Pancreatic Blood Flow and Insulin Output in Severe Hemorrhage

Ts, Lau; Taubenfligel, W; Levene, R. A.; Farago, G. A.; Chan, Henry Lik Yuen; Koven, Irving H.; Wr, Drucker

doi:10.1097/00005373-197210000-00008

Cited by 21 publications

(5 citation statements)

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“…1; table II). These findings are in accordance with most previous studies which have shown that the normal output of insulin is inhibited by hypotension and hypovolaemia (6 -8 , 10, 12, 13, 26, 27), although some investigators have reported an increment of insulin release during exsanguination in the dog (2,19). The powerful influence of the sympatho-adrenal system on insulin release during haemorrhagic hypotension is further stressed by the fact that insulin output is inhibited concomitant to a marked elevation of the extracellular glucose concentration.…”

Section: Discussionsupporting

confidence: 93%

Role of the Sympatho-Adrenal System in the Control of Endocrine Pancreas during Haemorrhage in Cats

Andersson¹,

Hoist²,

Järhult³

1979

Eur Surg Res

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Glucose, insulin and glucagon concentrations were determined before, during and after a 60-min period of haemorrhagic hypotension at 60 mm Hg in controls, adrenal-ectomized and splanchnicectomized cats. Peak increase of arterial plasma glucose concentration in response to haemorrhage was 13.7 ± 4.3 mM in controls, 10.2 ± 2.8 mΛf in adrenal-ectomized and 3.1 ± 1.7 mM in splanchnicectomized cats, respectively. Peak portal insulin decrease was 58 ± 8 and 36 ± 14 pmol/l in controls and adrenalectomized cats, respectively, whereas insulin levels increased slightly in splanchnicectomized cats during hypovolaemia. Portal plasma glucagon concentration rose by about 250 pmol/l in response to bleeding in all groups of cats. We conclude that the prompt hyperglycaemic and hypomsuünaemic response to haemorrhage in cats are caused by an adrenergic, ‘non-medullary’ mechanism, whereas the marked rise in pancreatic glucagon release seems due to factors unrelated to the sympatho-adrenal system.

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Section: Discussionsupporting

confidence: 93%

Role of the Sympatho-Adrenal System in the Control of Endocrine Pancreas during Haemorrhage in Cats

Andersson¹,

Hoist²,

Järhult³

1979

Eur Surg Res

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“…However, interpretations of pancreatic beta cell function based on peripheral insulin levels, particularly in low flow states, can be misleading (Hiebert et al 1972, Lau et al 1972). Thus, a previous report in the rhesus monkey, subjected to hemorrhagic hypotension of 50 mmHg, clearly showed a 90% reduction in the calculated pancreatic secretion rate, despite a rise in peripheral venous glucose levels by over 100% and insulin with 30% (Hiebert et al 1972).…”

Section: Discussionmentioning

confidence: 99%

“…Neither anesthetic effect nor variable experimental hemorrhagic conditions can fully explain, however, clear cut species differences which have been reported, Thus, dogs seem to demonstrate both hyperglycemia and hyperinsulinemia (Bauer et al 1969, Lau et al 1972) and respond normally to a glucose tolerance test (GTT) (Hiebert et al 1976).…”

Section: Discussionmentioning

confidence: 99%

Glucose, insulin and osmolality changes in rats sustaining different hemorrhage volumes

Ware

Ljungqvist

Norberg

et al. 1982

Acta Physiologica Scandinavica

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Plasma glucose, osmolality and insulin have been investigated during hemorrhage in non-starved rats. The rate of blood loss leading to hemorrhages of 44% and 55% of the estimated original blood volume determined the patterns of response. Substantial hyperglycemic hyperosmolality and insulin values appropriate for the raised levels of glucose were observed in the animals bleeding more rapidly. The slower rate of hemorrhage was associated with only moderate hyperglycemia and hyperosmolality, while the insulin values rose to very high levels, 45 times basal. It is postulated that altered glucose-insulin metabolism in haemorrhage may have important consequences for fluid homeostasis, and the rate of bleeding is the fundamental factor steering this effect.

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“…Endotoxin administration to experimental animals induces a pronounced hypoglycemia (glucose levels of less than 70 mg/dl in mice [27]) which arises from several discrete metabolic alterations (2,12,(15)(16)(17)(18)32). Hypoglycemia also occurs in humans during acute bacterial sepsis and endotoxic shock (1,20). Impaired hepatic gluconeogenesis plays a major role in this response (19,33).…”

mentioning

confidence: 99%

Influence of endotoxin treatment on dexamethasone induction of hepatic phosphoenolpyruvate carboxykinase

McCallum¹,

Seale²,

Stith³

1983

Infect Immun

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Decreased glucocorticoid binding has been observed at a time after endotoxin (3 to 6 h) when imparied liver enzyme induction is known to occur. This study was undertaken to characterize the early time course of hypoglycemia and decreased liver phosphoenolpyruvate carboxykinase (PEPCK) activity in intact and adrenalectomized mice given endotoxin. In addition, altered steroid induction of hepatic PEPCK was examined in adrenalectomized mice given dexamethasone at intervals before and after a median lethal dose of endotoxin. Intact mice demonstrated a dramatic hyperglycemia at 1 h after endotoxin treatment, a response absent in adrenalectomized mice. Plasma glucose levels were significantly reduced from control values at 3 and 6 h posttreatment, with the most pronounced endotoxin-induced hypoglycemia seen in adrenalectomized mice. Hepatic PEPCK activity in intact mice given endotoxin was decreased at 3 and 6 h after treatment, although no change from basal, noninduced levels was seen in poisoned adrenalectomized mice. The increased increment in hepatic PEPCK activity due to fasting of intact control mice was reproduced in adrenalectomized control mice by the administration of dexamethasone. Furthermore, the induction of hepatic PEPCK by dexamethasone was inhibited by 1 h after endotoxin treatment, with enzyme activity falling to basal, noninduced levels by 6 h posttreatment. At these same time intervals after endotoxin treatment, no evidence of histopathology in the liver or adrenal glands was seen. These results coincide with changes in steroid binding seen previously and indicate that endotoxin treatment produces significant alterations in glucocorticoid action at the subcellular or molecular level.

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Pancreatic Blood Flow and Insulin Output in Severe Hemorrhage

Cited by 21 publications

References 0 publications

Role of the Sympatho-Adrenal System in the Control of Endocrine Pancreas during Haemorrhage in Cats

Role of the Sympatho-Adrenal System in the Control of Endocrine Pancreas during Haemorrhage in Cats

Glucose, insulin and osmolality changes in rats sustaining different hemorrhage volumes

Influence of endotoxin treatment on dexamethasone induction of hepatic phosphoenolpyruvate carboxykinase

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