Common carotid haemodynamic and metabolic effects of acutely administered nifedipine in human subarachnoid haemorrhage.

Although the drugs known as "calcium antagonists" exert inhibitory actions on vascular smooth muscle, there are no quantitative data concerning the clinical use of these vasodilator agents in human subarachnoid haemorrhage. In the present clinical study, we have measured the effects of nifedipine (20 mg tablet) on common carotid artery diameter (D) blood flow velocity (V) common carotid blood flow (CCBF) as an index of cerebral blood flow, systolic (Qs) and diastolic (Qd) blood flow fractions using a pulsed Doppler apparatus and on carotid arterial pressure (CAP), heart rate (HR) and oxygen consumption (VO2). Eight patients with subarachnoid haemorrhage were studied during anaesthesia for cerebral angiography. Thirty minutes after sublingual nifedipine, diameter (P less than 0.05), blood flow velocity (P less than 0.001), CCBF (P less than 0.001), Qs (P less than 0.05), and Qd (P less than 0.05) increased with a decrease in Qs/Qd ratio (P less than 0.05). carotid vascular resistance (CVR) fell (P less than 0.02) and oxygen consumption of the brain increased (P less than 0.01). Systolic, diastolic, and mean carotid blood pressure, heart rate, and arteriovenous difference in oxygen were unchanged. The increase in CCBF was closely correlated with the vascular resistance in the control state (r = 0.928, P less than 0.001) and with oxygen consumption (r = 0.869, P less than 0.001). We conclude that in vivo, nifedipine exerts a preferential action on cerebral vessels, vasodilating large arteries and arterioles. This action is more powerful if the vessels are already vasoconstricted. Thus, the use of nifedipine could be fruitful in cerebral ischaemia that is secondary to subarachnoid haemorrhage.