Depression of plasma lipid fractions and inhibition of platelet aggregation by action of glucagon

Abstract

Venous blood was taken from 20 normal people following an overnight fast, and glucagon (1 mg) dissolved in 1.0 ml diluent was given i.v. Blood was taken at 1, 2, and 3 hr. Control studies were done in seven of the subjects at another time by administering the diluent only. Glucagon caused significant depression of plasma total lipid, and triglyceride at 1 and 2 hr, while plasma total cholesterol was significantly depressed at 2 hr. Epinephrine-induced platelet aggregation was studied in the hourly specimens of platelet-rich plasma (PRP) by measuring change in optical density (OD). Epinephrine caused both primary and secondary platelet aggregation in the 0-hr PRP of ten subjects and primary aggregation only in the other ten. Intravenous glucagon caused significant inhibition of secondary platelet aggregation at 2 and 3 hr. Secondary platelet aggregation was not inhibited when there was no depression of plasma lipids following glucagon (two of ten subjects). Glucagon (1 mg) dissolved in 1.0 ml diluent was given subcutaneously to five of the subjects at another time, and the studies were repeated. Depression of plasma total lipid, triglyceride, and cholesterol was greater than when glucagon was given i.v. Magnitude and duration of the depression were both increased. Secondary platelet aggregation induced by epinephrine was also inhibited. It was concluded that depression of plasma lipids by transfer of the lipid to platelets by action of glucagon is associated with inhibition of epinephrine-induced platelet aggregation.