SPLANCHNIC SYMPATHETIC-NERVE ACTIVITY AND CIRCULATING CATECHOLAMINES IN THE HYPERTHERMIC RAT

The mechanisms responsible for the initial rise in splanchnic vascular resistance with environmental heating are controversial, and those responsible for the subsequent fall in splanchnic resistance in the severely hyperthermic animal are unknown. Thus we examined the effect of environmental heating on plasma catecholamine concentration, splanchnic sympathetic nerve activity (SNA), and select blood chemistries. In one study, 25 male Sprague-Dawley rats (270-300 g) were assigned to one of five groups on the basis of their core temperature (T(c), 37, 39, 41, 43, or 44-degrees-C) at death. Heart rate (HR), mean arterial pressure (MAP), and T(c) were monitored during heat stress under alpha-chloralose anesthesia 12.5 mg.ml-1.h-1). At each predetermined T(c), an aortic blood sample was drawn and analyzed for mean plasma concentration of norepinephrine (NE), epinephrine (E), Na+, K+, and lactate. From 41 to 43-degrees-C, NE and E rose significantly, and the animals became hyperkalemic and lactacidemic. In a separate study, we quantitated SNA from the greater splanchnic nerve during heat exposure of artificially respired animals anesthetized with pentobarbital sodium (50 mg/kg). MAP, splanchnic SNA, and T(c) were recorded. T(c) was elevated from 37.0 +/- 0.12 to 41.3 +/- 0.18 0.18-degrees-C in 70 min by increase of ambient temperature to 38-degrees-C in an environmental chamber. Splanchnic SNA was 54 +/- 8 spikes/s at a T(c) of 37-degrees-C and increased significantly as T(c) exceeded 39-degrees-C (P < 0.05). These results provide direct evidence that the sympathetic nervous system is involved in heat-induced splanchnic vasoconstriction and indicate that the decline in splanchnic vascular resistance in the hyperthermic rat observed in previous studies cannot be attributed to a decline in SNA or to a fall in circulating catecholamines but may be related to hyperkalemia and lactacidemia.