Adrenal and pancreatic endocrine responses to hypoxia in the conscious calf.

Abstract

SUMMARY1. Pancreatic and adrenal responses to intense hypoxia have been examined in conscious unrestrained calves 3-5 weeks after birth.2. The outputs of both cortisol and corticosterone from the right adrenal gland rose steadily in response to hypoxia and this cortical secretary response was accompanied by a pronounced increase in blood flow through the gland. The changes in both steroid output and adrenal blood flow corresponded with those which occur in response to supramaximal doses of corticotrophin in calves of the same age.3. Neither adrenaline nor noradrenaline were released in significant amounts from the adrenal medulla until the arterial Po0 had fallen below 15 mmHg. Such severe hypoxia caused secretion of catecholamines at rates comparable with those recorded during maximal stimulation of the sympathetic innervation to the gland in anaesthetized calves. The response to intense hypoxia in these conscious calves differed from that which occurs under anaesthesia in that the amount of adrenaline released was invariably greater than that of noradrenaline.4. Severe hypoxia produced a rapid but transient increase in plasma glucagon concentration, followed by a pronounced rise in plasma glucose concentration in animals with abundant liver glycogen. No change in plasma insulin concentration was observed during hypoxia although it rose subsequently in response to hyperglyeaemia. 5. Bilateral section of the splanchnic nerves virtually abolished the release of catecholamines in response to hypoxia but the adrenal cortical and pancreatic responses did not appear to be affected.

Adrenal medullary responses to stimulation of the splanchnic nerve in the conscious calf.

“…In older calves, such as those used in the present study, in which the 'adrenal clamp' technique has been employed to quantify catecholamine output to physio- Comline & Silver, 1966 logical stimuli in conscious animals, adrenaline has again been the predominant amine released (Bloom et al 1975(Bloom et al , 1976(Bloom et al , 1977(Bloom et al , 1978. The results of the present experiments show that greater amounts of adrenaline than noradrenaline are also released from the gland in response to direct stimulation of the innervation when the stimulus frequency falls within the physiological range, the experiments are carried out in conscious animals and 'stress' is avoided by employing a stimulus below discernible behavioural threshold.…”

“…Thus, adrenaline is the predominant amine release in response to hypoglycaemia, 2-deoxyglucose or hypoxia in calves 3-5 weeks after birth (Bloom, Edwards, Hardy, Malinowska & Silver, 1975; Bloom, Edwards, Hardy & Silver, 1976;Bloom, Edwards & Hardy, 1977. In contrast, more noradrenaline than adrenaline is released in response to various stimuli, including splanchnic nerve stimulation, intra-arterial ACh and asphyxia, in anaesthetized calves of the same age (Silver, 1960;Comline & Silver, 1966) and the ratio between the amounts of the two amines released from the gland under these conditions differs markedly from the proportions in which they are stored in the gland (Comline & Silver, 1966).…”

<b>Adaptation to hypoxia: Changes in the level of erythrocyte 2.3-diphosphoglycerate and liver </b><b>adenylates </b>

“…First, hypoxic stress results in marked increase in plasma glucose (2), lactate (2), fatty acids (3), cortisol (2), and catecholamines (2), which are known to induce the degradation of adenine nucleotides (19). The increased level of catecholamines during hypoxia (2,6) could be responsible for the degradation of adenine nucleotides. Second, liver adenylate content decreased more rapidly under starved-hypoxic conditions than under fed-hypoxic conditions.…”

“…in a slight decrease in the liver adenylate pool under starved conditions (18). Hypoxia-induced increase in catecholamines and cortisol would favor an increased glycogenolysis and hepatic gluconeogenesis (2,3,6,17), which can provide blood glucose, a good substrate for anaerobic metabolism in many tissues under hypoxic conditions, and for the synthesis of erythrocyte 2,3-DPG. When fed ad lfbffruiz before and during hypoxia, little or no depletion of liver glycogen and no stimulation of hepatic gluconeogenesis may occur at the first stage; thus, the liver adenylate pool remains unchanged for 3 days.…”

“…Some metabolic changes to a deficient oxygen supply may act in most tissues: an elevation of erythrocyte 2,3-diphosphoglycerate (2, (10), an increased rate of glycolysis (13), and adenine nucleotide degradation (7, 14~16) under the conditions causing tissue hypoxia. The increase in erythrocyte 2,3-DPG during hypoxia, which is considered to be the most important factor favoring oxygen release at tissue level (10), is explained by the activation of erythrocyte phosphofructokinase (EC 2.7.1.11) due to respiratory alkalosis in hypoxia (8).…”