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Biomedical subjects

B C Wexler

Publications and source records attributed to B C Wexler.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

ACTH content of pituitary glands of arteriosclerotic breeder vs. non-arteriosclerotic virgin rats.

Acid extracts were made of the pituitary glands of non-arteriosclerotic male and female virgin rats and arteriosclerotic, male and female breeder rats. The ACTH content of these pituitary glands was determined by measuring the amount of corticosterone produced by the adrenal glands of healthy but hypophysectomized rats when challenged by the various ACTH acid extracts. The pituitary glands of the arteriosclerotic animals were significantly heavier than non-arteriosclerotic rats and contained decreased amounts of ACTH commensurate with the severity of the pituitary donor's arteriosclerosis. Similarly, arteriosclerotic donors had heavier adrenal glands but contained considerably less corticosterone than non-arteriosclerotic virgin rats. Male breeder rats developed microscopic aortic lesions involving intimal mesenchymal cell and ground substance alterations whereas the female breeder lesions progressed from intimal ground substance and connective tissue changes to medial elastolytic degeneration and eventual medial cartilaginous and osseous metaplasia. Histopathologic examination of the pituitary and adrenal glands demonstrated hyperplasia of basophil and other cytologic elements of the pituitary gland including colloid-filled cysts and lipid depletion of the zona glomerulosa as well as hemorrhage and thrombosis of the adrenal cortex of the arteriosclerotic breeder rats. The hypothesis is made that repeated breeding leads to abnormal hypothalamic regulation of pituitary gland synthesis and release of ACTH, which, in turn, contributes to abnormal adrenal glandular function conditioning the aortic wall toward abnormal changes in mesenchymal cell activity and metabolism of connective tissue ground substance.

Adrenal Glands↗
PubMedDate not supplied

Aortic hexosamine, [35S]sulfate uptake, and calcium metabolism related to early arterial degenerative changes induced by lactation and forced weaning in breeder rats.

The relation of lactation and weaning to the development of early arterial lesions in the female breeder rat was investigated. Changes in aortic hexosamine and 35S-uptake, which are indicative of ground substance metabolism were correlated with changes in aortic calcium, phosphorus, and 45Ca-uptake during lactation and weaning. Lactation was associated with reduced aortic hexosamine content and lowered uptake of [S]sulfate. Further dynamic changes in aortic metabolism of these substances occurred following weaning in conjunction with an intense calcium uptake in the aorta of some, but not all, of the post-lactation animals. These latter changes were associated with the beginning aortic calcifications. Histopathologically, early arterial lesions developing during lactation, consist of intimal accumulations of mucopolysaccharide capped over by collagen. With repeated breeding cycles, these early lesions become exacerbated with extensive medial calcification occurring in areas rich in mucopolysaccharide and collagen particularly around degenerating elastic fibers. The hormones associated with reproduction and lactation may have a conditioning effect on these arterial connective tissue alterations and the development of arterial degenerative changes.

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Changes in LH and prolactin in arteriosclerotic femal breeder rats.

Serum levels of LH and prolactin were measured in repeatedly-bred, arteriosclerotic female rats. Serum LH was abnormally decreased on the afternoon of proestrus and estrus. The extent of the depression of circulating LH levels parallels the severity of the arteriosclerosis. Serum prolactin was significantly increased above normal at proestrus, and the degree of prolactin increase was also correlated with the degree of severity of arteriosclerosis. It is suggested that frequent and repeated pregnancies affect the hypothalamic-pituitary-adrenal-gonadal axis leading to hormonal and metabolic imbalance, which may play a causal role in the pathogenesis of the spontaneous arteriosclerosis which appears in repeatedly-bred rats.

Animals↗
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Metabolic responses following isoproterenol-induced myocardial infarction in arteriosclerotic breeder vs. non-arteriosclerotic virgin and ovariectomized female rats.

Intact and ovariectomized, non-arteriosclerotic female rats and arteriosclerotic, breeder female rats were subjected to myocardial infarction by the administration of 2 subcutaneous injections, 24 hr apart, of the beta-adrenergic stimulator, isoproterenol. The animals were sacrificed at regular hourly intervals following each injection and then on days 4, 6, 8, 10, 12, and 16 thereafter. Measurement of serum insulin and free fatty acids (FFA) demonstrated a blunted response in these metabolic parameters in the case of the ovariectomized virgin rats. The non-arteriosclerotic, intact virgin rats exhibited dynamic changes in serum insulin, glucose, FFA and corticosterone (Cmpd. B) following both isoproterenol injections, whereas the arteriosclerotic breeder rats manifested elevated levels of these parameters on Day 1, but did not display any increases in serum levels, except for FFA, following the second isoproterenol injection on Day 2. In spite of the hormonal alterations brought about by the gonadectomy and their differing metabolic response, the ovariectomized females did not have a mortality rate significantly different from the intact females. Thus, the presence or absence of ovarian estrogens seemingly does not affect the progress of an isoproterenol-induced myocardial infarction.

Animals↗
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Adrenocortical suppression and myocardial infarction in non-arteriosclerotic (virgin) and arteriosclerotic (breeder) rats.

Non-arteriosclerotic, virgin and arteriosclerotic, breeder rats were treated with aniline to suppress adrenal steroidogenic capacity and responsiveness to the stress of acute myocardial infarction. After two weeks of aniline treatment, some of the non-arteriosclerotic and arteriosclerotic animals were given two injections of isoproterenol, spaced 24 h apart, to induce massive myocardial infraction. On the 3 rd day, when myocardial necrosis reaches its zenith, the animals were sacrificed. Aniline-induced adrenal insufficiency caused increased mortality, absence of congestive heart failure, cardiac and adrenal enlargement but no evidence of the characteristic intense catabolism and increased corticoid production which attends acute myocardial infarction. Serum enzymes, e.g., SGOT, SGPT and LDH, triglycerides, but not glucose, free fatty acids and cholesterol, became acutely elevated in animals treated with aniline and isoproterenol. Animals developed a fatty liver, beta cell degranulation, post hypophy-sectomy-like changes in their adrenal cortices, unusually severe infarction, marked distention of intermuscular spaces, frequent foci of dystrophic calcification and cartilaginous metaplasia of the papillary muscles. It is believed that aniline-induced adrenal suppression altered the usual pathophysiologic response to acute myocardial infarction.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Comparative effects of prolactin, perphenazine and reserpine on non-arteriosclerotic (virgin) vs arteriosclerotic (breeder) rats.

Non-arteriosclerotic, virgin and arteriosclerotic breeder rats were subjected to chronic treatment with prolactin or prolactin-releasing drugs such as perphenazine and reserpine for 12 weeks. Males and females responded to the prolactin as evidenced by increased milk secretion, adrenal hyperplasia and thymus gland involution. Although the prolactin- and reserpine-treated animals gained weight and manifested pituitary gland basophilia, the perphenazine-treated animals showed considerable loss of body weight as well as involution of the pituitary gland, ovaries and testes, suggesting a condition of induced hypopituitarism. Chronic treatment with prolactin, both directly and indirectly, caused uniform increases in serum enzymes, e.g., CPK, SGOT, SGPT and LDH, lipids, e.g., triglycerides, free fatty acids and cholesterol, glucose and BUN. Corticosterone production was enhanced by prolactin, reduced by perphenazine and unaffected by reserpine. Prolactin did not induce any arterial disease in the arteriosclerosis-resistant, virgin rats but it did cause eracerbation of the usual severity of arteriosclerosis in the hilar renal arteries of the arteries sclerosis-prone, breeder rats as well as an increased incidence of "old" and "new" foci of myocardial necrosis, characteristically found in breeder rats. It is suggested that hypothalamic control of prolactin as well as ACTH release may play a role in the spontaneous arteriosclerosis which develops in repeatedly-bred, male and female rats.

Alanine Transaminase↗
PubMedDate not supplied

Aldosterone, deoxycorticosterone and corticosterone differences between arteriosclerotic breeder vs nonarteriosclerotic virgin rats.

The circulating levels of the major adrenal steroids, corticosterone (Cmpd. B), deoxycorticosterone (DOC), and aldosterone were compared in male and female, arteriosclerotic, breeder and non-arteriosclerotic virgin, Sprague--Dawley rats under resting conditions, i.e., quiescence, and after exposure to a mild stress, i.e., movement from one room to another just prior to autopsy. Under resting conditions, the arteriosclerotic animals had significantly greater circulating levels of Cmpd. B, DOC and aldosterone than the non-arteriosclerotic animals. Both the arteriosclerotic and non-arteriosclerotic animals were able to respond adequately to the mild stress stimulus. However, the female breeder rats which manifest the most severe aortic sclerosis, showed the greatest increase in Cmpd. B and aldosterone in response to the mild stress. Although no statistically significant differences could be found between female breeders with grossly visible aortic sclerosis of clear, minimal, moderate, or severe degree, it was apparent that adrenal steroid responsiveness becomes progressively compromised with increasing severity of arteriosclerosis, e.g., unusually high or low levels of Cmpd. B and aldosterone under both quiescent and mild stress conditions. It is suggested that there may be some connection between abnormal hypothalamic-pituitary-adrenal-gonadal function in repeatedly-bred and the pathogenesis of their naturally-occurring ateriosclerosis.

Aldosterone↗
PubMedDate not supplied

Hyperlipidemia, hyperglycemia and hypertension in repeatedly bred parents of the obese spontaneously hypertensive rat (obese/SHR) unaccompanied by arteriosclerosis.

A sub-strain of male and female spontaneously hypertensive rats (SHR) capable of having massively obese or non-obese offspring were bred repeatedly or were maintained as virgin controls. When the male and female breeders had sired or given birth to 5 litters of young, they were autopsied along with their 10-month-old celibate brothers and sisters. Virgin and breeder SHR developed high blood pressure (250 +/- 10 mm Hg). Breeder rats were significantly heavier than their virgin cohorts; pituitary and adrenal glands, hearts, and kidneys were significantly enlarged while thymi were severely involuted in breeder vs virgin SHR. The hyperlipidemia, fatty liver, hyperglycemia, and islet hyperplasia, characteristic of virgin SHR, were greatly exacerbated in breeder SHR. Blood levels of corticosterone, deoxycorticosterone, and aldosterone were greatly elevated in breeder vs virgin SHR. Although breeder rats of genetically normotensive strains develop aortic sclerosis, none of the breeder SHR developed aortic sclerosis. Instead, intimal fibrinohyalin lesions appeared confined to the testes and ovaries. It is suggested that the anatomical appearance or resistance of the arterial wall to the development of lesions is genetically mediated but this genetic programming may be modified by metabolic and hormonal factors with particular emphasis on the participation of adrenocorticoids.

Adrenal Cortex↗
PubMedDate not supplied

Histopathological reactivity of carotid arteries of normotensive Sprague-Dawley vs spontaneously hypertensive rats to ligation injury.

The common carotid arteries of normotensive non-arteriosclerotic Sprague-Dawley (S-D) rats, mildly hypertensive but arteriosclerotic breeder S-D rats, severely hypertensive but non-arteriosclerotic virgin spontaneously hypertensive rats (SHR), and severely hypertensive breeder SHR were ligated to induce injury. Three weeks post-ligation, the animals were killed and histopathological sections of the ligated artery demonstrated myointimal proliferation without occlusion in the normotensive S-D rats but myointimal proliferation with occlusion in the severely hypertensive SHR. Breeder S-D rats with moderate hypertension manifested a high incidence of total occlusion by combined myointimal proliferation and thrombosis. Severely hypertensive breeder SHR manifested a high incidence of massive thrombi containing cholesterol clefts causing total occlusion of the injured artery. It is suggested that the severity of the hypertension and the hormonal-metabolic milieu conditions the morphologic response of the arterial wall to injury.

Animals↗
PubMedDate not supplied

Comparative effects of unilateral and bilateral carotid artery ligation in the spontaneously hypertensive rat.

Male and female, spontaneously hypertensive rats (SHR) with blood pressures ranging from 190-210 mmHg were subjected unilateral or bilateral carotid artery ligation. Representative numbers of animals were killed 2, 4, 6, 8, 10, 12, 24 and 48 hours later. Severe cerebral ischemia caused a significant and protracted increase in the pre-existent high blood pressure, the enzymes CPK, SGOT and LDH triglycerides, free fatty acids, glucose, and corticosterone. Despite these marked pathophysiologic changes, the brains of these animals were free of real damage except for cerebral edema and scattered petechiae. Some of the animals developed massive atrial thrombi and myocardial infarcts. It is suggested that severe cerebral ischemia precipitated the myocardial infarcts through the aegis of the hypothalamic-pituitary-adrenal stress response.

Animals↗
PubMedDate not supplied

Myocardial necrosis induced by breeding in stroke-prone/SHR.

Virgin and breeder, spontaneously hypertensive and stroke prone rats (SHR/SP) were observed from weaning until 130 +/- 10 days of age. Blood pressure rose rapidly, reaching 230--240 mm Hg. After the birth of the second litter of pups, male and female breeders began to die suddenly, due to myocardial necrosis and congestive heart failure. At autopsy, the brains of virgin and breeder SHR/SP were swollen but were free of any pathologic changes. There were no significant alterations in the blood chemistry of virgin rats but breeder SHR/SP had super-normal enzyme levels, CPK, SGOT, SGPT and LDH, hyperglycemia, hyperlipidemia, and hypersecretion of corticosterone. Breeder SHR/SP developed PAN-like lesions of the mesenteric arcades and adrenal cortex along with severe fibrino-hyalin lesions of the testicular and ovarian arteries. It is suggested that alterations in hypothalamic-pituitary-adrenal function associated with the reproductive effort conditioned these SHR/SP to develop myocardial necrosis rather than stroke and the development of unusual hypertensive arteriopathy.

Alanine Transaminase↗
PubMedDate not supplied

Enovid-induced exacerbation of high blood pressure in stroke-prone rats (SHR).

Male and female, normotensive Wistar:Kyoto rats, spontaneously hypertensive rats (SHR), and Stroke-prone SHR (SHR/SP) with severe hypertension were treated with a contraceptive drug (Enovid) from the time of weaning until they became 180 days old. Although the Envoid-treated SHR and SHR/SP had exacerbations of their high blood pressure, none of the animals developed renal or cerebral damage. Chronic treatment with Enovid caused testicular and ovarian atrophy and a significant increase in circulating corticosterone. It is suggested that the potentially deleterious effects, e.g., stroke, hypertension, hyperglycemia, hyperlipidemia, etc., of chronic treatment with contraceptive drugs is largely determined by pre-existing genetically endowed proneness or resistance.

Animals↗