Mechanisms producing tachycardia in conscious baboons during environmental heat stress

The involvement of changes in sympathetic activity, changes in cardiac efferent vagal activity, sympathetic activity, changes in cardiac efferent vagal activity, and nonautonomic mechanisms in producing the rise in heart rate (HR) during the heat stress-induced hyperthermia was studied in seven unanesthetized, chronically instrumented baboons (Papio anubis and P. cynocephalus). The experimental protocol consisted of subjecting the baboon to environmental heating (EH) of sufficient intensity (40-45°C) to raise arterial blood temperature (T(bl)) 2-3° C in 1-2 h while in one of four states: 1) normal (control), 2) β-adrenergic receptor blockade induced by propranolol, 3) cholinergic receptor blockade induced by atropine, and 4) combined β- and cholinergic receptor blockade induced by propranolol and atropine together. HR rose linearly with T(bl) during EH in all four states (correlation coefficient ≥ 0.97 in all cases) with average HR-T(bl) regression coefficients (slopes) being 20.5 ± 1.2 (SE) beats·min^-1·°C for the normal state, 12.2 ± 0.5 beats·min^-1·° C^-1 for the β-blockade state, 13.3 ± 1.1 beats·min^-1·°C^-1 for the combined β- and cholinergic receptor blockade state, and 8.4 ± 0.8 beats·min^-1·°C^-1 for the combined β- and cholinergic receptor blockade state. Thus nonautonomic mechanisms account for about 40% of the tachycardia in heat-stressed baboons with the remaining 60% produced by combined vagal withdrawal and sympathetic activation. Furthermore application of a multiplicative model of autonomic control of HR to these data suggests that about 75% of the autonomic component is produced by vagal withdrawal.