Hyperglycaemia induced by drugs

Self Cite

Leimdorfer, Arana & Hack (1947) have shown that in the cat an intracisternal injection of adrenaline produces a long-lasting hyperglycaemia, which they attributed to a central action of the adrenaline. The hyperglycaemia was not reproduced by an intraperitoneal injection of adrenaline. In contrast, the hyperglycaemia produced in the rabbit by the injection of adrenaline into the lateral cerebral ventricle is fuliy accounted for by its absorption into the blood stream, since it is reproduced by intraperitoneal injection and is not affected by bilateral splanchnicotomy (Hasselblatt & Sproull, 1961). It appeared therefore that the hyperglyeaemic response of the cat to intracisternal and of the rabbit to intraventricular adrenaline might result from different mechanisms.However, the present experiments show that one difference between the two species is that, whereas in the rabbit adrenaline given byintraperitoneal injection readily elicits a hyperglycaemic response (Hasselblatt & Sproull, 1961), in the cat it does not. This is not due to a difference in the sensitivity of the two species to the metabolic action of adrenaline because, when infused intravenously, adrenaline is found to be as effective in the cat as in the rabbit. The hyperglyeaemic response of the cat to an intracisternal injection of adrenaline could therefore well be accounted for by absorption.The importance of this mechanism was established in the present experiments by the effect of bilateral splanchnicotomy on the hyperglycaemic response, but a central component, mediated by the splanchnic nerves, was also revealed.According to Leimdorfer (1950), noradrenaline given in small doses by intracisternal injection is, like adrenaline, effective in raising blood glucose concentration. If the hyperglyeaemic effect of intracisternally injected adrenaline or noradrenaline is largely due to systemic absorption noradrenaline should in this respect be the less effective, since it is well known that noradrenaline has a much weaker metabolic action than adrenaline.Previous estimates of the relative hyperglycaemic potency ofnoradrenaline vary greatly, between

contrasting

confidence: 61%

“…Blood glucose concentration was determined by the specific glucose oxidase method of Huggett & Nixon (1957), and the procedure followed was the same as that described by Hasselblatt & Sproull (1961).…”

Section: Methodsmentioning

confidence: 99%

Hyperglycaemia produced by intracisternal injection of adrenaline in cats

Sproull¹

1963

Self Cite

“…A Collison cannula was aseptically implanted under pentobarbitone sodium anaesthesia into the left lateral cerebral ventricle, as originally described by Feldberg & Sherwood (1953). In rabbits the point of insertion was either 7 mm lateral to the midpoint of the sagittal suture as described by Hasselblatt & Sproull (1961) The reserpine was dissolved in pyrogen-free distilled water; the solution was kept in the dark and cold but warmed to room temperature before injection. The monoamines were dissolved in pyrogen-free NaCl solution (0.9 g/100 ml.)…”

Section: Methodsmentioning

confidence: 99%

Temperature effects of reserpine injected into the cerebral ventricles of rabbits and cats

Banerjee¹,

Burks²,

Feldberg³

et al. 1968

SUMMARY1. In unanaesthetized rabbits and cats reserpine was injected through a chronically implanted cannula in the left lateral cerebral ventricle, and rectal temperature was recorded.2. In rabbits the reserpine (0-5-0.6 mg) caused a rise in temperature, frequent defaecation and sedation. On repeating the intraventricular injections at 24 hr intervals the rise in temperature was not obtained with the second or third injection, but defaecation and sedation still occurred. When the hyperthermic response to intraventricular reserpine had disappeared the anterior hypothalamus still responded to intraventricular noradrenaline which produced a rise in temperature.3. In cats the reserpine (0.5-0.75 mg) caused a biphasic change in temperature, i.e. an initial fall followed by a rise, frequent defaecation, and catalepsy. On repeating the intraventricular injections at 24 hr intervals the initial hypothermic phase of the temperature response was not obtained with the second or third injection, but the late rise, defaecation and catalepsy were still produced. When the hypothermic phase had disappeared the hypothalamus still responded to intraventricular noradrenaline or adrenaline which produced a fall, and to intraventricular 5-hydroxytryptamine (5-HT) which produced a rise in temperature.4. It is concluded that the rise in temperature in rabbits and the initial fall produced in cats is not due to a direct action of reserpine on the cells of the anterior hypothalamus but to noradrenaline released from adrenergic

“…Three samples were taken in each experiment before the adrenaline was given. Blood glucose concentration was determined by the specific glucose oxidase method of Huggett & Nixon (1957), and the procedure followed was the same as that described by Hasselblatt & Sproull (1961).…”

Section: Drug8mentioning

confidence: 99%

The origin of the hyperglycaemic response to intracisternal adrenaline in the cat: the site of systemic absorption and of central action of adrenaline from the subarachnoid space

Sproull¹

1963

Self Cite

An intracisternal injection of adrenaline in the cat produces a pronounced hyperglycaemia which has been attributed by Leimdorfer, Arana & Hack (1947) to a central action of the amine. However, it has recently been shown that this hyperglycaemia is largely attributable to peripheral action following absorption of the adrenaline into the blood stream, although a central component, mediated by the splanchnic nerves, does contribute to the resultant hyperglycaemia (Sproull, 1963).The present experiments, carried out to determine the site or sites of the systemic absorption and of the central action of intracisternally injected adrenaline, have shown that the main sites on and through which adrenaline acts from the subarachnoid space lie in the tuberal region on the ventral surface of the brain. METHODSCats of 2-4 kg body weight were anaesthetized with amytal sodium, 170-200 mg, injected intraperitoneally, and tracheotomy was performed. For the withdrawal of blood samples a vinyl cannula, 0-90 mm external diameter x 0-45 mm bore, was passed into the inferior vena cava through the saphenous vein.Direct introduction of adrenaline into the cisterna magna The cistema was exposed by removing the muscles over the atlanto-occipital membrane and then incising the dura and arachnoid. To retain the cerebrospinal fluid, the cats were placed on the belly, in a head-down ('gargoyle') position, with full flexion of the atlantooccipital joint, which was elevated to make the cistema magna become the highest point in the subarachnoid space. The adrenaline, in various doses, was dropped directly into the cisterna, after removal of some of the cerebrospinal fluid. In some experiments, in order to prevent ready access of the adrenaline to either the dorsal, lateral, or ventral surfaces of the medulla or the junction between the medulla and spinal cord, the area to be excluded from the adrenaline was covered with blood clot. After removing the surrounding cerebrospinal fluid, fresh blood immediately followed by thrombin (Parke, Davis & Co.) was applied to the area. An adherent clot instantly formed. The posterior cranial fossa was then refilled