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Acta Physiologica 2011; Volume 202, Supplement 684
The Joint Conference (FAMÉ 2011) of the LXXVth Meeting of the Hungarian Physiological Society, XVIth Meeting of the Hungarian Society of Anatomists, Experimental Section of the Hungarian Society for Experimental and Clinical Pharmacology and Hungarian Society for Microcirculation and Vascular Biology
6/8/2011-6/11/2011
Pécs, Hungary
HUMAN AND RAT CEREBRAL ARTERIES CONSTRICT TO INCREASE IN FLOW. A NOVEL ASPECT OF THE AUTOREGULATION OF CEREBRAL BLOOD FLOW.
Abstract number: P87
Toth1,2 P., Rozsa2 B., Springo2 Zs., Doczi3 T., Koller1,2 Á.
Introduction:
It is well established that elevation of pressure increases vasomotor tone, which play a substantial role in the regulation of cerebral blood flow (CBF). Interestingly, responses of cerebral vessels to increases in flow vary and have not been studied in human cerebral arteries. We hypothesized that increases in flow elicit constrictions of isolated human and rat cerebral arteries and aimed to elucidate the underlying mechanisms.
Methods:
Changes in diameter of isolated cerebral arteries of human (HCA) and middle cerebral arteries (MCA) of rat were measured to increase in flow, pressure and to their simultaneous increase. Then extrapolated (e)CBF was calculated. Flow-induced response was obtained in the presence of inhibitors of known mechanisms of action. Reactive oxygen species (ROS) were detected by ethidium bromide (EB) fluorescence.
Results:
HCA and MCA constricted to increases in flow (human: from 74±4.9 to 63±5%, rat: from 63.8±0.8 to 48.8±1.5% of passive diameter at 80 mmHg, p<0.05). Simultaneous increase in intraluminal flow+pressure further reduced the diameter compared to pressure induced changes (pressure: from 84±3 to 53±4%, pressure+flow: from 83.8±3 to 36±3%, p<0.05), leading to constant eCBF. Flow-induced constrictions were abolished by HET 0016 (inhibitor of synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE), inhibition of COX, blocking TXA2 (TP) receptor) and attenuated by scavenging ROS. Flow-enhanced ROS formation was significantly reduced by HET 0016 (control: 0.05±0.02, flow: 0.18±0.04, flow+HET 0016: 0.07±0.02 integrated intensity/total area).
Conclusions:
We found that in human and rat cerebral arteries 1) increases in flow elicit constrictions, 2) the mechanism of flow-induced constriction of cerebral arteries involves enhanced production of ROS, COX activity and mediated by 20-HETE via TP receptors, 3) and propose that simultaneous operation of pressure- and flow-induced constrictions is necessary to explain an effective autoregulation of CBF.
Support:
American Heart Association, Founders Affiliate, 0855910D,NIH PO-1 HL-43023, OTKA K71591 and K67984
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 684 :P87