[The effects of the vasodilator nitroprusside on haemodynamics and myocardial oxygen consumption during drug induced myocardial depression (author's transl)].
The effect of the vasodilator nitroprusside (NP) on haemodynamics and myocardial oxygen consumption during drug induced myocardial oepression was examined in dogs (n = 7). The investigations were performed on closed chest dogs lightly anaesthetized with piritramide and N2O/O2 (ratio 2:1) under controlled ventilation and after beta-adrenergic blockade (1.5 mg/kg propranolol). After a loading dose and a continuous infusion of 0.3 mg/kg X min of pentobarbitone left ventricular maximum dp/dt was reduced to 50% of the control level, which was taken for granted as a standardized myocardial depression. Using an infusion of NP at a mean rate of 7 microgram/kg X min mean arterial pressure was then lowered to 80 mmHg for 20 min. The vasodilator therapy led to an increase in cardiac output and in stroke volume by 16%. Since the calculated endsystolic volume of the left ventricle decreased simultaneously (19%), the ejection fraction increased from 38% to 46%. There was also a significant reduction in left ventricular enddiastolic pressure (46%), which is supposed to result from the combined effects of an improved myocardial performance, a pooling of blood in peripheral vessels (indicated by decreases in enddiastolic volume by 6%, in mean pulmonary arterial pressure by 25% and in central venous pressure by 45%) and an increased ventricular compliance. Since the myocardial wall tension, a major determinant of myocardial energy demand, was lowered by increased ventricular compliance and reduced pre- and afterload, the oxygen consumption of the heart decreased by 22%. The smaller demand was supplied by an unchanged coronary blood flow. The narrowing of the a-v oxygen difference of the heart indicated a coronary dilatation (10%). The results obtained from this study support the clinical observations that NNP may improve an imbalanced ratio between myocardial oxygen supply and demand, in patients with impaired cardiac performance.
D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output / Q000187:drug effects; D002496:Central Venous Pressure / Q000187:drug effects; D004285:Dogs; D005260:Female; D005292:Ferricyanides / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D009206:Myocardium / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects; D010424:Pentobarbital / Q000494:pharmacology
D005292:Ferricyanides; D009599:Nitroprusside; D010424:Pentobarbital
Kardiovaskuläre Wirkungen von Natriumnitroprussid während einer Myokarddepression.