Munchausen Zollinger-Ellison syndrome.
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Adult↗
Biomedical subjects
K R Gillon
Publications and source records attributed to K R Gillon.
Effect of single-dose omeprazole on intragastric acidity and volume during obstetric anaesthesia.
Various antacid or antisecretory agents are used to reduce the risk to patients of aspiration of gastric contents during general anaesthesia and a trial of the gastric proton pump inhibitor, omeprazole, is reported here. Twenty women admitted for elective Caesarean section under general anaesthesia received a single 80-mg oral omeprazole dose at 2000 hours on the evening before surgery. Intragastric pH and volume were measured immediately after induction of anaesthesia and on completion of surgery. Eighty-five percent of pH measurements at induction and extubation and 80% and 95% of volume measurements at induction and extubation respectively met the defined success criteria (pH greater than or equal to 2.5, volume less than 25 ml). Omeprazole treatment was well tolerated by the women and Apgar scores and subsequent progress of the babies were acceptable. These results indicate that gastric acidity and volume were acceptable in the majority of women after omeprazole treatment, but the interval from drug administration to induction of anaesthesia may have been too long in some cases and resulted in unacceptably low pHs.
Adult↗
Water content, vasoactive intestinal polypeptide and substance P in intact and crushed sciatic nerves of normal and streptozotocin-diabetic rats.
Observations on streptozotocin-diabetic rats have confirmed overhydration of peripheral nerve. As in previous studies, the sorbitol and fructose content, when expressed in terms of wet weight of nerve was found to be increased and myo-inositol decreased. The reduction in myo-inositol content was less, although still significant, when expressed in terms of protein content. Nerve water content increased during Wallerian degeneration following a crush injury in both normal and diabetic animals, but was relatively less in the latter. Vasoactive intestinal polypeptide (VIP) concentrations were significantly increased in diabetic nerve, those for substance P being normal. Both became severely reduced during Wallerian degeneration following nerve crush and ligature. The significance of these findings is discussed. The accumulation of water in the endoneurial compartment may be related to impaired extraction by the perineurium, to which the increased VIP content may contribute. These changes are unlikely to be responsible for nerve fibre damage.
Animals↗
The pathology of diabetic neuropathy and the effects of aldose reductase inhibitors.
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Aldehyde Reductase↗
Free and total lipid myo-inositol concentrations decrease with age in human brain.
An active transport system maintains myo-inositol in the brain at a much higher concentration than in the blood. Free and total lipid inositol has been analysed in samples of normal human anterior temporal cortex of different ages. At age 20 the concentration of inositol was 60 mumols/g protein, and it fell steadily to half that concentration at age 90. There was a similar fall with age in the total inositol lipid concentration.
Adult↗
Sorbitol, inositol and nerve conduction in diabetes.
Motor nerve conduction velocity was lower in streptozotocin-diabetic rats than in controls. Treatment with the aldose reductase inhibitor Sorbinil restored conduction velocity to normal. Diabetic rats had an increased concentration of sorbitol and reduced free inositol in sciatic nerve. Sorbinil corrected both defects. Inositol administration to diabetic rats also restored conduction velocity to normal. Genetically diabetic mice had reduced concentrations of inositol in sciatic nerve but fructose and sorbitol were normal. Glucose concentration was considerably increased.
Animals↗
Transport of myo-inositol into endoneurial preparations of sciatic nerve from normal and streptozotocin-diabetic rats.
myo-Inositol transport by a viable rat sciatic-nerve preparation is described. Such 'endoneurial' nerve preparations accumulated myo-inositol by an energy-dependent saturable system. Streptozotocin-diabetes reduced myo-inositol transport into sciatic nerve by approx. 40%. Elevated medium glucose concentration reduced myo-inositol transport into control nerves to a similar extent. Fructose and sorbitol did not inhibit myo-inositol transport. Inclusion of an aldose reductase inhibitor in the medium counteracted the reduced myo-inositol transport caused by elevated glucose concentration. The importance of these results to the problem of diabetic neuropathy is discussed.
Adenosine Triphosphate↗
Myo-inositol and sorbitol metabolism in relation to peripheral nerve function in experimental diabetes in the rat: the effect of aldose reductase inhibition.
A possible relationship between increased sorbitol concentration and decreased myo-inositol concentration in peripheral nerves of diabetic rats has been examined. To this end, sorbinil, an aldose reductase inhibitor, was used either to prevent or reverse elevation of nerve sorbitol concentration in diabetic rats. Sorbinil treatment at 20 mg . kg-1 . day-1 prevented elevation of nerve sorbitol levels in early diabetes and reduced sorbitol concentration from 2.38 to 0.51 mumol/g in rats diabetic for 10 weeks. This treatment reduced the increase in nerve fructose concentration and prevented the reduced myo-inositol concentration found in diabetic rat nerve (control 3.63, diabetic 2.40, diabetic/sorbinil, 3.56 mumol/g). Sorbinil treatment did not prevent a significant slowing of motor-nerve conduction velocity at 10 weeks although treatment reduced the extent of slowing. Sorbinil treatment at 25 mg . kg-1 . day-1 reduced elevated sorbitol and fructose concentrations in diabetic in diabetic rat nerve and normalised myo-inositol concentration. Myo-Inositol treatment at 650 mg . kg-1 . day-1 did not affect the elevated concentrations of sorbitol, fructose or glucose in peripheral nerves of diabetic rats, but it did restore reduced myo-inositol concentration. Both sorbinil and myo-inositol treatment partially reversed the slowing of motor-nerve conduction velocity in diabetic rats. These results are discussed in relation to the involvement of sorbitol and myo-inositol metabolism in the aetiology of diabetic neuropathy.
Aldehyde Reductase↗
Free and lipid inositol, sorbitol and sugars in sciatic nerve obtained post-mortem from diabetic patients and control subjects.
Sciatic nerves removed post-mortem from diabetic patients and normal subjects were analysed by gas chromatography for glucose, fructose, sorbitol and myo-inositol. The concentrations of free and lipid inositol were significantly lower in nerves from the diabetic than from the control group. Concentrations of glucose, fructose and sorbitol were higher in the nerves of the diabetic patients.
Aged↗
Axonal transport of noradrenaline and noradrenergic transmission in rats with streptozotocin-induced diabetes.
The accumulation of noradrenaline in constricted sciatic nerves was measured in 6 month diabetic rats (streptozotocin 35 mg/kg) and 4 day diabetic rats (streptozotocin 70 mg/kg) together with two groups of age-matched control animals. There was no alteration in the amount of noradrenaline accumulated in the nerves of the diabetic animals when compared with the controls. The vasa deferentia of the long-term diabetic animals showed an impaired response to stimulation of their noradrenergic nerves and a hypersensitivity to exogenous noradrenaline. These vasa were not wasted and showed a normal contractility in response to potassium chloride. Vasa deferentia from the short-term diabetic rats showed no abnormalities of function. Vasa deferentia from all groups of rats were also examined at the ultrastructural level. Specimens from all the chronically diabetic animals contained many abnormal nerve terminals. These lesions were not seen in vasa from the short-term diabetic rats. Taken together these findings indicate that rats with chronic streptozotocin-induced diabetes exhibit pathological changes in the noradrenergic nerves supplying the vas deferens. These animals do not, however, show an impairment of the axonal transport of noradrenaline.
Animals↗