Abstract
Electrocardiography (ECG) was performed for SART stressed (repeated cold stressed) mice which had changes in blood pressure and blood flow to examine the effects of this treatment on heart function. In the ECG of mice subjected to SART stress for 5 days, potentiations of the R and T voltage, a shortening of the PQ interval, a prolongation of the QRS interval, and a slight increase of the heart rate were observed; and such changes in the EGG were maintained for several days. Recovery from all these changes was observed after a single dose or consecutive administrations of propranolol. From these results, it is considered that sympathetic nerve activity may be increased in the function of the heart in SART stressed mice, as contrasted to the partial vagotonia in the duodenum. Neurotropin (NSP), a nerve sedative, was then administered to mice once daily for 5 days during the SART stress. ' NSP prevented the changes of the PQ and QRS interval in SART stressed mice, but could not prevent the potentiation of the R and T voltage and the heart rate increase. In particular, the potentiations of the R and T voltages were thought to be induced by the increase of sympathetic nerve activity; therefore, it is thought that NSP may not have direct actions at least on the sympathetic nerve sites in autonomic nervous systems.
