Experiments were performed on unanesthetized @entity35 (n=6) to determine the systemic hemodynamics during chemoreflex activation by intravenous KCN. @entity35 chronically instrumented with ultrasonic flow probes in the ascendant aorta were submitted to KCN injections (30 microg/kg) before and after sequential administration of the autonomic blockers @entity3897 and @entity1169 . In the control period KCN injections produced a 60% reduction in heart rate (HR) and a 46% elevation in blood pressure (BP), while cardiac output (CO) decreased 76%, @entity64 volume (SV) decreased 40%, and calculated total peripheral resistance (TPR) increased 900%. @entity3897 administration increased resting HR, whereas no change was observed in CO or BP. Chemoreflex-induced @entity1168 was markedly attenuated (26%), and the pressor response was potentiated (59%) after @entity3897 administration. CO and TPR responses were both attenuated after @entity3897 administration (68% and 718%, respectively). Sequential administration of @entity1169 decreased HR but did not change the cardiovascular responses to KCN injections compared with the responses observed after @entity3897 administration. In conclusion, CO is greatly reduced during KCN-evoked chemoreflex. Besides the intense @entity1168 , a decrease in SV contributed to this reduction. Bradycardic response was most dependent on the cardiac parasympathetic activation, and the reduction in SV was probably most dependent on the increased cardiac afterload due to the sudden increase in BP.

Hemodynamics of chemoreflex activation in unanesthetized XXXX .

@entity1169 :: ('MESH:D011433', 'Chemical') :: ['propranolol'] @entity64 :: ('MESH:D020521', 'Disease') :: ['stroke'] @entity3897 :: ('MESH:D001285', 'Chemical') :: ['Atropine', 'atropine'] @entity35 :: ('10116', 'Species') :: ['Rats', 'rats'] @entity1168 :: ('MESH:D001919', 'Disease') :: ['bradycardia']
@entity35 :: (10116,Species) :: ['rats']
