HEMODYNAMICS OF CHEMOREFLEX ACTIVATION IN UNANESTHETIZED RATS

Experiments were performed on unanesthetized rats (n=6) to determine t he systemic hemodynamics during chemoreflex activation by intravenous KCN. Rats chronically instrumented with ultrasonic flow probes in the ascendant aorta were submitted to KCN injections (30 mu g/kg) before a nd after sequential administration of the autonomic blockers atropine and propranolol. In the control period KCN injections produced a 60% r eduction in heart rate (HR) and a 46% elevation in blood pressure (BP) , while cardiac output (CO) decreased 76%, stroke volume (SV) decrease d 40%, and calculated total peripheral resistance (TPR) increased 900% . Atropine administration increased resting HR, whereas no change was observed in CO or BP. Chemoreflex-induced bradycardia was markedly att enuated (26%), and the presser response was potentiated (59%) after at ropine administration. CO and TPR responses were both attenuated after atropine administration (68% and 718%, respectively). Sequential admi nistration of propranolol decreased HR but did not change the cardiova scular responses to KCN injections compared with the responses observe d after atropine administration. In conclusion, CO is greatly reduced during KCN-evoked chemoreflex. Besides the intense bradycardia, a decr ease in SV contributed to this reduction. Bradycardic response was mos t dependent on the cardiac parasympathetic activation, and the reducti on in SV was probably most dependent on the increased cardiac afterloa d due to the sudden increase in BP.