Search PubMed⌕ Search

Biomedical subjects

E Stark

Publications and source records attributed to E Stark.

At least 91 records · Page 5Linked to original sources

Evidence that the mediobasal hypothalamus is involved in serotonergic stimulation of renin secretion.

The effect of the serotonin-releasing drug parachloroamphetamine (PCA) on plasma renin activity was studied in rats 4 days after surgical lesions of the mediobasal hypothalamus, anterolateral deafferentation of the mediobasal hypothalamus, posterolateral deafferentation, or hypophysectomy. PCA increased plasma renin activity in sham-operated rats, but it failed to increase plasma renin activity in rats with mediobasal hypothalamic lesions or posterolateral deafferentation. The response to PCA was unaffected by anterolateral deafferentation and enhanced by hypophysectomy. There were no significant differences in plasma renin activity in lesioned, deafferented, and hypophysectomized rats injected with saline. The data indicate that the mediobasal hypothalamus is part of the pathway by which central serotonergic neurons affect renin secretion, and that the effect is not mediated via hormones of the pituitary gland.

Amphetamines↗

Doctors in spite of themselves: the limits of radical health criticism.

This paper distinguishes a materialist from a medical approach to health (including as medical the clinical, epidemiological, sociological, environmental, and radical approaches). Three themes are developed. The first concerns a broad definition of medicine. Derived from the actual strategies that capital and labor adopt to health, this definition encompasses all attempts to manage the social factors responsible for ill-health as "conditions" while maintaining (or concealing) the contradictory basis for these conditions in capitalist social relations. The second theme concerns the roots of medicine. Radicals treat scientific medicine as a tool introduced by capitalists and a professional elite to maximize profits, increase productivity, and control women and other oppressed minorities. The materialist view, by contrast, emphasizes the role of worker initiatives in transforming the relations responsible for epidemic disease in the 19th century and the extent to which this transformation led directly to the utility of medical care after 1900. The fact that modern medicine can acknowledge its dependence neither on these initiatives nor on the progress of suffering created through the accumulation process is far more important than the market position of doctors in determining medicine's limits and the ideology of professional doctors. The third theme concerns the utility of a materialist epidemiology for reinterpreting many of the same issues examined by radicals, including medicalization, victim blaming, professional ideology, elitism, the exclusion of certain oppressed groups from "the sick role," and medicine's failure to combat the diseases of stress. The basic contention is that a revolutionary health strategy is impossible as long as medical care remains the centerpiece of our analysis.

Epidemiology↗

[Functional maturation of the human corticotropin releasing factor-adrenocorticotropic hormone system during intrauterine life. An in vitro study].

Radioimmunoassay was used to determine ACTH secretion by cultured hypophyses of human fetuses from the 6th to the 30th week of intrauterine life and their responsiveness to hypothalamic extracts obtained from adult animals. CRF-like activity in the human hypothalamus was measured within the 6th to the 32nd week of prenatal development from changes in ACTH release by cultured cells of the adult rat hypophysis. It was established that starting from weeks 6-7 of embryogenesis, the human fetal hypophysis is capable of synthesizing and secreting immuno-reactive ACTH in vitro. The human fetus hypothalamus of the first trimester of gestation contained no CRF-like substance. The fetus hypothalamus of the second and third trimesters of pregnancy manifested a considerable amount of CRF-like substance. It is suggested that CRF appears at the end of the first trimester of pregnancy.

Adrenocorticotropic Hormone↗

[Transluminal dilatation of renal artery stenoses for treatment of renovascular hypertension (author's transl)].

Transluminal angioplasty according to Grüntzig was performed for 10 stenoses in 7 patients with renovascular hypertension. Nine out of 10 renal artery stenoses were passable and could be dilated. Definite angiographic improvement could be shown in each case. The degree of stenosis could be decreased from 86% to 38% on average. At the narrowest point the diameter was enlarged by a factor of 3.1. The pressure gradient at the stenosis fell on average from 147 to 26 mm Hg. The maximal arterial blood pressure which was on average 254/124 mm Hg before drug treatment, and 169/97 mm Hg after high dosage antihypertensive treatment, fell to 140/84 mm Hg immediately after dilatation. Before dilatation there was a definite increase in peripheral plasma renin activity in every case which fell from 41 to 12 ng AI/ml . h. In one out of 5 patients restenosis occurred after 3 months which could again be successfully dilated. In the two younger patients blood pressure 3 to 9 months later was normal even without antihypertensives. In the older patients normal blood pressure could be maintained with mild antihypertensive treatment.

Adult↗

Effects of paraventricular lesions on stimulated ACTH release and CRF in stalk-median eminence of the rat.

The effects of destroying the paraventricular nucleus (PVN) of the rat hypothalamus on pituitary-adrenal function were studied. Four days after PVN lesions were placed with a rotating knife, the basal plasma corticosterone level was normal, but the corticosterone response to electrical stimulation of the medial basal hypothalamus, surgical trauma, and ether-venesection stress was significantly inhibited. Four and 8 days after PVN lesioning and adrenalectomy, the basal plasma ACTH level was lower, and the rise of plasma ACTH level elicited by a 3-min ether inhalation was significantly smaller than in the adrenalectomized controls. Corticotropin-releasing factor (CRF) activity in the stalk-median eminence extracts from PVN-lesioned rats was significantly less than in the control extracts. The weight of the adrenals was decreased by both 2 and 4 wk after PVN destruction, and 2 wk after hemiadrenalectomy, the compensatory adrenal hypertrophy was inhibited. The plasma corticosterone response to ether-venesection stress was inhibited only temporarily because it returned to normal by the end of the 4th postoperative week. The results are consistent with the hypothesis that a substantial portion of CRF-containing fibers in the stalk-median eminence region either originate from or run though the PVN or its immediate vicinity.

Adrenal Glands↗

Corticoliberin activity of rat neurohypophysis is distinct from vasopressin.

Electrical stimulation of the neural lobe of the pituitary resulted in an increase of corticosterone secretion in both normal and Brattleboro rats. Bioassaying the corticoliberin (CRF) activity of stalk-median eminence and neural lobe extracts obtained from normal and Brattleboro rats revealed that the endogenous vasopressin was not a prerequisite of ACTH-releasing potency. Arginine-8-vasopressin failed to potentiate the CRF activity of the different extracts. These data suggest that a nonvasopressin substance(s) with CRF activity can be released from the neurohypophysis of the rat, and it may contribute to activating the pituitary-adrenal axis under certain experimental conditions.

Adrenocorticotropic Hormone↗

Lack of correlation between hypothalamic serotonin and the ether-induced ACTH secretion in adrenalectomized rats.

The central serotonergic system was manipulated using a serotonin receptor antagonist (cyproheptadine), electrolytic lesioning of the raphe nuclei and neurochemical destruction of the serotonergic terminals in the hypothalamus. The effects of these interventions on ether-induced ACTH secretion were studied in adrenalectomized rats. Serotonin, norepinephrine and dopamine concentrations were measured in the medial basal hypothalamus (MBH) or in individual nuclei of the hypothalamus and of certain midbrain regions. Cyproheptadine pretreatment inhibited ether-induced ACTH hypersecretion in adrenalectomized animals. Neither the electrolytic lesions of the midbrain raphe nuclei, nor the neurotoxic destruction of the hypothalamic serotonergic terminals (by intraventricular administration of 5,6-dihydroxytryptamine) caused any alteration of stimulated ACTH secretion after ether inhalation and/or long-term corticoid deficiency. These results suggest a lack of correlation between the activity of the central serotonergic system and the ACTH releasing effect of ether-stress in adrenalectomized rats.

5,6-Dihydroxytryptamine↗

Effects of treatment with adrenocorticotrophin on the hypothalamo-pituitary-adrenal system.

Long-term treatment with adrenocorticotrophin (ACTH) inhibited the stress-induced response of the hypophysial-adrenocortical system 24 h after the final ACTH injection. The mechanism of this phenomenon was studied in both normal and adrenalectomized rats, the latter receiving corticosterone at various doses. The effect of electrical stimulation of the medial basal hypothalamus on the concentration of corticosterone in plasma (an indicator of ACTH secretion), the corticotrophin releasing factor (CRF) content of the stalk median eminence (SME), the ACTH content of the pituitary gland and the in-vitro release of ACTH by the pituitary gland incubated with or without addition of SME extract were investigated. Electrical stimulation of the medial basal hypothalamus failed to induce a rise in concentrations of corticosterone in plasma of normal rats treated with ACTH; moreover the levels of hypothalamic CRF and hypophysial ACTH were significantly decreased. Hemipituitary glands of ACTH-treated rats released markedly less ACTH in vitro in response to SME extract than did the control glands. This indicated that long-term hormone administration caused a serious impairment of the responsiveness of the corticotrophic cells toward CRF. Pituitary ACTH content and in-vitro responsiveness of pituitary glands obtained from ACTH-treated, adrenalectomized rats receiving corticosterone replacement seemed to be dependent on the amount of exogenous corticosteroid, but not on that of exogenous ACTH. Our previous and present findings suggest that long-term treatment with ACTH elicits repeatedly increased secretion of endogenous corticosterone, impairing the stress-induced CRF-ACTH release at both the hypothalamic and hypophysial levels. Our data challenge the view that ACTH itself is able to inhibit its own secretion.

Adrenalectomy↗

Possible inhibitory influence of gamma-aminobutyric acid on growth hormone secretion in the rat.

Increasing the levels of endogenous gamma-aminobutyric acid (GABA) by treating rats with GABA-transaminase inhibitors (ethanolamine-O-sulphate and gamma acetylenic GABA) resulted in a decrease in plasma levels of GH. Diminishing GABAergic activity by inhibiting GABA synthesis with 3-mercaptopropionic acid or by blocking GABA receptors with bicuculline increased plasma concentration of GH. The presence of GABA was without effect on the basal, somatostatin-inhibited or high K+-stimulated secretion of GH by hemipituitary glands in vitro. The results suggest that GABA inhibits secretion of GH under the given experimental circumstances.

4-Aminobutyrate Transaminase↗

Reevaluation of the pituitary-adrenal response to ether in rats with various cuts around the medial basal hypothalamus.

ACTH release elicited by ether inhalation or ethervenesection and measured by changes in plasma corticosterone level was studied in rats at various time intervals after placing a complete or an anterolateral cut around the medial basal hypothalamus (MBH). There was no rise in 'resting' plasma corticosterone after acceptable isolations and, in 5 out out of 6 series of experiments, the complete or long anterolateral cuts prevented the rise in plasma corticosterone normally induced by ether stress. In contrast, ethervenesection elicited a significant increment of plasma corticosterone when the basal region of the lateral retrochiasmatic area (RCAL) was not completely transected. Possible reasons why these experiments failed to confirm previous findings are discussed. These results support the hypothesis that corticoliberin-containing fibers enter the MBH from outside and that most of these fibers run through the RCAL on their way towards the neurohemal regions of the infundibulum.

Adrenocorticotropic Hormone↗

Effect of electrical stimulation of the neurohypophysis on ACTH release in rats with hypothalamic lesions.

Electrical stimulation of the neural lobe (NL) of the pituitary induces a rise in plasma corticosterone indicating the release of adrenocorticotropin (ACTH) in rats pretreated with dexamethasone, morphine and pentobarbitone. 7-8 days after placing an anterolateral cut around the medial basal hypothalamus (MBH), the rats failed to respond with ACTH release to electrical stimulation of the NL; the number of nerve fibers and terminals in the NL decreased to less than 5% of the normal; and ACTH releasing activity of acid extracts of the NL was undetectable using both in vivo and in vitro tests, which are insensitive to vasopressin. After lesions of the paraventricular nuclei the stimulation of the NL elecited a rise of plasma corticosterone that was significantly less than that in the controls. These results suggest that the NL of the pituitary contains electrically excitable fibers capable of releasing corticotropin-releasing factor (CRF; distinct from vasopressin) and that these fibers probably originate from outside the MBH, with a portion of them coming from or through the paraventricular nuclei or their immediate vincinity.

Adrenocorticotropic Hormone↗

The rise of plasma ACTH induced by ether is mediated through neural pathways entering the medial basal hypothalamus.

The effect of ether stress on the release of immunoreactive ACTH was studied in rats with an antero-lateral cut around the medial basal hypothalamus. Ether failed to raise the plasma ACTH level of rats in which an antero-lateral hypothalamic cut and adrenalectomy had been performed 7 to 8 days previously. Plasma ACTH was also unchanged in rats exposed to ether 2 h after an antero-lateral cut. These data suggest that intact neural pathways entering the medial basal hypothalamus from the antero-lateral direction are necessary for the ACTH releasing action of ether stress.

Adrenal Glands↗

Changes in corticotrophin releasing factor of the stalk median eminence in rats with various cuts around the medial basal hypothalamus.

The activity of corticotrophin releasing factor (CRF) in extracts of the stalk median eminence (SME) complex proper (average protein content, 30.6 micrograms) of male rats was assayed by monolayer cultures of anterior pituitary cells using the release of immunoreactive ACTH. Extracts which were equivalent to 0.025 SME of control rats usually had detectable CRF activity, while there was no detectable activity in extracts of 0.4 SME equiv. taken 8 days after complete surgical isolation of the medial basal hypothalamus (MBH). The activity of CRF in extracts from rats with an anterolateral cut around the MBH was at least ten times less than that in the control rats. One day after placing an anterolateral cut around the MBH the ACTH releasing activity of the SME was not significantly different from that of the control animals but activity decreased significantly 3 days after the operation and was at least ten times less than in the control animals on day 7 after the operation. It is suggested that most of the CRF activity of the SME is contained in nerve fibres entering the neurohaemal region from outside the MBH and that transection of these fibres produced the fall in CRF content of the SME in rats with partial or total surgical isolation of the MBH.

Animals↗

Medicine and patriarchal violence: the social construction of a "private" event.

Our objectives are to describe the pattern of abuse associated with battering and to evaluate the contribution of the medical system and of broader social forces to its emergence. A pilot study of 481 women who used the emergency service of a large metropolitan hospital in the U.S. shows that battering includes a history of self-abuse and psychosocial problems, as well as repeated and escalating physical injury. In addition, although the number of battered women using the service is 10 times higher than medical personnel identify, the pattern of abuse that constitutes battering emerges only after its initial effects are presented and in conjunction with specific medical intervnetions and referrals. Examination of intervention and referral patterns suggests a staging process by which battering is socially constructed. At first, the physical trauma associated with abuse is medicated symptomatically. But the patient's persistence, the failure of the cure, and the incongruity between her problems and available medical explanations lead the provider to label the abused woman in ways that suggest she is personally responsible for her victimization. Although secondary problems such as depression, drug abuse, suicide attempts, or alcoholism derive as much from the intervention strategy adopted as from physical assault or psychopathology, they are treated as the primary problems at psychiatric and social service referral points where family maintenance is often the therapeutic goal. One consequence of this referral strategy is the stabilization of "violent families" in ways that virtually insure women will be abused in systematic and arbitrary ways. The use of patriarchal logic by medical providers ostensibly responding to physical trauma has less to do with individual "sexism" than with the political and economic constraints under which medicine operates as part of an "extended patriarchy." Medicine's role in battering suggests that the services function to reconstitute the "private" world of patriarchal authority, with violence if necessary, against demands to socialize the labors of love.

Emergency Service, Hospital↗