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Biomedical subjects

B L Furman

Publications and source records attributed to B L Furman.

At least 73 records · Page 4Linked to original sources
PubMed1980

Bordetella pertussis respiratory tract infection in the mouse: pathophysiological responses.

The influence of living Bordetella pertussis on the induction and duration of pathophysiological reactions in mice infected intranasally with graded doses of culture was studied. Lethally infected mice showed loss of body weight, spleen atrophy, pronounced hypothermia and hypoglycemia, and highly elevated levels of leukocytes and serum immunoreactive insulin. Sublethally infected mice showed normal weight gain, practically normal temperature, spleen enlargement, lesser pronounced hypoglycemia, lower but significantly elevated levels of leukocytes and serum immunoreactive insulin, and histamine sensitization. Intensity of each reaction was related to the degree of lung infectivity. Hypothermia and leukocytosis were highly correlated. Concentration of serum immunoreactive insulin was closely related to the level of leukocytosis but not to the level of glucose. The strain and age of mice significantly affected the degree and duration of the reactions. The results suggest that the intranasally infected mouse may provide a useful model for investigations on whooping cough.

Aging↗
PubMed1980

Blockade of adrenaline-induced hyperglycaemia in the anaesthetized cat by continuous infusion of phentolamine and propranolol.

1 The effects of adrenoceptor blocking drugs on the metabolic responses to adrenaline infusion (1 microgram kg-1 min-1) have been studied in the anaesthetized, fasted cat. 2 Propranolol, in doses (0.25 or 1 mg/kg) which prevented completely adrenaline-induced tachycardia, reduced but did not abolish adrenaline-induced hyperglycaemia. 3 Phentolamine infusion, at a rate (15 micrograms kg-1 min-1 after a priming dose of 2.5 mg/kg) which reversed the pressor effect of adrenaline, reduced but did not abolish adrenaline-induced hyperglycaemia. 4 The continuous infusion of a combination of phentolamine (15 micrograms kg-1 min-1 after a priming dose of 2.5 mg/kg) and propranolol (5 micrograms kg-1 min-1 after a priming dose of 0.25 mg/kg) prevented completely the hyperglycaemia response to adrenaline infusion over a 6 h period. 5 The increase in blood lactate concentration produced by adrenaline was prevented completely by the combined infusion of propranolol and phentolamine but was not modified by phentolamine alone.

Anesthesia↗
PubMed1980

In vitro metabolic effects of gliclazide and glibenclamide in the rat.

The actions of gliclazide and glibenclamide on glucose uptake and glycogen deposition by rat hemidiaphragm and glucose utilization by rat epididymal adipose tissue have been examined in vitro. Neither drug exerted an insulin-like action on muscle or adipose tissue with respect to glucose uptake, glycogen deposition or glucose utilization. Neither gliclazide nor glibenclamide augmented the stimulating action of insulin on glucose uptake or glycogen deposition in the rat hemidiaphragm. In a high concentration (1 microgram ml-1), but not in lower concentrations, glibenclamide enhanced the action of insulin in stimulating glucose utilization by rat epididymal adipose tissue. Gliclazide was without any significant effect. Twenty eight day oral treatment with gliclazide did not increase basal or insulin-stimulated glucose uptake or glycogen deposition in rat hemidiaphragm muscle or glucose utilization by epididymal adipose tissue. It is concluded that in normal rats sulphonylureas do not exert important insulin-like actions or insulin potentiating effects.

Adipose Tissue↗
PubMed1979

The effects of levodopa on plasma glucose in two strains of rat.

The effects of levodopa on plasma glucose were examined in two strains of rats. In fasted Wistar rats levodopa produced a dose-dependent hyperglycaemic response which was augmented by pretreatment with nialamide. This response in nialamide-treated rats was prevented by pretreatment with phentolamine and converted to a hypoglycaemic response. Phentolamine increased the plasma concentration of immunoreactive insulin (IRI). In phentolamine-pretreated rats levodopa produced a further marked increase in the plasma IRI concentration. It is suggested that the prevention of levodopa hyperglycaemia by phentolamine is due to the marked increase in the plasma IRI concentration produced by pretreatment with phentolamine. Moreover the fall in the plasma glucose concentration produced by levodopa in phentolamine-pretreated rats is likely to be due, at least in part, to the additional increase in the plasma IRI concentration produced by levodopa under these conditions. In contrast, in fasted Sprague-Dawley rats pretreated with nialamide, levodopa produced either no effect on plasma glucose, or in larger doses, a marked hypoglycaemic effect followed by death. This hypoglycaemic effect was accompanied by a decrease in the plasma IRI concentration.

Animals↗
PubMed1979

Effects of levodopa and dopamine on plasma 11-hydroxycorticosteroid concentrations in mice.

The effects of levodopa on the plasma concentration of 11-hydroxycorticosteroids and glucose were examined in mice. In fasted, nialamide treated mice, but not in fed mice, levodopa produced a significant decrease in the plasma concentration of 11-hydroxycorticosteroids. This was accompanied by a significant and marked decrease in the plasma glucose concentration. These effects of levodopa could be mimicked by relatively small doses of dopamine injected intracerebroventricularly but not intravenously. The integrity of the hypothalamic-pituitary adrenal axis in nialamide-treated mice was suggested by the elevation in plasma 11-hydroxycorticosteroids produced by fasting or by insulin induced hypoglycaemia. These results indicate that in the mouse, as in other species, levodopa can inhibit stress provoked increases in the secretion of 11-hydroxycorticosteroids.

11-Hydroxycorticosteroids↗
PubMed1979

Impaired plasms immunoreactive insulin response to glucose in elderly hypertensive patients with abnormal clucose tolerance.

Oral glucose tolerance and the plasma immunoreactive insulin response to oral glucose were measured in 42 elderly hypertensive patients. Twenty-four of these patients showed abnormal glucose tolerance curves an 18 had normal curves. Patients with abnormal glucose tolerance showed significantly lower plasms immunoreactive insulin concentrations at 30 min and 60 min after the glucose load compared with patients with normal glucose tolerance. The patients in the two groups did not appear to differ in any other clinical or biochemical characteristics.

Aged↗
PubMed1978

[Nature and pathogenic significance of vertebral osteochondrosis].

On the basis of literary data the authors demonstrate that spinal osteochondrosis is due to aging changes in the biochemism and structure of intervertebral discs. Under the influence of such factors as physical, overtension, overcooling of the organism, osteochondrosis may acquire a pathogenic significance in the appearance of some diseases. This in its turn may be due to the development of supplementary processes in the discs and adjacent tissues. The authors discuss the insufficiently studied problem of overcooling of the organism in the development of sacro-lumbar radiculitis, underlining the facts of influence of overcooling on the hemodynamics and metabolism of the organism.

Adult↗
PubMed1977

Effects of levodopa and dopamine of plasma glucose concentration in mice.

In nialamide-treated, fasted mice levodopa produced a dose-dependent hypoglycaemic response. The response was also seen in pargyline-treated mice but not in animals which were not treated with a monoamine oxidase inhibitor. Dopamine did not affect plasma glucose under these conditons. In doses which were ineffective when injected i.v., both levodopa and dopamine produced hypoglycemia when injected intracerebroventriculary (i.c.v.). The hypoglycaemic response to levodopa was prevented by the dopamine antagonists, haloperidol and pimozide. The possible involvement of 5HT in the hypoglycaemic response to levodopa was suggested by the blockade of the response by cyproheptadine and methysergide together with the observations that hypoglycaemia is produced by 5HTP and by i.c.v. 5HT. p-Chlorophenylalanine (PCPA) also reduced the response to levodopa but the usefulness of PCPA as an inhibitor of 5HT synthesis in these experiments in doubtful since it also inhibited the hypoglycaemic effects of 5HTP and i.c.v. 5HT. Hypoglycaemia produced by levodopa did not appear to involve stimulation of insulin secretion since plasma IRI levels were not increased by levodopa and the hypoglycaemia was accompanied by a elevation of plasma FFA and no significant change in the liver glycogen content. It is suggested that the hypoglycaemic effect of levodopa is mediated through dopamine acting in the brain, although the involvement of 5HT in the response and the mechanisms involved remain to be determined.

Animals↗
PubMed1975

Effect of ICI 66082, a beta-adrenoceptor blocking drug on blood glucose in the rat.

ICI 66082, a cardioselective beta-adrenoceptor blocking agent, was found to produce hypoglycaemia in fasted rats. In fed rats a hyperglycaemic response was observed. The drug produced hypoglycaemia in fed adrenalectomised animals. The hypoglycaemic response to ICI 66082 was accompanied by elevations in plasma immunoreactive insulin (IRI) concentrations. The drug also reduced plasma glucose and increased IRI in moderately alloxan-diabetic rats. In severely diabetic animals The drug did not increase IRI concentrations and did not unequivocally lower plasma glucose concentrations. In vitro experiments showed ICI 66082 to increase glucose uptake by rat diaphragm muscle and epididymal adipose tissue. the hypoglycaemic response may be mediated by increases in plasms IRI concentrations with a possible contribution from direct effects of the drug on peripheral glucose utilization. As these responses differ from those published in relation to other beta-adrenoceptor blocking drugs it is unlikely that the effects are due to beta-adrenoceptor blockade. However, like other beta-adrenoceptor blocking drugs ICI 66082 reduced isoprenaline-mediated increase in plasma IRI.

Adipose Tissue↗