No abstract

The involvement of changes in sympathetic activity, changes in cardiac efferent vagal activity, and nonautonomic mechanisms in producing the rise in heart rate (HR) during 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 degrees C) to raise arterial blood temperature (Tbl) 2-3 degrees C in 1-2 h while in one of four states: 1) normal (control), 2) beta-adrenergic receptor blockade induced by propranolol, 3) cholinergic receptor blockade induced by atropine, and 4) combined beta- and cholinergic receptor blockade induced by propranolol and atropine together. HR rose linearly with Tbl during EH in all four states (correlation coefficient greater than or equal to 0.97 in all cases) with average HR-Tbl regression coefficients (slopes) being 20.5 +/- 1.2 (SE) beats X min-1 . degrees C for the normal state, 12.2 +/- 0.5 beats X min-1 . degrees C-1 for the beta-blockade state, 13.3 +/- 1.1 beats X min-1 . degrees C for the cholinergic blockade state, and 8.4 +/- 0.8 beats X min-1 . degrees C-1 for the combined beta- 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.

SUMMARY. The influence of environmental heat stress on the arterial baroreflex control of heart rate (HR) was studied in eight conscious, chronically instrumented baboons. Inflations of balloon occluders around the inferior vena cava (IVC) and thoracic descending aorta (DA) were used to produce acute, graded changes in mean arterial blood pressure (MABP) in 5 mm Hg intervals ranging from ±5 to ±25 mm Hg. After determination of the HR responses to changes in MABP in the normothermic baboon (blood temperature <37.6°C), the animal was subjected to environmental heating to produce hyperthermia. When blood temperature reached approximately 39.5°C, HR responses to graded DA and IVC occlusions were again determined. During hyperthermia, the HR sensitivity (AHR/AMABP) to MABP changes was markedly diminished for reductions in MABP and significantly enhanced for increases in MABP. To determine whether these alterations in the HR response to changes in MABP were due to an alteration of the baroreflex control of HR, full, sigmoid-shaped HR-MABP curves for both the normothermic and hyperthermic states were constructed and characterized by total HR range, estimated slope of the steep portion of the curve, and MABP at the midpoint of the HR range (BPM). During hyperthermia (1) the whole HR-MABP curve shifted significantly upward by 35-40 beats/min, (2) total HR range, the estimated slope, and BP50 did not change, and (3) the control point (pre-occlusion HR-MABP value) shifted upward along the steep portion of the HR-MABP curve. In six of the eight baboons, full HR-MABP curves were also constructed during either /?-adrenergic blockade or cholinergic (Ch)-receptor blockade in the normothermic and hyperthermic state. Similar to that seen for the unblocked heart, the whole HR-MABP curves were also shifted upward during hyperthermia in this group of baboons with no alteration in the total HR range, the estimated slope, or BP r , 0 . The upward shift in the HR-MABP curve during Ch-receptor blockade, unlike during /S-receptor blockade, was much greater than that which could be attributed only to the local effect of blood temperature. Although the control point was also shifted upward along the steep portion of the curve during /?-or Ch-receptor blockade, the upward shift observed during /S-adrenergic blockade was similar to that observed in the unblocked state. Thus, a heat stress-induced hyperthermia produces a rise in HR without significantly altering the characteristics of the reflex control of HR by arterial baroreceptors. To rely solely on changes in HR sensitivity may lead to erroneous conclusions as to the effect of a particular stress on the baroreceptor reflex control of HR. Further, these results indicate that: (1) the upward shift in the HR-MABP curve is mediated by both the local effect of blood temperature on HR and cardiac sympathetic efferent neurons which are independent of the baroreceptor reflex, and (2) the upward shift in the control point is mediated predominantly by vagal withdrawal, probably as part of the comp...

The mechanisms involved in producing intestinal vasoconstriction during a hyperthermia-producing intestinal vasoconstriction during a hyperthermia-producing environmental heat stress are unknown. Five conscious baboons (Papio anubis), each with chronically implanted catheters and a flow probe around the superior mesenteric artery, were subjected to environmental heating (Ta 40-45 degrees C) to raise their arterial blood temperature (Tbl) 2.0-2.6 degrees C to approximately 39.5 degrees C. Accompanying the gradual rise in Tbl was a fall in mean superior mesenteric artery blood flow (MSMF) and a progressive rise in superior mesenteric vascular resistance (SMR). At peak Tbl, MSMF had fallen 28.8 +/- 0.6% (mean +/- SE) and SMR had risen 50.2 +/- 4.2%. To determine the involvement of the sympathetic nervous system in producing this intestinal vasoconstriction, the baboon was subjected to environmental heating after induction of alpha-adrenergic receptor blockade by phenoxybenzamine or phentolamine. In this state, the rise in Tbl was accompanied by no change in MSMF and a slight, but not statistically significant, rise (7.8 +/- 3.8%) in SMR. Since alpha-receptor blockade nearly completely abolishes intestinal vasoconstriction during heat stress, this intestinal vasoconstriction must be mediated primarily by elevated sympathetic outflow.

This study, carried out in two parts, sought to determine the importance of vasopressin (VP), the renin-angiotensin system (RAS), and the sympathetic nervous system in the dehydration-produced attenuation of hindlimb (cutaneous) vasodilation during environmental heating (EH). Baboons, chronically instrumented for blood sampling and for measurement of mean iliac blood flow (MIBF), arterial pressure, and core temperature (Tc), were subjected to EH while in euhydrated and dehydrated (64-72 h of water deprivation) states. EH consisted of exposure to an elevated ambient temperature (40-42 degrees C) until Tc reached 39.5 degrees C. In part I, indexes of the above vasoconstrictor systems were measured. Base-line plasma renin activity (PRA) and VP and norepinephrine concentrations were all significantly elevated by dehydration. In addition, the increase in PRA during EH was accentuated by dehydration. In part II, the effects of blockades of the RAS, the pressor action of VP, and the innervation of the hindlimb on hindlimb vasodilation during EH were assessed. None of these blockades, singly or together, reversed the dehydration-produced attenuation of the increase in MIBF during EH. Thus we conclude that other mechanisms are responsible for the dehydration-produced attenuation of cutaneous vasodilation in baboons during EH.

Dehydration attenuates the increase in limb skin blood flow elicited by environmental heating (EH). This study sought to determine which of the two primary effects of dehydration, increased body fluid osmolality or decreased body fluid volume, was primarily responsible for this cutaneous vasoconstrictor bias in baboons. Unanesthetized chronically instrumented baboons were exposed to EH while in euhydrated state, after 65-69 h of water deprivation (dehydration), after infusion of a small volume of hypertonic (20%) saline to raise plasma osmolality and sodium concentration to dehydration levels, and after injections of the diuretic furosemide over a 64-h period to produce an isosmotic fall in extracellular fluid volume. EH consisted of an acute elevation of ambient temperature to 39.5-42.0 degrees C until internal temperature reached 39.5-39.8 degrees C. The normal increases in external iliac artery blood flow and iliac vascular conductance during EH were unchanged by hyperosmolality but were attenuated by 39 and 31%, respectively, after furosemide treatment and by 42 and 46%, respectively, during dehydration. Thus the fall in extracellular fluid volume is the component of dehydration that attenuates the increase in hindlimb blood flow during EH in the same way as dehydration itself.

The characteristics and control of the increase in plasma renin activity (PRA) during environmental heating (EH) were determined in 12 unanesthetized, chronically catheterized baboons. Each EH experiment consisted of a 1.5- to 4-h exposure to an ambient temperature of 39-44 degrees C until core temperature (Tc) reached 39.5-40.0 degrees C. These EH experiments were done on the baboon in an unblocked state and during beta-adrenergic receptor blockade produced by propranolol when on normal-to-high salt intake (NHSI) and on low-salt intake (LSI). PRA rose linearly with Tc during EH, but the increase in PRA was considerably larger when the baboon was on LSI. The PRA-Tc linear regression coefficients were 2.32 and 5.98 ng angiotensin I X ml-1 X h-1 X degrees C-1 in NHSI and LSI states, respectively. This rise in PRA during EH was completely eliminated during beta-blockade in both NHSI and LSI states. It is concluded that heat stress activates the sympathetic nervous system to stimulate beta-receptor-mediated renin secretion by the kidney, this activation is controlled primarily by internal thermoreceptors, and variations in salt intake alters only the magnitude of the increase in PRA during heat stress, not the mechanisms that produce it.

The cutaneous vasodilation and renal vasoconstriction in baboons during environmental heating (EH) appear to be produced predominantly by sympathetic vasoconstrictor withdrawal and activation of the renin-angiotensin system, respectively. Since these mechanisms may be influenced differently by sodium depletion, this study examined the hypothesis that sodium depletion would have a differential effect on cutaneous and renal vascular responses to EH. Sodium depletion was produced in chronically instrumented baboons by placing them on low-salt intake for 8-19 days along with diuretic administration. EH consisted of exposing the baboon to an ambient temperature of 40-42 degrees C until core temperature (Tc) reached 39.8-40.0 degrees C. Both control plasma renin activity (PRA) and the rise in PRA with Tc during EH were considerably larger in sodium-depleted baboons. However, the magnitudes of the progressive increases in iliac vascular conductance (used as an index of hindlimb cutaneous vasodilation) and renal vascular resistance with rising Tc during EH were unaltered by sodium depletion. Therefore, neither cutaneous nor renal vascular responses to EH are influenced by elevated PRA and other changes accompanying sodium depletion in the baboon.