Effects of hydralazine and nitroprusside on cardiopulmonary function when a decrease in cardiac output complicates a short-term increase in pulmonary vascular resistance.
We investigated the short-term cardiopulmonary effects of nitroprusside and hydralazine when cardiac output (CO) was reduced by a short-term increase in pulmonary vascular resistance (PVR). In six anesthetized, ventilated dogs, small autologous blood clots, injected over 1 to 2 hr, increased right ventricular afterload. When CO had fallen approximately 40%, dogs were treated with nitroprusside and subsequently with hydralazine. Both drugs reduced biventricular filling pressures (p less than .05), but only hydralazine increased CO and stroke volume (p less than .05). Although mean blood pressure and pulmonary artery pressure remained constant with hydralazine, systemic vascular resistance and PVR decreased (p less than .01). In contrast, although nitroprusside reduced blood pressure and systemic vascular resistance (p less than .01), it did not affect PVR and pulmonary artery pressure. When CO is significantly reduced because of a short-term increase in PVR, hydralazine may be superior to nitroprusside in improving cardiopulmonary function.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004285:Dogs; D005292:Ferricyanides / Q000494:pharmacology*; D006830:Hydralazine / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology*; D011655:Pulmonary Embolism / Q000188:drug therapy / Q000209:etiology; D011667:Pulmonary Veins / Q000502:physiology; D013318:Stroke Volume / Q000187:drug effects; D013997:Time Factors; D014655:Vascular Resistance / Q000187:drug effects
D005292:Ferricyanides; D009599:Nitroprusside; D006830:Hydralazine