Hemodynamic and platelet response to the bolus intravenous administration of porcine heparin.
There is considerable evidence that under some conditions intravenous heparin infusion may cause or at least enhance platelet aggregation in vivo. Reports of heparin-induced vasodilatation and decreases in arterial blood pressure have not been accompanied by simultaneous observations of the platelet response. In this study both the hemodynamic and platelet response to the bolus administration of porcine intestinal mucosa sodium heparin were monitored in 24 cardiac and 12 vascular surgery patients. Mean arterial blood pressure decreased 7.1 +/- 0.8 mmHg as a result of a 247 +/- 34 dyne X sec/cm5 decrease in systemic vascular resistance. Platelet count, platelet volume distribution, and beta-thromboglobulin levels did not change with heparin infusion. These responses did not differ when comparing the 155 unit/kg group and the 400 unit/kg group or the 400 unit/kg groups treated with different commercial preparations. The single patient who did have a decrease in platelet count and a severe rise in beta-thromboglobulin with heparin died intraoperatively of a massive myocardial infarction. Large increases in platelet factor 4 with heparin administration were not associated with platelet release but were dependent on whether or not the patient was treated with preoperative subcutaneous or intravenous heparin. There was no evidence that heparin-induced vasodilatation was mediated by platelet aggregation and release.
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006493:Heparin / Q000008:administration & dosage / Q000494:pharmacology*; D006801:Humans; D007275:Injections, Intravenous; D010976:Platelet Count; D010978:Platelet Factor 4 / Q000032:analysis; D013552:Swine; D001620:beta-Thromboglobulin / Q000032:analysis
D001620:beta-Thromboglobulin; D010978:Platelet Factor 4; D006493:Heparin