title: Constrictor response of small pulmonary arteries to acute pulmonary hypertension during left atrial pressure elevation.
abstract: Acute elevations in left atrial pressure (LAP) were induced by altering the volume of air within a balloon inserted into the left atrium; the changes in internal diameter (ID) of small muscular pulmonary arteries (100-600 microns ID) in response to the associated rises of pulmonary arterial pressure (PAP) were measured using an X-ray TV system on the in vivo cat lung. When LAP was elevated to 14 +/- 1, 24 +/- 1, and 30 +/- 1 mmHg, PAP was increased to 21 +/- 1, 30 +/- 1, and 37 +/- 1 mmHg, respectively. With PAP ranging from 16 (control value) to 21 mmHg the ID did not dilate significantly. With PAP of 30-37 mmHg significant ID dilation occurred. The magnitude of the ID dilation (16%) with PAP of 37 mmHg, however, was significantly smaller than that (20%) with PAP of 30 mmHg despite the greater pressure rise. When the elevated PAP of 30-37 mmHg was quickly returned to the control level by rapid balloon deflation, the ID constricted significantly below the control level. The magnitude of the ID constriction was proportional to the degree of the preceding PAP rise and was maximal in the arteries of 200-400 microns ID. A papaverine hydrochloride injection combined with the balloon deflation completely abolished the ID constriction. A phentolamine injection, on the other hand, significantly attenuated the constriction with approximately half of the constriction persisting. The results indicate that an increase in vascular smooth muscle tone occurred in the small muscular pulmonary arteries, particularly those of 200-400 microns ID, in response to the acute rise of PAP above 30 mmHg during the LAP elevation. In addition, the data suggest the partial participation of catecholamines in the active contraction of vascular smooth muscle. The arterial contraction may serve to protect the pulmonary capillaries from an excessive hydrostatic pressure and pulmonary edema.
authors.affiliation: Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Suita, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Shirai
authors.forename: I
authors.initials: I
authors.lastname: Ninomiya
authors.forename: K
authors.initials: K
authors.lastname: Sada
mesh_terms: D000792:Angiography; D000818:Animals; D016275:Atrial Function; D001783:Blood Flow Velocity; D001794:Blood Pressure; D002415:Cats; D006325:Heart Atria / Q000187:drug effects; D006976:Hypertension, Pulmonary / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D010208:Papaverine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011312:Pressure; D011651:Pulmonary Artery / Q000187:drug effects / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D010208:Papaverine; D010646:Phentolamine