DECREASED DIGITAL FLOW PERSISTS AFTER THE ABATEMENT OF COCAINE-INDUCED HEMODYNAMIC STIMULATION

This study determined whether the development of delayed ischemic sequ elae due to cocaine use-after the return of arterial blood pressure (B P) and heart rate to near-baseline values-may be attributable to regio nal vasoconstriction which persists beyond the acute systemic hemodyna mic response. Five cocaine-using volunteers received intravenous infus ions of saline placebo and cocaine 0.50 mg/kg several days apart in a double-blinded cross-over design. The intensity and duration of the co caine-induced decrease in peripheral blood flow (as documented by lase r Doppler flowmetry of the finger) were compared to the increases in B P (obtained with a Dinamap(R)) and heart rate using paired t-test and repeated-measures analysis of variance. A significant increase in BP a nd a significant decrease in finger flow were noted by the first time point (5 min). Within 15 min, cocaine induced a 36% +/- 5% increase in BP and a 73% +/- 18% decline in finger flow (P < 0.05 for difference between percent change in BP and percent change in flow). Dinamap(syst olic) and Dinamap(diastolic) returned to within 15% of baseline within 30 min, while finger flow remained more than 50% below baseline for t he remainder of the 60-min study period (P < 0.05). Changes in heart r ate paralleled those in BP. Except for isolated cases of documented co ronary vasoconstriction in patients presenting with complications afte r cocaine use, this study is the first to document the persistence of cocaine-induced vasoconstriction of a sensitive vascular bed beyond th e hypertensive response. It thus helps to explain the development of i schemic injury after cocaine use despite a stable rate-pressure produc t.