Mechanism of increased susceptibility to fibrillation of the hypothermic mammalian heart in situ.

The susceptibility of auricles and ventricles to fibrillation during hypothermia of isolated hearts, and of hearts in situ in anaesthetized cats, was estimated by measuring the threshold for the production of fibrillation by electrical stimulation. Hypothermia reduced the threshold of in situ hearts, but increased the threshold of isolated perfused hearts and of heart-lung preparations. The increased sensitivity of in situ hearts to fibrillation could be induced by cooling the head only, and was abolished by cutting the vagi. At normal body temperature, section of the vagi had no influence on the fibrillation threshold. In contrast, cutting the sympathetic increased the fibrillation threshold of in situ hearts at normal temperature, but had no influence on the threshold during hypothermia. It was concluded that the increased susceptibility of anaesthetized animals to fibrillation could be attributed to changes in the central nervous control of the heart induced by the cooling of the head.