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Biomedical subjects

B C Wexler

Publications and source records attributed to B C Wexler.

At least 19 recordsLinked to original sources
PubMed1985

Anti-opiate (naloxone) suppression of Cushingoid degenerative changes in obese/SHR.

Young and mature, genetically obese and non-obese, spontaneously hypertensive rats (SHR) were injected with saline (controls) or naloxone for 12 weeks. Naloxone stilled the hyperphagia to a normal intake in the obese SHR (Obese/SHR) so that young Obese/SHR did not develop their usual massive obesity and mature Obese/SHR that had become massively obese were reduced to leanness. The naloxone-treated young, obese and non-obese SHR (controls) exhibited marked reduction of the weight of their pituitary and adrenal glands, whereas the pituitary and adrenal glands of naloxone-treated mature, obese and non-obese/SHR were greatly increased in weight. The elevated systolic blood pressure of the obese and non-obese rats was reduced after chronic treatment with naloxone. Naloxone treatment caused reduction of blood ACTH, corticosterone, and beta endorphin levels but elevated growth hormone levels. The characteristic hyperinsulinemia, hyperlipidemia, hyperglycemia, elevated BUN levels, and the Cushingoid spectrum of degenerative changes found in Obese/SHR did not appear in naloxone-treated rats.

Adrenal Glands↗
PubMed1985

Prolonged protective effects following propranolol withdrawal against isoproterenol-induced myocardial infarction in normotensive and hypertensive rats.

Young adult, male and female, normotensive Sprague-Dawley (S-D) and spontaneously hypertensive rats (SHR) were injected with propranolol three times daily for 3 weeks. None of the animals manifested signs of withdrawal when the injections were terminated. Seven days later, the animals were challenged with a dose of isoproterenol which would produce massive myocardial infarction and 50-60% mortality in non-treated animals. The propranolol pretreatment caused marked tranquilizing and blood pressure lowering effects in SHR exclusively. Despite the 7-day propranolol withdrawal period, very few animals died and myocardial damage was minimal. However, blood pressure levels dropped to shock-like levels, blood CPK and LDH levels showed dynamic increases, there was marked hypertriglyceridaemia, and plasma corticosterone rose to supranormal levels. Microscopically, the hearts of the propranolol pretreated animals showed little evidence of necrosis but the SHR hearts manifested large atrial and ventricular thrombi. It is suggested that in the rat, propranolol treatment causes positive myocardial protective effects mediated through hormonal and metabolic changes and propranolol withdrawal does not lead to hypersensitivity to catecholamines. In fact, the beta-blocking effects of propranolol remain effective for some time after withdrawal.

Animals↗
PubMed1984

Dexamethasone suppression of cushingoid degenerative changes in obese spontaneously hypertensive rats (SHR).

Male and female, young (2 months old) and mature (10 months old), obese and nonobese, spontaneously hypertensive rats (SHR) were treated with dexamethasone, 5 micrograms/rat and 10 micrograms/rat, respectively, subcutaneously (SC) 2 times daily for 5 months. Steroid treatment stilled the voracious appetite of the obese SHR, and the massively obese, mature animals were reduced to almost normal size. The young, steroid-treated, obese SHR did not develop their genetically programmed corpulency. The untreated, young and mature, obese SHR ate voraciously, became massively obese, and developed their characteristic Cushing's disease-like spectrum of degenerative changes, eg, hypertension, hyperlipidemia, hyperglycemia, muscle wasting, kidney stones, thin skin, and accelerated aging. The blood pressure of the steroid-treated animals was lowered concomitant with reduced levels of circulating ACTH, beta endorphin, insulin, triglycerides, and cholesterol. Dexamethasone caused hyperlipidemia, hyperglycemia, and increased BUN levels in young obese and nonobese SHR only. The mature obese SHR had giant-sized thymus glands that were further enlarged with steroid treatment; dexamethasone was thymolytic in young, obese and nonobese SHR. Dexamethasone caused severe reduction of pituitary and adrenal gland size, simulating the condition of hypophysectomy. These findings demonstrate that dexamethasone suppression of the pituitary-adrenal axis palliates and prevents the spontaneous development of Cushingoid degenerative changes in these genetically obese and hypertensive rats.

Adrenal Glands↗
PubMed1983

Resistance of obese and non-obese, spontaneously hypertensive rats to alloxan-induced diabetes.

Male, 5 months old, massively obese, spontaneously hypertensive rats (Obese/SHR) were given 10 mg alloxan/100 g b.w., s.c., to induce diabetes. Control Obese and non-obese/SHR were given saline. Insulin therapy was withheld. All of the animals were killed at 6 months of age. Alloxan caused a slight but statistically significant increase in blood pressure, pituitary and adrenal glandular hyperplasia, hyperlipidemia, hyperglycemia, and increased BUN levels. The giant sized islets of Langerhans in Obese/SHR showed only partial degranulation of the insulin-producing beta cells concomitant with residual but apparently adequate blood insulin levels, whereas the islets of non-obese/SHR exhibited virtually total beta cell degranulation and only trace amounts of blood insulin. The alloxanized, non-obese rats were severely emaciated; the alloxanized Obese/SHR maintained their obesity. Alloxan-treated, Obese and non-obese/SHR manifested gross and microscopic degenerative changes suggesting acceleration of the normal aging process. The genetically-programmed pathogenesis of diabetes, obesity, hypertension, and Cushingoid pathophysiology of Obese/SHR may be due to hyperadrenocorticism.

Adrenal Cortex↗
PubMed1983

Cushingoid pathophysiology of old, massively obese, spontaneously hypertensive rats (SHR).

Male and female, massively obese and nonobese, spontaneously hypertensive rat (SHR) which are hypersensitive to stress were kept under quiescent conditions; they were autopsied at 15 months of age. The blood pressure of the Obese/SHR plateaued at 166 mmHg versus 198 mmHg for the nonobese/SHR. The once massive thymi vanished in the Obese/SHR accompanied by greatly enlarged adrenal glands, pituitary basophilia, greatly elevated levels of adrenocorticotrophin, corticosterone, deoxycorticosterone, aldosterone, fatty liver, hyperlipidemia, and hyperglycemia. The Obese/SHR were hyperadrenocorticoid compared with their nonobese siblings and manifested a Cushingoid spectrum of degenerative changes (e.g., thin skin, hypertension, diabetes, kidney stones, and accelerated aging). The provision of a nonstressful environment is believed to have dampened the usual chronic hyperadrenocorticism and prolonged the lifespan of the Obese/SHR.

Adrenal Cortex Hormones↗
PubMed1983

Hypersensitivity of spontaneously hypertensive rats to heat and ether before the onset of high blood pressure.

Hypertension-prone, male, spontaneously hypertensive rats (SHR; n = 60) and normotensive, male, Sprague-Dawley rats (S-D; n = 60) were exposed to the relatively innocuous stimulus of heat and ether when they were 40 days of age, just before the usual onset of high blood pressure in SHR. The animals were decapitated 0, 2, 5, 15, and 60 min postexposure to heat and ether. Blood levels of corticosterone, aldosterone, PRL, GH were measured concomitant with pituitary content of GH and PRL and adrenal content of ascorbic acid and cholesterol. The foregoing constituents were used as an index of pituitary-adrenal responsiveness. Changes in circulating corticosterone, PRL, GH, and especially aldosterone indicated that before the onset of their high blood pressure, SHR are much more responsive to noxious stimuli than normotensive S-D. The pattern of change in the pituitary content of GH and PRL, adrenal ascorbate, and cholesterol were also indicative of SHR hypersensitivity. These findings suggest that adrenal steroidogenesis and the stress response pattern in SHR vs. normotensive rats may be unique.

Adrenal Glands↗
PubMed1983

Jogging reduces obesity and hypertension in obese/SHR.

Young Obese/SHR, genetically destined to become obese were made to run three times daily, averaging 2740 ft/day. Siblings of these young Obese/SHR which were allowed to remain sedentary, developed voracious appetites, massive obesity, hyperlipidemia, diabetes, hypertension, hyperadrenocorticism, muscle wasting, kidney stones, thin skin, and accelerated aging. The Obese/SHR that exercised did not become obese, their blood lipid, glucose, BUN, blood pressure, and hyperadrenocorticism were reduced, but their testes and ovaries became prematurely atrophic.

Adrenocorticotropic Hormone↗
PubMed1983

Hormonal and metabolic changes during acute myocardial infarction in normotensive vs hypertensive rats.

Male and female, normotensive, Sprague-Dawley (S-D) rats, and spontaneously hypertensive rats (SHR) were subjected to acute and massive myocardial infarction with isoproterenol. Some of the animals were pre-treated (7 days) with the prolactin-lowering drug, bromocryptine. SHR survived in greater numbers than S-D but developed massive congestive heart failure of late onset. The adrenal glands and hearts became greatly hypertrophied in parallel with severely involuted thymus glands. ECG tracings demonstrated intense tachycardia and myocardial ischaemia. Bromocryptine reduction of prolactin (PRL) showed no effect on ECG tracings but reduced triglyceride, free fatty acid, total cholesterol and glucose levels. Isoproterenol caused dynamic increase in glucose, free fatty acids and triglycerides. CPK levels demonstrated greater cardiac damage in S-D vs SHR; greatly elevated SGOT and SGPT levels confirmed the presence of fatty liver in S-D and SHR. Myocardial infarction caused marked increase in circulating PRL in females only and sustained increases in aldosterone and corticosterone. SHR survivors had a high incidence of atrial and ventricular thrombi, left ventricular aneurysms, and intense fibroplasia and cartilaginous metaplasia in areas adjacent to damaged myocardium. It is suggested that adrenal steroidogenesis during an acute myocardial infarct favours survival and more complete myocardial repair in females vs males, and preexisting hypertension in SHR is associated with hormonal and metabolic response patterns different from normotensive S-D rats.

Animals↗
PubMed1982

Differences in adrenal cholesterol, ascorbic acid, circulating corticosterone and aldosterone during the onset of hypertension in SHR vs WKy rats.

Young adult male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats were killed under strictly quiescent conditions when they became 24, 32, 44, 60, 90 and 120 days of age. Systolic blood pressure was measured just prior to autopsy. Adrenal glands were assayed for ascorbic acid and total cholesterol content, and examined histologically. At 60 days of age, the blood pressure of the SHR became abnormally elevated, reaching severely elevated levels by 120 days of age. The adrenal glands of SHR were consistently smaller than those of WKy but their zonae glomerulosae stained intensively positive for lipid. Adrenocortical ascorbate and cholesterol content remained consistently and significantly lower in SHR vs WKy as did circulating corticosterone levels. Plasma aldosterone levels rose concomitantly with rising blood pressure in SHR and became progressively lower with age in normotensive WKy. These findings suggest that corticosteroidogenesis is different in SHR vs normotensive WKy rats.

Adrenal Glands↗
PubMed1982

Genetically mediated resistance to naturally occurring aortic sclerosis in spontaneously hypertensive as against Sprague-Dawley and Wistar-Kyoto breeder rats.

Male and female, normotensive, Sprague-Dawley (S-D), Wistar-Kyoto (WKy), and spontaneously hypertensive rats (SHR) were bred repeatedly until the females had given birth to and nursed 6 litters of pups. At the close of the 2nd, 4th and 6th breeding, breeder males and females, along with celibate males and females of equal age, were killed. S-D and WKy breeder rats manifested progressively increasing adiposity and high blood pressure with each successive breeding; breeder SHR showed mild exacerbation of their pre-existing high blood pressure. Adrenocortical hyperplasia and thymus-gland involution suggested increasing pituitary-adrenal activity in breeder rats. Circulating aldosterone levels decreased with repeated breeding in parallel with increased deoxycorticosterone and corticosterone secretion. The repeatedly bred normotensive rats manifested worsening aortic sclerosis as against little or no aortic sclerosis in the repeatedly bred SHR. Breeder SHR developed fibrinohyalin intimal lesions limited exclusively to the arterioles of the testis and ovary. Virgin rats did not develop any vascular disease. It is suggested that a diverse spectrum of adrenal steroids in breeder HSR combined with genetic direction control the morphogenesis of arterial disease in breeder SHR.

Animals↗
PubMed1981

Spontaneous hypertension ion cross-suckled rats.

Genetically normotensive Sprague-Dawley rats nursed by spontaneously hypertensive foster mothers develop sustained high blood pressure. Some factor related to the genetically programmed hypertension of the foster mother is probably transmitted to the infant rats through her milk. Alternatively, the hyperkinetic behavior of the mother may activate a hypertensinogen in young having the proper constellation of genes.

Animal Population Groups↗
PubMed1981

Furosemide-induced hyperuricemia, hyperglycemia, hypertension and arterial lesions in nonarteriosclerotic and arteriosclerotic rats.

Male and female, Sprague-Dawley rats, with and without arteriosclerosis, were subjected to chronic treatment with furosemide for 4 weeks. Furosemide-treated rats manifested increased adrenal and kidney weights along with an increase in blood pressure; rats with pre-existing arteriosclerosis showed considerable reduction in heart and body weights. Furosemide-treated animals displayed an increase in circulating levels of creatine phosphokinase, lactic dehydrogenase, free fatty acids, glucose, BUN and uric acid. Circulating levels of triglycerides, total cholesterol, and corticosterone were subnormal, whereas aldosterone was distinctly elevated. Despite these metabolic derangements, de novo arterial disease did not appear in virgin rats without pre-existing arterial disease. However, furosemide-treated virgin rats did develop grossly visible apical and left-ventricular foci of myocardial necrosis, i.e., 12% in males, 9% in female virgins. Breeder rats with pre-existing arteriosclerosis manifested exacerbation of their arterial disease, e.g., intimal calcification of the epicardial coronary arteries along with foci of myocardial fibrosis and islet beta-cell granule depletion. Adrenocortical lipid alterations appeared in all animals treated with furosemide. It is suggested that this spectrum of metabolic and histopathologic degenerative changes may have been caused by secondary aldosteronism due to the chronic treatment with furosemide.

Animals↗
PubMed1981

Allopurinol amelioration of the pathophysiology of acute myocardial infarction in rats.

Adult, male, Sprague-Dawley rats were subjected to an acute and massive myocardial infarct with isoproterenol. Some of the animals were treated with the anti-hyperuricemic agent, allopurinol, either before or during the induction of myocardial infarction. Autopsy of animals at hourly and daily intervals demonstrated that treatment with allopurinol provided protection against the untoward pathophysiologic changes which attend this kind of experimental infarct. Allopurinol was anti-arrhythmic and caused improved myocardial repair accompanied by reduced fluctuations in circulating CPK, SGOT, SGPT, LDH, and myoglobin. Changes in blood lipids, glucose, and BUN suggests that allopurinol exerts some of its myocardial protective effects through its positive influence on protein metabolism. Allopurinol appears to alter adrenal steroidogenesis which may also play a role in the myocardial salutary effects of this drug.

Allopurinol↗