Morphine hyperglycaemia

Feldberg, W.; Gupta, K. C.

doi:10.1113/jphysiol.1974.sp010539

Cited by 44 publications

(39 citation statements)

References 7 publications

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“…Recently, it has been shown that a number of drugs which, on intraventricular injection affect blood pressure, heart rate, respiration or blood glucose, act in this way (Feldberg & Guertzenstein, 1972;Guertzenstein, 1973;Bousquet & Guertzenstein, 1973;Edery & Guertzenstein, 1974;Feldberg & Gupta, 1974;Guertzenstein & Silver, 1974;Dey, Feldberg & Wendlandt, 1975).…”

Section: Introductionmentioning

confidence: 99%

Vasopressin Release by Nicotine: The Site of Action

Bisset

Feldberg

Guertzenstein

et al. 1975

British J Pharmacology

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In cats anaesthetized with chloralose the release of neurohypophysial hormones was examined after injection of nicotine into the cerebral ventricles or cisterna magna or its topical application through perspex rings to the ventral surface of the brain stem. The release was measured by assaying the hormones in samples of venous blood Injected into a lateral or the third cerebral ventricle, nicotine (0.5 to 1 mg) produced release of vasopressin without oxytocin. When the aqueduct was cannulated, preventing access to the fourth ventricle and to the subarachnoid space, this release did not occur. Vasopressin was also released without oxytocin when nicotine (0.25 to 2 mg) was injected into the subarachnoid space through the cisterna magna. With this route of administration the nicotine did not enter any part of the ventricular system. Applied through paired perspex rings placed across the ventral surface of the brain stem, nicotine again produced release of vasopressin without oxytocin. The amount of nicotine placed in each ring was usually 80 μg, but a release was obtained with 10 μg and in one experiment with as little as 5 μg. The bilateral region on the ventral surface of the brain stem where nicotine acts when producing release of vasopressin lies lateral to the pyramids and in a longitudinal direction, 6 to 9 mm caudal to the trapezoid bodies. The vasopressin release by nicotine injected intraventricularly or intracisternally, or applied topically to the ventral surface of the brain stem was not due to absorption of nicotine into the blood stream, nor to blood pressure effects. It is concluded that nicotine acts on the ventral surface of the brain stem probably by activating the central projection to the supra‐optic and possibly also the paraventricular nuclei of afferent pathways in the sinus and vagus nerves which control the release of vasopressin in response to changes in blood volume or distribution.

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Section: Introductionmentioning

confidence: 99%

Vasopressin Release by Nicotine: The Site of Action

Bisset

Feldberg

Guertzenstein

et al. 1975

British J Pharmacology

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“…No experiments were done to determine the site of action of these substances although it is probably the same as that on which morphine acts when producing its hyperglycaemic effect, i.e. the ventral surface of the brain stem (Feldberg & Shaligram, 1972;Feldberg & Gupta, 1974), it would appear that apomorphine is about half, and pethidine at most about a third to a sixth as potent as morphine. With codeine no hyperglycaemia was obtained but if its potency were about a tenth that of morphine, no effect would have been detected with the sensitivity of the method used.…”

Section: Discussionmentioning

confidence: 99%

“…As the sulphate salt of morphine was used in all previous experiments to produce hyperglycaemia on intraventricular injection (Borison et al, 1962;Feldberg & Shaligram, 1972;Feldberg & Gupta, 1974;, this experiment, performed with the hydrochloride, shows that hyperglycaemia is not an effect of the sulphate moiety but of morphine itself.…”

Section: Methodsmentioning

confidence: 99%

“…For injections into the left lateral ventricle or for infusions into the fourth ventricle, a Collison cannula was implanted in an aseptic operation under pentobarbitone sodium anaesthesia. The method for cannulating the lateral ventricle was that described by Feldberg & Shaligram (1972), and for the fourth ventricle, that of Feldberg & Gupta (1974). The injections or infusions of drugs were made after recovery from operation, a few days later, without anaesthesia.…”

Section: Methodsmentioning

confidence: 99%

“…The hyperglycaemia is a central effect, but it does not stem from an action on structures in the walls of the third ventricle as suggested by these authors. Recent experiments indicate that the structures on which morphine acts when producing this effect are situated near the ventral surface of the brain stem caudal to the trapezoid bodies and are reached after the drug has passed into the subarachnoid space through the lateral recesses (Feldberg & Shaligram, 1972;Feldberg & Gupta, 1974;Dey, Feldberg & Wendlandt, 1975).…”

Section: Introductionmentioning

confidence: 99%

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Hyperglycaemia Produced by Drugs With Analgesic Properties Introduced Into the Cerebral Ventricles of Cats

Dey

Feldberg

1975

British J Pharmacology

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1The effects on blood glucose of four substances with analgesic properties (apomorphine, pethidine, codeine and etorphine) and of prostaglandin El were examined in unanaesthetized cats. They were applied by the intraventricular route being either injected into a lateral ventricle or infused into the fourth ventricle through implanted Collison cannulae. 2 Apomorphine gave rise to pronounced hyperglycaemia in a dose of 0.75 mg which produced scarcely any hyperglycaemia on intravenous injection. It was more effective on infusion into the fourth ventricle than on injection into a lateral ventricle and was approximately half as potent as morphine in provoking hyperglycaemia. 3 Codeine produced no hyperglycaemia in doses of 0.75 and 1.5 mg. 4 Pethidine had a weak hyperglycaemic action in doses of 0.75 and 1.5 mg, but the effect was not regularly obtained. Potency of the drug was at most only a third to a sixth that of morphine. 5 Etorphine produced strong hyperglycaemia on infusion into the fourth ventricle in a dose of 10,ug. Unlike apomorphine or morphine it was more potent on injection into a lateral ventricle when it produced a strong hyperglycaemic response in doses of 5 or 1 ,g, which were subthreshold on infusion into the fourth ventricle. However, this response may have been brought about indirectly as a result of severe asphyxia and of convulsions associated with the injections. On infusion into the fourth ventricle, etorphine was about 75 times as potent as morphine in producing hyperglycaemia. 6 Prostaglandin E1 had no hyperglycaemic action when infused into the fourth ventricle in a dose of 400 ng.

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Opiates modulate insulin action in vivo in dogs

et al. 1984

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To investigate the influence of opiates on insulin action in vivo, we induced mild physiological hyperinsulinaemia (15-20 mU/l) in five trained conscious dogs in the absence or presence of ongoing infusion with the opiate agonist D-met2-pro5-enkephalinamide (DMPE, 0.5 micrograms X kg-1 X min-1), or the opiate antagonist naloxone (1.25 mg followed by 1 microgram X kg-1 X min-1). The effects on glucose production and glucose utilization were measured by isotope dilution using 3-3H-glucose. Glucose fell similarly over 30 min in response to insulin in controls (0.021 +/- 0.003 mmol X l-1 X min-1), and both the DMPE and naloxone studies (0.016 +/- 0.002 mmol X l-1 X min-1 and 0.017 +/- 0.003 mmol X l-1 X min-1, respectively). In control dogs, insulin lowered glucose by transiently suppressing production by 0.028 +/- 0.006 mmol X kg-1 X min-1 at 20-30 min without changing utilization. In contrast, in both the DMPE and naloxone studies insulin lowered glucose by markedly raising utilization at 20 min by 0.094 +/- 0.017 and 0.139 +/- 0.022 mmol X kg-1 X min-1, respectively. Furthermore, insulin failed to suppress production in both DMPE and naloxone studies and, as plasma glucose fell, production rose in both treatment groups at 20 min by 0.045 +/- 0.012 and 0.089 +/- 0.022 mmol X kg-1 X min-1 respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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Morphine hyperglycaemia

Cited by 44 publications

References 7 publications

Vasopressin Release by Nicotine: The Site of Action

Vasopressin Release by Nicotine: The Site of Action

Hyperglycaemia Produced by Drugs With Analgesic Properties Introduced Into the Cerebral Ventricles of Cats

Opiates modulate insulin action in vivo in dogs

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