The effect of captopril on renal, coronary, and systemic hemodynamics in patients with severe congestive heart failure.
The effects of captopril (CPT), an oral angiotensin-converting enzyme (ACE) inhibitor, on systemic failure (CHF). In 15 patients, CPT decreased mean arterial pressure from 75 +/- 3 to 60 +/- 3 mm Hg associated with a 16% increase in cardiac output, a 24% reduction in systemic vascular resistance, and a 36% decrease in pulmonary capillary wedge pressure (all p less than 0.01). Despite the improved cardiac output, renal blood flow, creatinine clearance, and sodium excretion did not rise during the first 2 days of CPT therapy. In eight patients, coronary sinus blood flow diminished from 98 +/- 11 to 82 +/- 9 ml/min (p less than 0.01) following drug administration in association with a fall in arterial pressure and heart rate but no change in coronary sinus oxygen inhibitor failed to improve renal hemodynamics. In addition, initial CPT administration produced a decrease in coronary blood flow that was related to a decrease in myocardial oxygen requirements.
D002216:Captopril / Q000494:pharmacology* / Q000627:therapeutic use; D006328:Cardiac Catheterization; D003404:Creatinine / Q000652:urine; D005260:Female; D006321:Heart / Q000187:drug effects*; D006333:Heart Failure / Q000188:drug therapy* / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007668:Kidney / Q000187:drug effects*; D008297:Male; D011188:Potassium / Q000652:urine; D011392:Proline / Q000031:analogs & derivatives*; D012964:Sodium / Q000652:urine; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology* / Q000627:therapeutic use
D014665:Vasodilator Agents; D011392:Proline; D002216:Captopril; D012964:Sodium; D003404:Creatinine; D011188:Potassium