Effects of Enflurane on Release of Insulin by Pancreatic Islets in Vitro

Ewart, Robin; Rusy, Ben F.; Bradford, Mark W.

doi:10.1213/00000539-198112000-00007

Cited by 21 publications

(14 citation statements)

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“…A prior study demonstrated that isoflurane reduced the Glu metabolism, induced hyperglycaemia, and inhibited pancreatic insulin release (Zuurbier et al 2008). In another study, enflurane anaesthesia reportedly inhibited pancreatic insulin release and elevated blood glucose (Ewart et al 1981). Our study showed similar effects on serum insulin and glucose in dogs anaesthetized with either propofol-isoflurane or emulsified isoflurane.…”

Section: Discussionsupporting

confidence: 74%

Comparison between emulsified isoflurane and propofol/isoflurane combination on plasma thyroid hormones, insulin, glucose, and glucagon in dogs

Jiang

Lin

et al. 2014

Acta Vet. Brno

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It is important to determine the varying effects of anaesthesia agents on the endocrine function. In this study, the effects of emulsified isoflurane and propofol-isoflurane on the endocrine function were compared in dogs. Sixteen dogs were randomly divided into two groups: one group (G1) of dogs were induced with intravenous 5 mg/kg propofol and maintained with inhaled 2-2.5% inspiratory isoflurane in 100% oxygen; second group (G2) of dogs were induced with intravenous 1 ml/kg emulsified isoflurane and maintained with intravenous 8 ml/kg/h emulsified isoflurane. Blood samples to determine the endocrine function were collected prior to induction of anaesthesia and at 15 min, 30 min, 60 min, 2 h, 6 h, and 24 h after drug administration. Serum triiodothyronine and tetraiodothyronine concentrations in G1 increased significantly (P < 0.05) at 15 min and were higher than in G2. Serum insulin at 15 min and 30 min were significantly (P < 0.05) higher in both G1 and G2. Serum insulin in G1 was higher after anaesthesia than in G2. Serum glucagon decreased at 15 min, 30 min, and 60 min, without significant changes (P > 0.05). Serum glucose increased at 15 min and 30 min after anesthesia, and was significantly higher in G1 than in G2 (P < 0.05) at 60 min. In conclusion, both emulsified isoflurane and propofol-isoflurane anaesthesia affected triiodothyronine, tetraiodothyronine, and insulin in dogs, but emulsified isoflurane anaesthesia had a minimal effect on triiodothyronine and tetraiodothyronine. With its less deleterious effect on the endocrine function, emulsified isoflurane may be more suitable for canine anaesthesia.

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Section: Discussionsupporting

confidence: 74%

Comparison between emulsified isoflurane and propofol/isoflurane combination on plasma thyroid hormones, insulin, glucose, and glucagon in dogs

Jiang

Lin

et al. 2014

Acta Vet. Brno

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“…Volatile anesthetics, such as sevoflurane, attenuate insulin secretion by activating Table 6. Changes in blood glucose levels during insulin tolerance tests in groups S-ITT, SL-ITT, and P-ITT adenosine triphosphate-sensitive potassium channels in β-islet cells (2)(3)(4)(5). We previously found that propofol anesthesia enhances insulin secretion in rats (6,7).…”

Section: Discussionmentioning

confidence: 97%

“…Volatile anesthetics, such as sevoflurane, activate adenosine triphosphatesensitive potassium channels in β-islet cells, resulting in attenuated insulin secretion (2)(3)(4)(5). Although the precise mechanisms have not been elucidated, insulin secretion is significantly enhanced in rats under propofol anesthesia (6,7).…”

Section: Introductionmentioning

confidence: 99%

Comparison of mechanisms underlying changes in glucose utilization in fasted rats anesthetized with propofol or sevoflurane: Hyperinsulinemia is exaggerated by propofol with concomitant insulin resistance induced by an acute lipid load

Kitamura

Kawamura

et al. 2014

BST

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“…Hyperglycemia commonly occurs in the perisurgical period. Some of this is due to the intercurrent illness, but studies with the anesthetics isoflurane, halothane, and enflurane were shown to inhibit insulin secretion in isolated islets (Ewart et al, 1981;Desborough et al, 1993). It is generally agreed that the inhibition observed in these experiments is not due to an inhibition of glucose oxidation, but is associated with a small (but significantly different from controls) inhibition of islet adenylyl cyclase activity (Ewart et al, 1985).…”

Section: Acetylcholine and Cholinesterase Inhibitorsmentioning

confidence: 99%