External carotid artery (ECA) vasoconstriction may defend internal carotid artery (ICA) blood flow during acute hypotension. We hypothesized that α1-receptor blockade-induced delay in ICA recovery to the baseline level from acute hypo-perfusion is related to attenuated ECA vasoconstriction. ICA and ECA blood flow were determined by duplex ultrasound during thigh-cuff release induced acute hypotension while the α1-receptor blocker prazosin (1 mg/20 kg-1) was administered to nine seated young healthy males. Both ICA (mean ± SD; 17 ± 8%, P=0.005) and ECA (37 ± 15%, P<0.001) blood flow decreased immediately following occluded thigh-cuff release with a more rapid ICA blood flow recovery to the baseline level (9 ± 5 sec) than for the ECA blood flow (17 ± 5 sec; P=0.019). ICA blood flow recovery from hypo-perfusion was delayed with prazosin (17 ± 4 sec vs. CONTROL 9 ± 5 sec, P=0.006) whereas ECA recovery remained unchanged (P=0.313) despite a similar reduction in mean arterial pressure (-20 ± 4 mmHg vs. CONTROL -23 ± 7 mmHg, P=0.148). These findings suggest that α1-receptor blockade-induced attenuation of the ICA blood flow response to acute hypotension is unrelated to the reduction in ECA blood flow. Sympathetic nervous system via the ECA vascular bed does not contribute to dynamic CA during acute hypotension.
- cerebral blood flow
- external carotid artery blood flow
- internal carotid artery blood flow
- transcranial Doppler