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Biomedical subjects

B C Wexler

Publications and source records attributed to B C Wexler.

At least 91 records · Page 5Linked to original sources

Cardiovascular function in nonarteriosclerotic versus arteriosclerotic rats.

Cardiovascular function of arteriosclerotic (breeders) and nonarteriosclerotic (virgins) male am exercise was examined in the denervated gracilis muscle of the anesthetized dog. The data show that 1) on initiation of heavy exercise, the effluent blood PO2 and pH fall markedly and then rise slowly but remain depressed relative to control during 60 min of exercise hyperemia, while the initial increases in [K+] and osmolality rapidly approach and eventually reach preexercise levels. 2) The enhanced vasodilator activity of venous blood from exercising muscle is attenuated when effluent blood PO2 or pH is corrected to preexercise levels; it is completely abolished when both are corrected. 3) Induced reduction of PO2 or pH in the arterial inflow, and thus venous outflow, of resting muscle produces a fall in resistance; simultaneous reductions of both to levels seen in heavy exercise produce a fally in resistance to near that observed during exercise. Since the enhanced vasodilator activity of venous blood from the contracting muscle was abolished by simultaneous correction of the PO2 and pH, it seems likely that these factors, acting directly or indirectly, are the prinicipal chemicals responsible for the maintenance of the vasodilation seen in canine skeletal muscle during heavy exercise.

Animals↗

Serum insulin changes in arteriosclerotic breeder female rats versus non-arteriosclerotic virgin rats.

Immunoreactive serum insulin (IRI), glucose, free fatty acids (FFA), and corticosterone (Cmpd. B) were measured in non-arteriosclerotic virgin versus arteriosclerotic, breeder female rats exhibiting normal 4-day cycles. In the arteriosclerotic breeder females, the normal increase in IRI during proestrus and estrus did not occur. The IRI levels during these times were comparable to the minimal levels found during metestrus in the non-arteriosclerotic virgin rats and were even lower than the IRI levels or ovariectomized rats. Since both young and old non-arteriosclerotic virgin rats had similar IRI patterns, the lack of cyclic insulin change in the arteriosclerotic breeder rats is not considered to be age-related. Instead, these changes are ascribed to hypothalamic-pituitary-adrenal hyperactivity associated with repeated reproductive activity and the development of arteriosclerosis.

Animals↗

Metabolic response after isoproterenol-induced myocardial infarction in arteriosclerotic breeder vs nonarteriosclerotic virgin intact and gonadectomized male rats.

Male, nonarteriosclerotic (virgin) intact and castrated, Sprague-Dawley rats and male, arteriosclerotic (breeder) rats were subjected to an acute and massive myocardial infarct, by treating them with two large, subcutaneous doses of isoproterenol, spaced 24 hr apart. Serum insulin and glucose rose abruptly after the first injection of isoproterenol, but not after the second injection. Free fatty acids rose, most markedly, in the intact, nonarteriosclerotic rats, less in the arteriosclerotic breeders, and least in the castrates. These changes in free fatty acids coincided with numerical survival, i.e., greatest number of survivors in castrates. The castrated males also manifested the least amount of congestive heart failure and showed the greatest capacity to affect myocardial repair. It is suggested that reduced androgen levels may have an ameliorative effect on the usual pathogenesis of isoproterenol-induced myocardial infarction in rats.

Animals↗

Serum prolactin levels in rats following isoproterenol-induced myocardial infarction.

Circulating prolactin levels were monitored in nonarteriosclerotic, arteriosclerotic, and hormonally sterilized male and female Sprague-Dawley rats during the acute necrosis and repair phases of myocardial infarction induced by isoproterenol. Male rats are particularly prone to succumb to acute myocardial ischemia but reduction of androgen levels by neonatal sterilization improved survival considerably. Circulating prolactin levels are greatly increased, particularly in females, during acute myocardial ischemia. Since androgens suppress the hypothalamic center for prolactin release, prolactin levels were delayed and transitory in males. It is suggested that the superior survival of female rats may be related to their greater production of prolactin during acute stages of myocardial ischemia, which would dampen the tachycardia-inducing effects of the potent beta-adrenergic stimulating agent, isoproterenol.

Androgens↗

Polyarteritis nodosa induced in arteriosclerotic, male and female breeder rats by chronic alloxan diabetes.

Male and female virgin rats and breeder rats with naturally-occurring diabetes, hypertension and arteriosclerosis, were made severely diabetic with a single, subcutaneous injection of alloxan (10 mg/100 g b.w.), after an 18 h fast. During five months of unrelenting diabetes, some animals became obese while others became emaciated. Only the emaciated animals survived but they were blind, their adrenal glands were hemorrhagic, hypertrophied and thrombosed, thymi involuted, kidneys swollen, hearts reduced in size while testes and ovaries were atrophic. Serum CPK, SGOT and SGPT were elevated concomitant with extensive cardiovascular damage, hepatic steatosis and generalized catabolism. Circulating triglycerides and free fatty acids were markedly elevated with total cholesterol only slightly increased. BUN and serum calcium levels were also greatly elevated. Sub-normal Cmpd. B levels indicated impaired adrenal steroidogenesis. Virgin rats developed arteriosclerosis and male and female breeder rats showed exacerbation of their pre-existing aortic sclerosis as well as P.A.N. lesions in their small-sized arteries. It is believed that severe diabetes causes exacerbation of the endogenous hormonal milieu resulting from abnormal hypothalamic-pituitary-adrenal function induced by repeated breeding, which conditions the connective tissue components of the arterial wall of rats toward accelerated degenerative changes.

Animals↗

Adrenal glandular lipids and circulating corticosterone in severely diabetic rats.

Young, adult, female Sprague-Dawley rats were fasted for 18 h and then given a single s.c. injection of alloxan (10 mg/100 g body weight) which promptly induced a severe state of diabetes. The animals were killed at frequent time intervals during the 7-day study period in order to record the dynamic changes in their capacity for adrenal steroidogenesis and secretion as measured by fluorometric determination of their circulating corticosterone (Cmpd B) levels as well as by thin layer chromatographic identification of cortical lipid moieties used for steroidogenesis. In addition to severe polydypsia, polyuria and polyphagia, these animals manifested super-normal glucose, triglycerides, free fatty acids and cholesterol in their blood, severe hepatic steatosis, adrenal hyperplasia with lipid depletion from the mineralocorticoid producing z. glomerulosa, thymus gland involution and complete degranulation of their insulin producing islet beta cells. Despite an initial high output of Cmpd B and despite progressive cortical hyperplasia, the serum Cmpd B levels became reduced and many of the animals succumbed suddenly, due most likely to inadequate adrenocortical steroidogenesis. Adrenocortical lipids showed a progressive accumulation of free fatty acids, di- and triglycerides, suggesting that some lipid enzymatic defect could be responsible for the lack of conversion of these lipid entities essential for proper steroidogenesis.

Adrenal Glands↗