title: Reflex haemodynamic responses caused by distension of the uterus in anaesthetized pigs.
abstract: The present study was undertaken in anaesthetized pigs to determine whether distension of the uterus reflexly affects the aortic blood pressure, heart rate, left ventricular inotropic state and the coronary circulation. Experiments were performed in 17 pigs anaesthetized with alpha-chloralose and artificially ventilated. Coronary blood flow was measured with an electromagnetic flowmeter positioned around the origin of the left circumflex coronary artery. The uterus was distended by injecting 20 ml warm Ringer solution into a balloon positioned within the uterus (mean transmural pressure of about 17 mmHg). Distension of the uterus without controlling any haemodynamic variable caused an increase in aortic blood pressure. When this response was prevented, an increase in heart rate was obtained in each animal. When the heart rate and blood pressure responses were prevented, the distension did not cause significant changes in the maximum rate of change of left ventricular pressure, but always caused a decrease in mean coronary blood flow. In five pigs, the increase in heart rate and the decrease in mean coronary blood flow were graded by step increments of distension. In six pigs, the haemodynamic responses to distension of the uterus were not affected by the administration of atropine. In 12 pigs, which included the six given atropine, the increase in heart rate was abolished by the administration of propranolol and the increase in aortic blood pressure and the decrease in mean coronary blood flow were abolished by the subsequent administration of phentolamine. In the remaining five pigs, the haemodynamic responses caused by uterine distension were abolished by the administration of bretylium tosylate. The present study showed that distension of the uterus in anaesthetized pigs primarily caused reflex increases in heart rate and aortic blood pressure and coronary vasoconstriction. These reflex responses were mediated by efferent sympathetic mechanisms.
authors.affiliation: Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia di Novara, Università di Torino, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Vacca
authors.forename: A
authors.initials: A
authors.lastname: Battaglia
authors.forename: E
authors.initials: E
authors.lastname: Grossini
authors.forename: D A
authors.initials: DA
authors.lastname: Mary
authors.forename: C
authors.initials: C
authors.lastname: Molinari
authors.forename: N
authors.initials: N
authors.lastname: Surico
mesh_terms: D000344:Afferent Pathways / Q000187:drug effects / Q000502:physiology; D000768:Anesthesia, General; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D001950:Bretylium Tosylate / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects; D004525:Efferent Pathways / Q000187:drug effects / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D007001:Hypogastric Plexus / Q000502:physiology*; D008465:Mechanoreceptors / Q000502:physiology*; D009200:Myocardial Contraction / Q000187:drug effects; D010276:Parasympatholytics / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011312:Pressure; D011433:Propranolol / Q000494:pharmacology; D012018:Reflex / Q000187:drug effects / Q000502:physiology*; D013552:Swine; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*; D013565:Sympatholytics / Q000494:pharmacology; D014599:Uterus / Q000294:innervation*; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D010276:Parasympatholytics; D013565:Sympatholytics; D001950:Bretylium Tosylate; D001285:Atropine; D011433:Propranolol; D010646:Phentolamine