Cardiac output as a controller of ventilation through changes in right ventricular load.
Ventilatory responses to changes in right ventricular (RV) load were studied in spontaneous breathing anesthetized dogs. Moving average RV pressure leads to (PRV) was used as an index of the RV strain. RV load was changed in two ways: 1) cardiac output (Q) was increased by infusion of isoproterenol (0.7-1.2 micrograms/min) and reduced by infusion of vasopressin (0.3-0.5 U/min); and 2) RV pressure was increased independently on Q by partial balloon obstruction of the RV outflow. When Q was changed by drug infusion there was a linear correlation between leads to PRV and Q (avg r = 0.04). Well-correlated linear relationships were found between expired minute ventilation (VE) and leads to PRV (avg r greater than 0.03), the slopes and intercepts of which were not significantly different whether leads to PRV was changed by altering Q, partial obstruction of RV outflow, or combining both procedures. Bilateral vagotomy did not alter the VE/leads to PRV slope resulting from RV balloon inflations. It is suggested that the RV strain may act as a controller of ventilation and provide a link between Q and VE.
D000818:Animals; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D007545:Isoproterenol / Q000494:pharmacology; D011312:Pressure; D012119:Respiration; D014628:Vagotomy; D014630:Vagus Nerve / Q000502:physiology; D014667:Vasopressins / Q000494:pharmacology; D016276:Ventricular Function
D014667:Vasopressins; D007545:Isoproterenol