ANALYSIS OF RESPONSES TO VANCOMYCIN IN CAROTID BLOOD FLOW IN THE MALE-RAT

Vancomycin is known to cause vasodilation, and hypotension secondary t o histamine release. We studied the actions of two forms of vancomycin , a clinically available preparation, clinical vancomycin, and a resea rch grade preparation, laboratory vancomycin, in the presence of an H- 1 receptor blockade and during H-2 receptor blockade with Doppler flow probe analysis of carotid artery flow rate. Clinical vancomycin, labo ratory vancomycin, and histamine, increased the mean carotid artery bl ood flow from baseline in a dose-dependent manner. Diphenhydramine, H- 1 receptor antagonist, attenuated the increase in mean carotid artery blood flow for the highest dose of clinical vancomycin and for each do se of histamine. Famotidine, H-2 receptor antagonist, significantly at tenuated the increase in mean carotid artery blood flow for the highes t dose of clinical vancomycin, the two higher doses of laboratory vanc omycin, and with each dose of histamine. Both diphenhydramine and famo tidine attenuated the increase of mean carotid artery blood flow with clinical vancomycin, laboratory vancomycin, and histamine. These data suggest that the change in carotid flow produced by vancomycin, is dep endent, in part, on either H-1 or H-2 receptor activation.