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Biomedical subjects

B C Wexler

Publications and source records attributed to B C Wexler.

149 records · Page 9Linked to original sources
PubMedDate not supplied

Low protein fish vs low protein animal diet enhances the propensity for stroke in stroke-prone/SHR.

Weanling male and female, stroke-prone, spontaneously hypertensive rats (SHR/SP) were fed: 1) regular commercial rat chow, 2) low protein fish diet, 3) low protein fish diet + 1% saline, 4) low protein animal diet, and 5) low protein animal diet + 1% saline. The blood pressure of all of the SHR/SP rose rapidly reaching 240 mmHg at 90 days of age; blood pressure of low protein fish diet + 1% saline-fed SHR/SP rose most rapidly, reaching levels ranging from 258 to 300 mmHg. All of these animals developed acute strokes by 90 days of age; none of the other diet-fed SHR/SP manifested cerebral damage. The protein poor diets prevented normal growth, caused hypogonadism, and severely reduced pituitary and adrenal gland weights. The low protein diets were stressful causing significantly increased secretion of adrenocorticotrophic hormone and marked increases in triglyceride, free fatty acid, cholesterol, glucose, and B.U.N. levels. The mixed hemorrhagic-thrombogenic cerebral lesions occurred ipsilaterally in the parietal lobe, involved basal ganglia, and appeared in areas of brain tissue nourished by the middle cerebral artery. It is concluded that the inclusion of 1% saline drinking water with a low protein diet of fish tissue origin specifically, was synergistic in enhancing the propensity of SHR/SP rats to develop their genetically-programmed hypertension and stroke.

Animals↗
PubMedDate not supplied

Enovid-induced exacerbation of the propensity for stroke in low protein fish diet-fed stroke-prone/SHR.

Weanling, male and female, stroke-prone, spontaneously hypertensive rats (SP/SHR) were fed either a regular diet, a low protein diet derived from fish tissue + 1% saline drinking water, or the fish diet + 1% saline + daily injections of 0.1 mg Enovid/100 g bw/sc. After 48 days, the Enovid-treated animals developed acute and lethal strokes characterized by massive thrombonecrogenic lesions of the parietal lobe. The blood pressure of the Enovid-treated SP/SHR rose most acutely. The low protein fish diet was markedly catabolic and caused hyperlipidemia, hyperglycemia, elevated ACTH and beta-endorphin levels concomitant with reduced gonadotrophic function. Treatment with Enovid caused severe exacerbation of all of the foregoing changes. It is proposed that a low protein fish diet + 1% saline will accelerate the appearance of strokes in SP/SHR and that Enovid will enhance this effect through its anti-gonadotrophic activity and ability to stimulate increased pituitary-adrenal secretion.

Acute Disease↗
PubMedDate not supplied

Naloxone ameliorates the pathophysiologic changes which lead to and attend an acute stroke in stroke-prone/SHR.

Stroke-prone, spontaneously hypertensive rats (SP/SHR) were fed a low protein (8%) fish diet + 1% saline at the time of weaning; some were treated with Naloxone (0.4 mg/100 gms bw/sc/2 X daily/5 days per week). Naloxone-treated animals did not develop high blood pressure or strokes. Sixty-two days after feeding the low protein fish diet, blood pressure levels reached 260-300 mmHg and all of the non-treated animals exhibited acute and severe strokes; Naloxone treatment was again initiated for half of the SP/SHR. By Day 4 (post stroke), all of the non-treated SP/SHR were dead; Naloxone-treated SP/SHR survived until Day 12 (post stroke). Naloxone-treatment during the post-stroke period caused significant reduction of blood pressure, ACTH, and beta-endorphin levels concomitant with reduced cerebral edema and clearance of hepatic lipid infiltration. It is suggested that anti-opiate treatment may ameliorate the severe hypertension-inducing effects of a low protein fish diet and thereby prevent the appearance of strokes in SP/SHR as well as palliate the cerebral edema and fatty liver which characteristically appear in the immediate post-stroke period in fish-fed SP/SHR. The central mechanism of this palliative effect may be through reduced hypothalamic-pituitary-adrenal activity.

Acute Disease↗
PubMedDate not supplied

Chronic diabetes followed by chronic cerebral ischemia induced by bilateral carotid artery ligation in arteriosclerotic versus nonarteriosclerotic rats.

Male and female, arteriosclerotic (breeder) and nonarteriosclerotic (virgin), Sprague-Dawley rats were made severely diabetic with alloxan. Two weeks later experimental animals had both carotid arteries ligated to induce a state of acute cerebral ischemia. After six weeks of cerebral ischemia either with or without severe diabetes the animals were killed. Animals which survived either the acute induction of diabetes or cerebral ischemia did not manifest any new episodes of cerebral ischemia. Subjects with combined diabetes and cerebral ischemia manifested the greatest loss in body weight, adrenal hypertrophy and thymus gland involution, increased levels of serum CPK and SGOT, but decreased SGPT and LDH, hyperglycemia and hypertriglyceridemia, and the most extensive cerebral edema. It is suggested that diabetic rats may have a greater predilection toward cerebrovascular accidents because the diabetic state contributes not only to an exacerbation of atherosclerosis, but also complicates any condition of cerebrovascular ischemia by creating extracerebral edema.

Adrenal Glands↗