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- W1989538159 abstract "Use of extracorporeal circuits in cardiopulmonary bypass and hemodialysis often causes hypotension. To study a possible role of platelet-released serotonin, we perfused a rat hind leg by means of a heparin-coated (Edwards Lifesciences) extracorporeal shunt between carotid and femoral artery. The tube was loosely placed in a roller pump so that autoperfusion could instantaneously be replaced by pump perfusion. Aggregation of blood platelets was recorded continuously with a photometric device inserted into the tubing. Autoperfusion did not elicit platelet aggregation, and had no effect on aortic pressure or femoral resistance. Pump perfusion, however, immediately elicited strong platelet aggregation which diminished after ca 5 minutes but remained present for the next two hours of pumping. Aortic pressure initially decreased to 64 ± 9 % of pre-pump value, partly recovered, and then slowly fell to 69 ± 6 %. Femoral resistance showed a biphasic response: a short-lasting (ca 5 min) increase to 228 ± 31 % of initial value was followed by a sustained decrease to ca 60 %. The initial increase of femoral resistance was proportional to the amount of platelet aggregation, was accompanied by a four-fold increase of plasma serotonin in the tube, and could be prevented by 5-HT2A receptor blockade with ritanserin. The fall of aortic pressure remained absent after blockade of 5-HT2B mediated NO-release with pizotifen. General inhibition of NO-release with L-NA prevented both the decrease of aortic pressure and vasodilation in the leg. We conclude that the decrease of aortic pressure during pumping was caused by serotonin from aggregating platelets, via 5-HT2B receptor mediated NO-release." @default.
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- W1989538159 date "2001-03-01" @default.
- W1989538159 modified "2023-09-23" @default.
- W1989538159 title "HYPOTENSION DURING PUMP PERFUSION" @default.
- W1989538159 doi "https://doi.org/10.1097/00002480-200103000-00012" @default.
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