Platelet function studies in heart disease. VI. Enhanced platelet aggregate formation activity in congestive heart failure: inhibition by sodium nitroprusside.
We studied 11 patients with congestive heart failure and 10 normal volunteers for in vivo platelet aggregate formation activity. The patients with heart failure had significantly (p less than 0.01) more circulating platelet aggregates than the normal volunteers. During sodium nitroprusside infusion, the number of circulating platelet aggregates declined to normal levels and in vitro platelet aggregation responses to epinephrine and adenosine diphosphate were also suppressed significantly (p less than 0.01). This was associated with a 30% decline in systemic vascular resistance and a 28% increase in cardiac output. In other in vitro experiments, sodium nitroprusside was found to have direct, dose-related platelet aggregation inhibitory actions. This study suggests that an increase in vascular resistance in certain heart failure patients may in part be related to an increase in circulating platelet aggregates. Direct inhibition of platelet aggregation by sodium nitroprusside may be a mechanism of its beneficial effects in heart failure.
D000328:Adult; D001777:Blood Coagulation / Q000187:drug effects; D005292:Ferricyanides / Q000494:pharmacology*; D006331:Heart Diseases / Q000503:physiopathology*; D006333:Heart Failure / Q000097:blood*; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008875:Middle Aged; D009599:Nitroprusside / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects
D005292:Ferricyanides; D009599:Nitroprusside