title: Peripheral chemoreceptor modulation of the pulmonary vasculature in the cat.
abstract: The present study was undertaken to determine whether stimulation of the carotid and aortic bodies (cb and ab) could affect the pulmonary vasculature. Our hypothesis was that each promoted vasodilation and thus could modulate the pulmonary vasoconstrictor response to hypoxia. The experimental design of the first set of experiments took advantage of the facts that 1) the ab, but not the cb, increases its neural output in response to CO, whereas both respond to a decreased arterial PO2 (hypoxic hypoxia, HH) and 2) the aortic nerves in cats are easily transected. Hence, both cb and ab sent neural activity to the brain stem when the intact cat was exposed to 10% O2 in N2. Only the ab sent information during CO hypoxia (COH intact). Only the cb did so during HH in the cat in which the aortic nerves had been transected, removing the aortic body (HH abr); neither ab nor cb did so during COH abr. Fifteen anesthetized paralyzed artificially ventilated cats were fit with catheters in the femoral artery and vein, right and left atria, left ventricle, and pulmonary artery and with an aortic flow probe. In the HH intact and HH abr conditions, there was a significant rise in cardiac output, whereas pulmonary arterial pressure (Ppa) rose initially but then leveled off while cardiac output continued to rise. During the 15-min exposure to HH, pulmonary vascular resistance [PVR = (Ppa - Pla)/cardiac output, where Pla is left atrial pressure] rose initially and then decreased significantly at 2-3 min. In response to COH, PVR showed only a significant decrease. In the second set of experiments, seven cats were instrumented as above and had loops placed in the common carotid arteries for selectively perfusing the cbs. In response to a brief infusion of venous blood mixed with 0.3-0.5 micrograms NaCN, which selectively stimulated only the cb, aortic flow remained relatively constant while heart rate and Ppa - alveolar pressure difference decreased significantly; so also did PVR. These data are consistent with the hypothesis that stimulation of the ab and cb singly or together can provoke a significant pulmonary vasodilation in the anesthetized paralyzed artificially ventilated cat.
authors.affiliation: Department of Environmental Health Sciences (Division of Physiology), Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
authors.forename: R S
authors.initials: RS
authors.lastname: Fitzgerald
authors.forename: G A
authors.initials: GA
authors.lastname: Dehghani
authors.forename: J S
authors.initials: JS
authors.lastname: Sham
authors.forename: M
authors.initials: M
authors.lastname: Shirahata
authors.forename: W A
authors.initials: WA
authors.lastname: Mitzner
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002248:Carbon Monoxide; D002302:Cardiac Output / Q000502:physiology; D002344:Carotid Body / Q000502:physiology; D002415:Cats; D002628:Chemoreceptor Cells / Q000502:physiology*; D000860:Hypoxia / Q000139:chemically induced / Q000503:physiopathology; D008863:Microspheres; D009131:Muscle, Smooth, Vascular / Q000502:physiology; D010101:Oxygen Consumption / Q000502:physiology; D010477:Perfusion; D011652:Pulmonary Circulation / Q000502:physiology*; D014664:Vasodilation / Q000502:physiology
chemical_list: D002248:Carbon Monoxide