Clinical use of sodium nitroprusside in chronic ischemic heart  disease.  Effects on peripheral vascular resistance and venous tone and on ventricular volume, pump and mechanical performance.
Although hemodynamic benefit has been shown with sodium nitroprusside (NP) in acute coronary pump failure, complete understanding of the mechanisms of action of the agent on the cardiocirculation and its value in chronic ventricular dysfunction are lacking. This investigation evaluates the effects of NP on the systemic and regional arterial and venous beds and on cardiac dynamics, ventricular volumes, contractile state and myocardial energetics in long-standing congestive heart failure. Twelve patients with chronic coronary pump dysfunction received NP infusion to lower systolic pressure to 95-105 mm Hg. Left ventricular (LV) function was assessed directly by angiographic volumes and high fidelity pressure, and peripheral circulatory dynamics were determined simultaneously by forearm arterial and venous plethysmography. NP reduced mean arterial pressure (MAP) from 88.2 to 73.4 mm Hg (P less than 0.05) and significantly (P less than 0.05) enhanced the variables of LV performance: LV end-diastolic pressure (EDP) diminished from 18.5 to 9.9 mm Hg; ejection fraction rose from 0.47 to 0.55; percent of LV segmental shortening increased; and isovolumic and ejection indices of contractility improved. Concomitantly, NP reduced the indices of myocardial oxygen demands of ventricular tension time index and LVED volume index. These salutary effects on LV performance and energetics occurred secondary to peripheral arterial and venous dilation (P less than 0.05) produced by NP: total systemic vascular resistance was lowered from 1590 to 1310 dynes sec cm--5; forearm vascular resistance diminished from 46 to 37 mm Hg/ml/100 gm/min; and forearm venous tone fell from 14.2 to 10.1 mm Hg/cc. Depressed stroke index (SI) and cardiac index (CI) increased (P less than 0.05) with NP: despite the fall in LVEDP, when ventricular filling pressures with the agent were at levels slightly above normal. Dextran infusion given with NP to restore LVEDP to moderately elevated values increased SI and CI (P less than 0.05) when NP alone produced no change in stroke output. Thus, the peripheral vasodilator properties of nitroprusside improve LV function by reducing impedance to ventricular ejection, while MVO2 is diminished by decreasing LV preload and afterload through relaxing actions
D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D002306:Cardiac Volume / Q000187:drug effects*; D003327:Coronary Disease / Q000188:drug therapy*; D004341:Drug Evaluation; D005260:Female; D005292:Ferricyanides / Q000627:therapeutic use*; D006321:Heart / Q000187:drug effects*; D006334:Heart Function Tests; D006352:Heart Ventricles / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D009569:Nitric Oxide; D010101:Oxygen Consumption / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects*; D014665:Vasodilator Agents / Q000627:therapeutic use*; D014680:Veins / Q000187:drug effects*
D005292:Ferricyanides; D014665:Vasodilator Agents; D009569:Nitric Oxide