Endocrine responses to insulin hypoglycaemia in the young calf.

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SUMMARY1. The effect of somatostatin on the responses to moderate insulin hypoglycaemia and to 2-deoxyglucose has been examined in 2-3 week-old calves with cut splanchnic nerves.2. Intravenous infusions of somatostatin (150 p-mole.kg-1.min-1) completely suppressed release of glucagon, pancreatic polypeptide (PP) and insulin from the pancreas in response to 2-deoxyglucose (1-1 m-mole/kg i.v.).3. The same dose of somatostatin completely blocked the rise in plasma PP concentration that normally occurs in response to moderate insulin hypoglycaemia and significantly delayed the rise in plasma pancreatic glucagon concentration. The hypoglyeaemic response to insulin was also found to be intensified by the administration of somatostatin.4. It is concluded that each of the pancreatic neuroendocrine responses, that are now known to be mediated via the parasympathetic innervation, is suppressed in the presence of somatostatin in the young calf.

Section: Discussionmentioning

confidence: 99%

The effect of somatostatin on pancreatic endocrine responses mediated via the parasympathetic innervation in the conscious calf.

Bloom¹,

Edwards²,

Järhult³

1980

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“…Adrenal venous blood samples were analysed for cortisol and corticosterone, as above, and also for adrenaline and noradrenaline by a modification of Euler & Flooding's trihydroxyindole method (Euler & Floding, 1955) as previously described (Bloom et al 1975).…”

Section: Methodsmentioning

confidence: 99%

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

Bloom¹,

Edwards²,

Hardy³

et al. 1976

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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.

“…kg-1 min'. It is therefore possible to conclude that the limiting factor to steroid release under these conditions operates at pituitary or hypothalamic level rather than in the adrenal cortex itself (Hardy, Silver, Addison, Malinowska & Edwards, 1974;Bloom, Edwards, Hardy, Malinowska & Silver, 1975). …”

Section: Adrenal Responses In Conscious Calvesmentioning

confidence: 99%

The sensitivity of adrenal responses to synthetic adrenocorticotrophin in the conscious unrestrained calf.

Edwards¹,

Hardy²,

Malinowska³

1975

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SUMABRY1. Changes in cortisol and corticosterone output and blood flow from the adrenal gland have been determined in the conscious unrestrained calf during i.v. infusions of synthetic adrenocorticotrophin (Synacthen) at 0 5 ng . kg-' min-' (low dose), 5 ng . kg-' min-' (medium dose), 50 ng . kg-' min-' (high dose) and 500 ng.kg-' min-' (very high dose).2. Infusions at the low dose produced a rise in adrenal output of both cortisol and corticosterone to maximum values of approximately 100 and 30 ng. kg-' min-L respectively. Mean output of both steroids was significantly increased within 5 min, reached a maximum within 10 min and had fallen to resting levels 10 min after the infusion was discontinued.3. The effects of infusions at both the high and very high doses were closely similar; maximal cortisol outputs were within the range 600-800 ng . kg. -' min-' and corticosterone 350-500 ng . kg-' min-' in both groups.4. When the infusions were terminated, pronounced differences were observed in the rates at which steroid outputs declined. Basal levels were restored within 10 min following the low dose and within 60 min in medium dose animals, but both cortisol and corticosterone output were still elevated 2 hr after infusion in high dose animals. In calves infused at the very high dose, cortisol output did not fall significantly during this 2 hr period.5. The ratio of cortisol: corticosterone released from the adrenal gland immediately before infusion (3.2 + 0 3) approximated to the proportions in which the two steroids were found in the arterial plasma, but fell progressively to a minimum (1.3 + 0.1) with increasing doses of Synacthen. Conversely, the ratio of the steroids in the arterial plasma was increased during infusions at the low dose, but not at the higher doses. 6. No significant change in adrenal blood flow occurred during Synacthen infusion in low dose animals despite the increase in steroid output. In A. V. EDWARDS AND OTHERS medium dose animals blood flow through the gland rose during infusion by approximately 75 % while in both high and very high dose animals the flow increased by up to 300 %.7. In the three groups in which adrenal hyperaemia occurred, blood flow had fallen to within the resting range 45 min after infusion: in each case this fall was much more rapid than the fall in steroid output. No significant increase in aortic blood pressure or heart rate accompanied infusion of Synacthen, indicating that adrenal hyperaemia was dependent upon vasodilatation within the gland.8. Administration of cycloheximide (10 mg/kg) by i.v. injection either before or during an infusion of Synacthen, inhibited steroidogenesis without affecting the vasodilator response.