Reflex effects of lung inflation and inhalation of halothane, ether, and ammonia.
Anesthetized dogs were perfused at constant pressure from an external oxygenator after removing their hearts. Systemic vascular resistance (SVR) and spontaneous breathing effors were monitored while the lungs were ventilated briefly at a low frequency with several tidal volumes and at a low volume with several frequencies. Inflation depressed respiratory activity and transiently lowered SVR to a minimum from which it spontaneously partially recovered. The transient and sustained SVR changes were directly related to peak inflating pressure, independent of the mode of ventilation. Pressurization of the sublaryngeal extrapulmonary airways and addition of ammonia to lung inspirate were without effect. Ventilation with 7% ether had no effect, but at 13% it occasionally increased respiratory activity. Ventilation with 7% halothane depressed SVR and stimulated respiration, whereas 13% caused vasodilation and apnea. The magnitudes of SVR responses to halothane and to inflation were uncorrelated. All effects of inflation and inhalants were eliminated by vagotomy. We condluded that the systemic vessels appear to respond to changes in respiratory minute volume; that this is brought about by intrapulmonary receptors, perhaps of more than one type; that two classical "irritants" have little effect in dogs; and that halothane has effects on breathing and SVR consistent with stimulation of J-receptors.
D000641:Ammonia / Q000494:pharmacology*; D000818:Animals; D004285:Dogs; D005019:Ethyl Ethers / Q000494:pharmacology*; D005260:Female; D006221:Halothane / Q000494:pharmacology*; D008168:Lung / Q000294:innervation*; D008297:Male; D011661:Pulmonary Stretch Receptors / Q000502:physiology; D012018:Reflex / Q000502:physiology; D012119:Respiration; D013990:Tidal Volume; D014655:Vascular Resistance / Q000187:drug effects
D005019:Ethyl Ethers; D000641:Ammonia; D006221:Halothane