Studies on the mechanism of pulmonary vascular responses to miliary pulmonary embolism.
The nature and mechanisms of pulmonary vascular responses which follow miliary pulmonary embolism were examined in intact dogs in which the isolated left lower lobe was perfused at constant blood flow. Embolization of the lung with plastic microspheres increased total pulmonary vascular resistance, whereas, in contrast, vascular resistance of the isolated perfused left lower lobe which was protected from embolization was decreased. This vasodilation was prevented by chronic denervation of the lobe and by ganglionic blockade. Cervical vagotomy also blocked the response but atropine failed to alter the vasodilation. The response, which appeared to be reflex in origin and involve efferent sympathetic pathways, was prevented by beta-adrenergic receptor blockade produced by propranolol. Since the lobar vascular response to norepinephrine was significantly enhanced by propranolol, it was concluded that embolization of the lung evokes pulmonary vascular reflex vasodilation which is mediated over the sympathetic nervous system via a beta-adrenergic receptor mechanism.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001775:Blood Circulation; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D007545:Isoproterenol / Q000494:pharmacology; D008168:Lung / Q000098:blood supply; D005996:Nitroglycerin / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011651:Pulmonary Artery; D011655:Pulmonary Embolism / Q000503:physiopathology*; D014655:Vascular Resistance; D014664:Vasodilation / Q000187:drug effects
D001285:Atropine; D011433:Propranolol; D005996:Nitroglycerin; D007545:Isoproterenol; D000109:Acetylcholine; D009638:Norepinephrine