个温度区域，非冬眠哺乳动物通常会因心室颤动（VF）而出现循环骤停。冬眠动物的心脏对VF具有抗性，不仅对低温引起的VF有抗性，而且对局部应用乌头碱于心外膜诱导的VF以及通常会在非冬眠动物中引起VF的其他因素也有抗性。有几种机制可以解释在冬眠动物心脏中观察到的对VF的抗性。最重要的因素似乎是肾上腺素能神经支配模式的差异、冬眠动物脂质凝固点较低的不同物理化学性质、冬眠动物中可见的独特酶温度活性曲线以及细胞内钙处理方式的差异，与非冬眠动物心脏相比，这些差异使得冬眠动物心脏能够防止钙超载。
