Proceedings of The Physiological Society

University College Cork (2004) J Physiol 560P, C7



gulli,giosue ; Cooper,Victoria Luise; Claydon,Victoria Elisabeth; Hainsworth,Roger ;

1. Institute for cardiovascular Research, University of Leeds, Leeds, United Kingdom.

The delay, and not only the gain, of the baroreflex response (baroreflex sensitivity) play an important role in the maintenance of cardiovascular system stability. Additionally when postural changes induce sudden drops in blood pressure, a delayed response may fail to maintain sufficient cerebral perfusion pressure. We tested the hypothesis that the delay of the carotid baroreceptor reflex might be impaired in subjects with poor orthostatic tolerance. All the subjects involved in the study gave their written informed consent and the protocol was approved by the local ethical committee. An orthostatic test with 60 deg head-up-tilt, and progressive lower-body-negative-pressure was performed on 25 patients with histories of unexplained syncope and 11 control subjects (age 29 ± 8.6). Test was stopped at the onset of presyncope and time to presyncope was taken as a measure of orthostatic tolerance. Twelve patients had normal tolerance (normal patients, age=46±13), thirteen patients showed to have low orthostatic tolerance (early fainters, age=43±18). We measured beat-to-beat blood pressure (Finapres) and brachial artery blood flow velocity (Doppler ultrasonography). Before the test, we determined the response of forearm vascular resistance (mean arterial pressure/ mean brachial artery velocity) to loading/unloading of carotid baroreceptors by the application of neck suction/pressure (-/+30mmHg) to a chamber fitted overlying the carotid sinus. We measured the gain in the response (maximum percentage change from baseline value in vascular resistance divided by the neck collar pressure) and the latency in the response (delay in heartbeats of the maximum change in vascular resistance after neck-collar stimulation). Results are reported as mean±S.E.M. and differences were determined by repeated measures ANOVA. In the three groups there were no differences in the sensitivity of the vascular resistance response after baroreceptors loading/unloading. Following baroreceptors unloading the latency of the response was 15.2 ± 1.3 heartbeats in early fainters, 10.2 ± 0.9 heartbeats in normal patients and 11.4 ± 1.3 heartbeats in controls. The latency in blood pressure rise was 12.1 ± 1.2 heartbeats in early fainters, 8.7 ± 1.0 heartbeats in normal patients and 8.0 ± 1.0 in controls. The results following baroreceptors loading were more scattered. The early fainters had still the tendency to show prolonged latency. These results suggest that the delay in the baroreflex response may play an important role in posturally related syncope. When postural changes induce sudden drops in blood pressure (simulated by the baroreceptors unloading), a delayed response may lead to a failure to maintain sufficient cerebral perfusion pressure, even in the presence of a normal baroreflex gain.

Where applicable, experiments conform with Society ethical requirements