Abstract
Although reflex cardiovascular responses from skeletal muscle are thought to play a role in cardiovascular regulation during exercise, the mechanism of somatic afferent nerve stimulation is unknown. To evaluate the possibility that regional skeletal muscle hypoxemia or hypercapnia-acidosis might play a role in this response, the hindlimbs of 13 chloralose-urethane-anesthetized dogs were vascularly isolated below the renal vessels and perfused at a constant flow via an extracorporeal disk oxygenator-pump while the systemic cardiovascular system was monitored separately. When the oxygenator gas mixture was changed to create regional hindlimb hypoxemia (PO2 [partial pressure of O2], 290-27 mmHg, P < 0.001) there was an increase in heart rate (160-179 beats/min, P < 0.001), systemic blood pressure (99-111 mmHg, P < 0.001), systemic vascular resistance (95-194 mmHg.cntdot.min/l, P < 0.01), and brachial arterial resistance (19-38 mmHg.cntdot.min/ml, P < 0.02), but a decrease in aortic flow (1163-793 ml/min, P < 0.001) and brachial arterial flow (6.6-3.9 ml/min, P < 0.001). When the oxygenator gas mixture was changed to create regional hindlimb hypercapnia and acidosis (PCO2, 43-115 mmHg, P < 0.001; pH, 7.39-7.05, P < 0.001), there were no significant changes in any systemic cardiovascular parameters. Only hindlimb hypoxemia of the degree present during severe exercise and/or metabolite(s) secondary to hypoxemia can elicit cardiovascular adjustments similar to those observed during exercise.