The present series of experiments was designed to determine whether the piglet has mature cardiorespiratory responses to the administration of phenyl diguanie (PDG) similar to those reported in adult mammals. A total of 26 acutely instrumented piglets aged 2–23 days were lightly anesthetized with sodium pentobarbital. After control conditions were established, PDG was injected into the right atrium. Each animal was its own control for determination of presence and magnitude of aortic pressure, heart rate, respiratory rate and volume, and blood flow responses to test doses of PDG. A fall in blood pressure was observed in all animals within 2–4 sec after right atrial injection of PDG. Bradycardia occurred and a transient cardiac arrhythmia, consisting of 2nd and 3rd degree heart block, was observed in most animals; the latter has not been previously reported. Apnea followed by rapid shallow breathing was observed in most animals. This respiratory effect was more pronounced in the younger animals. After atropine, PDG elicited a monophasic rise in aortic pressure; the cardiac rhythm and rate changes were abolished. However, the apneic response was retained. Subsequent bilateral vagotomy abolished the hypotensive effect on PDG. Such results suggest the possibility that the piglet's cardiorespiratory response to the administration of PDG may be evoked by stimulation of type J pulmonary receptors. These have been postulated to be responsible for the triad of responses of hypotension, bradycardia, and apnea seen in other species after PDG administration.SpeculationAt present, there is no explanation for the apnea and bradycardia observed in premature infants with Respiratory Distress Syndrome and/or a large patent ductus arteriosus. Mild interstitial pulmonary edema has been postulated to be the physiologic stimulus for the type J (juxtacapuiary) pulmonary receptor. The authors speculate that the piglet's response to PDG which includes apnea, hypotension, and bradycardia may be mediated by artificial stimulation of the J receptor. It is possible that in the human neonate, an immaturely controlled or an inappropriately strong response to the pathophysiologic stimulation of pulmonary edema may be a mechanism for the clinical symptoms of apnea and bradycardia in the small neonate.