RESUMEN
Interactions of lung stretch receptor [LSR] activity with that of arterial chemoreceptor [ACR] stimulation on the cardiovascular system [CVS] during hypoxic hypercapnia [HH] and hypoventilation [HV] are studied in anesthetized cats. HV was induced by lowering the tidal volume to 45% of its normal value. At this condition HV with arterial blood oxygen and carbon dioxide tensions of 45 and 60 mmHg [PaO2 - 45 mmHg and PaCO2 = 60 mmHg] was induced and changes in CVS parameters were recorded. In the second run the tidal volume was kept constant and the same level of HH was induced by exposing the cat to a gas mixture of 6-8% O2, 10% CO2 in nitrogen. Results of this study revealed that stimulations of ACR during HH did not alter the heart rate but did elevate aortic flow [30%] and contractility [60%]. Despite Induction of systemic vasodilation at this stage, there was a 12% increase in mean arterial pressure [Pa]. Reduced LSR reflexes during HV increased the heart rate [20%] and contractility [90%]. Although aortic flow increased equally in both conditions, the absence of systemic vasodilation during HV caused a 40% rise in Pa. Hence it is concluded that the reduction of LSR reflexes will greatly potentiate the regulatory influences of ACR on CVS during systemic hypoxia and hypercapnia