Panting is a controlled increase in respiratory frequency accompanied by a decrease in tidal volume, the purpose of which is to increase ventilation of the upper respiratory tract, preserve alveolar ventilation, and thereby elevate evaporative heat loss. The increased energy cost of panting is offset by reducing the metabolism of nonrespiratory muscles. The panting mechanism tends to be important in smaller mammalian species and in larger species is supplemented by sweating. At elevated respiratory frequencies and body temperatures alveolar hyperventilation begins to develop but is accompanied by a decline in the control of carbon dioxide partial pressure in arterial blood, probably through central chemoreceptors. Most heat exchange takes place at the nasal epithelial lining, and venous drainage can be directed to a special network of arteries at the base of the brain whereby countercurrent heat transfer can occur, which results in selective brain cooling. Such a phenomenon has also been suggested in nonpanting species, including humans, and although originally thought to be a mechanism for protecting the thermally vulnerable brain is now considered to be one of the thermoregulatory reflexes whereby respiratory evaporation can be closely controlled in the interests of thermal homeostasis.

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SUMMARY1. Donkeys sweat on exposure to heat and in response to intravenous adrenaline infusion.2. Thermal sweating was abolished by the adrenergic-neurone blocking agent bethanidine but not by atropine.3. Sympathetic decentralization (by preganglionic sympathectomy) abolished thermal sweating but adreno-medullary denervation had no effect.4. Exercise resulted in sweating from both sympathetically innervated and decentralized skin and from the innervated skin of animals which had previously undergone adreno-medullary denervation.5. Insulin-induced hypoglyeaemia resulted in sweating from sympathetically decentralized skin and from innervated skin in two out of four animals. Adreno-medullary denervation abolished the sweat gland response to insulin administration.6. Cold exposure inhibited the response of innervated sweat glands but not that of decentralized glands to adrenaline infusion.7. It was concluded that heat-induced and exercise-induced sweating of the donkey is controlled by adrenergic nerves; adreno-medullary secretion may contribute to sweating during exercise, and that cutaneous blood flow is important in the response of the glands to humoral stimulation.

The effects of hypoxia upon renal and endocrine function are unclear. Normal water-loaded subjects were exposed to hypoxia for 1 h (inspired PO2 = 74 Torr) in a decompression chamber (5,100 m, n = 8) or by breathing 10.5% oxygen at ambient pressure (n = 4). In four of eight subjects exposed to hypobaric hypoxia: urine flows (V) decreased (mean = 56%), urine osmolality increased (340%), plasma arginine vasopressin (AVP) increased (2,700%), plasma cortisol increased (256%), and mean blood pressure (BP) decreased (18%). V correlated inversely with AVP (r = 0.71, P less than 0.01) while AVP increases correlated with falls in mean BP (r = 0.72, P less than 0.05). Similar results were observed in the subjects exposed to normobaric hypoxia. Plasma aldosterone fell in the four subjects who maintained V on exposure to hypobaric hypoxia, but plasma renin activity did not change. In both groups prolactin levels were variable and solute and creatinine excretion were unchanged. No changes were observed in controls or in subjects exposed to hypobaria alone. Acute hypoxic exposure may produce significant hypotension with consequent increased AVP secretion resulting in diminished V.

The effect of bilateral splanchnic nerve (SPLX) section in fetal sheep [116-121 days gestational age (dGA)] on subsequent adrenocortical function was investigated. Fetal cortisol release was stimulated by 1) ACTH-(1-24) administration (100 ng/min for 15 min) at 126-129 and at 132-135 dGA, and 2) nitroprusside-induced hypotension (50% reduction in fetal arterial blood pressure for 10 min) at 129-132 and 136-139 dGA. No differences were observed between SPLX and control fetuses (CONT) in basal arterial plasma concentrations of cortisol from 126-141 dGA. A significant effect of fetal age on basal cortisol was observed in both SPLX and CONT fetuses from 126-141 dGA. A significant (P less than or equal to 0.05) increase in fetal arterial concentrations of cortisol was achieved by ACTH-(1-24) infusion in SPLX and CONT and did not differ between groups at either 126-129 or 132-135 dGA. Hypotension induced a significant increase in fetal plasma cortisol concentrations in SPLX and CONT fetuses (P less than or equal to 0.05). SPLX fetuses secreted significantly less cortisol in response to hypotension than CONT fetuses at both 129-132 and 136-139 dGA (P less than 0.05). Fetal arterial plasma concentrations of immunoreactive ACTH in response to hypotension were not different between CONT and SPLX fetuses. We estimated the half-life of endogenous fetal plasma cortisol after both hypotension and infusion of ACTH-(1-24). There were no differences between either method of inducing cortisol release on the endogenous cortisol half-life, nor were any differences in cortisol half-life observed between SPLX and CONT. At 136-139 dGA the adrenomedullary response to hypotension was abolished in SPLX, confirming completeness of denervation. In conclusion, the splanchnic nerves do not appear to be involved in the normal increase in basal fetal plasma cortisol observed in late gestation in fetal sheep. However, splanchnic nerve modulation of secretion of cortisol in response to stress may be involved in the increased fetal adrenal sensitivity to stress observed late in gestation.