Abstract
The peripheral end of the right vagus was stimulated in acutely vagotomized rats under anesthesia at different body temperatures. A fairly abrupt increase in the R-R time on the electrocardiogram was observed when a critical stimulation frequency was reached. At a body temperature of 35[degree]C the critical frequency is 10 per second or more. On lowering of the body temperature to 28[degree]C the critical frequency is greatly reduced so that considerable slowing may be elicited at frequencies as low as one to five per second. Possible theoretical models to account for the critical frequency and its variation with temperature are considered. The temperature effect is too great to be accounted for either on the basis of the increased number of impulses which reach the heart per cardiac cycle, or the reduced rate of cholinesterase activity. The theory most consistent with the results is that each vagal impulse liberates or inactivates a substance, the concentration of which varies directly with heart rate. The interimpulse interval at the critical frequency would then represent the regeneration time of this substance. The temperature coefficient of the regeneration process appears to be about 3.3 per 10[degree]C.