EFFECT OF GENERALIZED SYMPATHETIC ACTIVATION BY COLD PRESSOR TEST ON CEREBRAL HEMODYNAMICS IN HEALTHY HUMANS

There is no general agreement regarding several aspects of the role of the sympathetic system on cerebral haemodynamics such as extent of ef fectiveness, operational range and site of action. This study was plan ned to identify the effect of a generalised sympathetic activation on the cerebral haemodynamics in healthy humans before it is masked by se condary corrections, metabolic or myogenic in nature. A total of 35 he althy volunteers aged 20-35 underwent a 5 min lasting cold presser tes t (CPT) performed on their left hand. The cerebral blood flow (CBF) ve locity in the middle cerebral arteries and arterial blood pressure wer e recorded with transcranial Doppler sonography and with a non-invasiv e finger-cuff method, respectively. The ratio of arterial blood pressu re to mean blood velocity (ABP/V-m)() and Pulsatility Index (PI) were calculated throughout each trial. CPT induced an increase in mean ABP (range 2-54 mmHg depending on the subject) and only a slight, though s ignificant, increase in blood velocity in the middle cerebral artery ( +2.4 and +4.4% on ipsi- and contralateral side, respectively). During CPT, the ratio ABP/V-m increased and PI decreased in all subjects on b oth sides. These changes began simultaneously with the increase in blo od pressure. The increase in ABP/V-m ratio is attributed to an increas e in the cerebrovascular resistance, while the concomitant reduction i n PI is interpreted as due to the reduction in the compliance of the m iddle cerebral artery. The results suggest that generalised increases in the sympathetic discharge, causing increases in ABP, can prevent co ncomitant increases in CBF by acting on both small resistance and larg e compliant vessels. This effect is also present when a slight increas e in blood pressure occurs, which suggests a moderate increase in the sympathetic discharge, i.e. when ABP remains far below the upper limit of CBF autoregulation. (C) 1998 Elsevier Science B.V. All rights rese rved.