Abstract
Experiments carried out on anesthetized cats showed that increasing blood flow, through the lobes of a lung, by 133% (SE 33%) generated an average of 0.75 impulses/s (SE 0.3) in 10 almost silent J receptors. Equivalent activity was produced by injecting 12-18 .mu.g phenyl diguanide/kg into the right atrium. Such activity caused marked reflex effects, i.e., apnea, rapid shallow breathing and reduction in the knee jerk. The reflex effects of J receptors were studied after blocking the activity from cardiac receptors by intrapericardial injections of xylocaine. This was necessary because left atrial injections of phenyl diguanide produced reflex respiratory effects and inhibition of the knee jerk. Hypoxia, but not hypercapnia, attenuated the reflex effects of J receptors, apnea being abolished if the Pa [arterial pressure], O2 fell below 35 mm Hg. This was a central effect as it occurred in spite of increased activity of J receptors following phenyl diguanide, and effects of hypoxia persisted after cutting both carotid nerves. The only invariable reflex effect of J receptors was a reduction in the total number and the average frequency of phrenic impulses in each breath. The changes in inspiratory time (ti) and expiratory time (te) following apnea were variable although most frequently both were reduced. In about half the observations the 1st effect before the apnea was a reduction in ti, in the other half it was a reduction in te. An input from J receptors inhibits inspiratory and expiratory mechanisms directly. In some cats apnea and rapid shallow breathing produced by J receptors continued after interrupting their activity by vagotomy and this did not diminish the reduction in ti or te; in other cats it did. The reduction in te was at times quite independent of changes in ti, i.e., pulmonary stretch receptor activity. J receptors must be stimulated during moderate exercise to levels that produce marked respiratory reflex effects and inhibition of muscles.