Analysis of factors that contribute to cardiovascular changes induced in the cat by graded levels of systemic hypoxia.

1. In cats anaesthetized with Saffan, which does not block afferent activation of the brain stem defence areas, we have analysed the cardiovascular changes induced by 3 min periods of graded systemic hypoxia (fraction of O2 in inspirate, Fi,O2, 0.15, 0.12, 0.08, 0.06). 2. At light levels of Saffan anaesthesia, hypoxia (particularly Fi, O2 0.08 and 0.06) or selective stimulation of carotid chemoreceptors evoked the pattern of tachycardia, decrease in renal and mesenteric vascular conductance (RVC, MVC), but increase in femoral vascular conductance (FVC) which is characteristic of the alerting‐defence response. This supports our view that activation of the defence areas is an integral part of the response to systemic hypoxia. 3. Hypoxia also induced an increase in frequency of augmented breaths which was graded with the level of hypoxia: 0.6 min‐1 at Fi, O2 0.21 to 1.1 min‐1 at Fi, O2 0.06; in some cats each of these was accompanied by a transient fall in arterial pressure (ABP) and increase in FVC. It is proposed that these responses were all part of a reflex elicited by lung irritant receptors and facilitated by peripheral chemoreceptors. However, their low rate of occurrence and the liability of the vasodilatation suggests they do not make major contributions to the overall response. 4. The above short‐lasting responses were superimposed upon gradual changes whose magnitudes were graded with the level of hypoxia: hyperventilation, slight tachycardia, but bradycardia at Fi, O2 0.6, small increases in ABP, FVC and MVC allowing femoral and mesenteric blood flow to increase, but decreases in RVC which maintained renal blood flow constant. 5. Vagotomy had no significant effect on these changes. Further, hyperinflation of the lungs with pressures of 10 mmHg evoked the Breuer‐Hering reflex but had no noticeable cardiovascular effect. It is proposed that, in the cat, reflex tachycardia and vasodilatation elicited by lung stretch receptors play no significant part in the response to hypoxia. 6. By contrast, after pneumothorax, with ventilation and thereby arterial PCO2 (Pa, CO2) maintained constant, graded hypoxia produced graded bradycardia, decrease in MVC and RVC and no change in FVC. Taken together, these results suggest that in the spontaneously breathing cat, the response to hypoxia is dominated by the effects of hypocapnia secondary to hyperventilation, which by inhibiting peripheral and central chemoreceptor activity effectively counteracts the primary bradycardia and peripheral vasoconstriction elicited by hypoxic stimulation of peripheral chemoreceptors. 7. These proposals are compared with those drawn for other species.