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Biomedical subjects

E R Levin

Publications and source records attributed to E R Levin.

65 records · Page 4Linked to original sources
PubMed1985

Severe hypertension induced by naloxone.

To evaluate the role of endogenous opioid peptides in regulating the blood pressure of hypertensive individuals, we administered the opiate antagonist, naloxone. One individual developed a severe hypertensive response, mean arterial pressure rising from a baseline of 107 mmHg to 147 mmHg 145 min after naloxone injection and infusion. After stopping naloxone, his blood pressure rapidly returned to baseline. Re-challenge with naloxone and clonidine resulted in a modest reduction of blood pressure in contrast to the profound hypotension induced by clonidine alone during a third session. Thus, endogenous opioids appear to regulate blood pressure in some hypertensive patients and opiate antagonists must be administered with caution to these individuals.

Blood Pressure↗
PubMed1985

Evidence for adrenocortical adaptation to severe illness.

During serious illness, there are characteristic increases in serum cortisol concentrations and urinary cortisol excretion. In the present studies, we investigated these changes in glucocorticoid metabolism in relation to adrenal androgen metabolism, as measured by RIA of dehydroepiandrosterone (DHA) and DHA sulfate (DHAS). A group of 23 seriously ill men with various disorders, ill for a week or longer, was age-matched to a control group of 25 men, and the following changes were found: 1) basal serum cortisol concentrations were elevated in the ill group (P less than 0.001), 2) basal serum DHA and DHAS concentrations tended to be lower in the ill group (P less than 0.1); 3) basal serum DHA to cortisol and DHAS to cortisol ratios were decreased in the ill group by 80.3% and 77.2%, respectively (P less than 0.001); 4) ACTH-stimulated serum cortisol concentrations increased by the same absolute amount in both groups, whereas the increase in stimulated DHA concentrations in the ill group was 57.2% less (P less than 0.05), indicating a defect in ACTH-stimulated DHA reserve in serious illness; 5) basal daily unconjugated DHA excretion was lower in the ill group (P less than 0.05); (6) basal daily cortisol excretion was higher in the ill group (P less than 0.05); and 7) the basal daily urinary unconjugated DHA to cortisol ratio was 85.4% lower in the ill group (P less than 0.001). Recently, Zipser et al. described the entity of hyperreninemic hypoaldosteronism in the seriously ill. Their findings combined with our own indicate a relative shift in the metabolism of adrenal pregnenolone in serious illness away from mineralocorticoids and adrenal androgens and toward glucocorticoids. The cause of this change is unknown. We speculate that this shift of relative biochemical pathway predominance may be a factor necessary for survival during chronic severe stress.

Adaptation, Physiological↗
PubMed1984

Studies of naloxone-induced secretion of beta-endorphin immunoreactivity in dogs.

The stimulating effect of naloxone on plasma beta-endorphin immunoreactivity (beta EI) was examined in dogs. Intravenous naloxone at 5, 1, or 0.1 mg/kg caused a significant increase in beta EI while doses of 0.01 or 0.001 mg/kg had no effect. The peak plasma beta EI levels occurred at 25 mins after naloxone. The neurotransmitter and antagonists metergoline, atropine, diphenhydramine and phentolamine all failed to significantly alter basal beta EI secretion; further, they all failed to prevent the increase in beta EI resulting from naloxone administration. Dexamethasone prevented the naloxone-induced rise in beta EI. Our results suggest naloxone's effect on beta EI is not mediated through several neurotransmitter systems known to affect ACTH secretion. Additionally, beta EI secreted in response to naloxone appears to originate mainly from the anterior lobe of the pituitary.

Animals↗
PubMed1984

Failure to confirm consistent stimulation of growth hormone by diazepam.

Diazepam has been reported to influence pituitary hormone secretion, with several studies claiming that diazepam provokes growth hormone release. Normal volunteers were therefore examined for anterior pituitary responsiveness to 10 mg diazepam i.v. and p.o. The drug had no significant effect on the secretion of prolactin or thyrotropin when compared to control saline injections in all subjects. Growth hormone response was variable; serum growth hormone increased significantly in only 4 of 10 patients after i.v. diazepam and in only 1 of 7 subjects tested with oral diazepam. Serum cortisol rose in only 1 subject, precluding a stress-related explanation for the increase in growth hormone. We conclude that diazepam inconsistently stimulates growth hormone secretion and should not be relied upon as a test of growth hormone reserve.

Administration, Oral↗
PubMed1981

Morphine and naloxone: effects on beta-endorphin immunoreactivity in canine plasma and secretions from rat pituitaries.

Morphine and naloxone were administered to five dogs to assess their effects on endogenous opioid release. Morphine (3 mg/20 kg) produced a significant (P less than 0.05) increase in plasma beta-endorphin immunoreactivity(beta EI) compared to saline control. The peak stimulation [19.2 +/- 4.97 baseline to 48.1 +/- 6.82 (SEM) pg/ml] occurred at +10 min and rapidly returned to preinjection levels at +60. At a dose 10 times equipotent to circulating basal beta EI, morphine (4-6 micrograms) failed to affect beta EI release. Naloxone, surprisingly, also caused a significant (P less than 0.025) release of beta EI. After naloxone, beta EI rose from a preinjection baseline of 36.4 +/- 5.82 pg/ml to a peak of 172 +/- 44.1 pg/ml at 45 min post injection. Naloxone pretreatment also obscured the effect of subsequently injected morphine (3 mg/20 kg). In three naloxone-treated dogs, gel chromatography of pooled basal and peak plasma revealed a preponderance of beta-lipotropin compared to beta-endorphin. To determine the site of stimulation of beta EI by opiates and opioids, a series of rat anterior pituitary incubations were performed. Neither morphine (10(-6) M) nor D-Ala2-methionine enkephalinamide (10(-6) M) nor naloxone (10(-6) M) had an effect significantly different from control medium on the release of beta EI from the pituitaries. In a second set of experiments we compared the effect on beta EI release of hypothalamic median eminence extract alone or with morphine. Hypothalamic median eminence extract at two concentrations produced significant release of beta EI, which was unaffected by the addition of morphine. These results suggest that stimulation of release of endogenous opioid peptides by opiates occurs at a suprapituitary level.

Animals↗
PubMedDate not supplied

Initial assessment of patient cognition in a rehabilitation hospital.

A descriptive study was undertaken to ascertain that the cognitive assessment done by nursing staff on patients' admission to a rehabilitation hospital specifically relates to the rehabilitation population. The study took place on a 40-bed general rehabilitation unit. Eighteen patients were evaluated consecutively using a modified mental status examination. Findings demonstrated that the initial cognitive assessment of the rehabilitation patient should include level of consciousness, orientation, insight, recall, attention, visual-spatial skills, affect, and speech. In this article, the authors describe the study results and illustrate the implications for rehabilitation nursing in a case study.

Cognition Disorders↗
PubMedDate not supplied

Endogenous opioids and opiate antagonists modulate the blood pressure of the spontaneously hypertensive rat.

Endogenous opioids have been implicated as modulators of the central nervous system regulation of blood pressure and heart rate. Whether these neuropeptides participate in blood pressure regulation in hypertension is unknown. To begin to study this question, we examined the response to opiate antagonists and agonists in the spontaneously hypertensive rat (SHR) and the normotensive Wistar-Kyoto (WKY) rat. The long-acting opiate antagonist naltrexone, 2.5 micrograms/kg, was injected into the lateral ventricle of the brain in awake, freely-moving SHR and produced a significant 19 mmHg decrease in mean arterial blood pressure compared to basal blood pressure (p less than 0.01); a decrease was not observed at a two logarithm lower dose. In contrast, naltrexone had no effect on the blood pressure of normotensive Wistar-Kyoto (WKY) rats. To evaluate a possible regulatory role for the predominantly kappa receptor active opioids, alpha- and beta-neo-endorphin, 10 micrograms each, was administered to SHR on separate days by intracerebroventricular injection. alpha- and beta-neo-endorphin caused significant decreases in mean arterial blood pressure of 11 and 9 mmHg respectively, effects reversed by pre-treatment with the opiate antagonist, naloxone. Heart rate was unaffected by any of the injected opioids or antagonists. Our naltrexone results support the hypothesis that an endogenous opioid(s) contributes to the hypertensive state of the SHR. Additionally, alpha- and beta-neo-endorphin can lower blood pressure in this model.

Animals↗
PubMedDate not supplied

Rapid actions of plasma membrane estrogen receptors.

Functional evidence for the existence of plasma membrane estrogen receptors in a variety of cell types continues to accumulate. Many of these functions originate from rapid signaling events, transduced in response to 17beta-estradiol (E(2)). It has been convincingly shown that E(2) activates phosphoinositol 3-kinase and protein kinase B/AKT, and stimulates ERK and p38 MAP kinases. In part, this stems from G-protein activation and the resulting calcium flux. As a result, the link between E(2) action at the cell membrane and discrete biological actions in the cell has been strengthened. There is now convincing in vitro evidence that E(2) can modulate the functions of neural and vascular cells via non-genomic actions. Thus, the actions of discrete pools of E(2) receptors are likely to contribute to the overall effects of the sex steroids.

Animals↗
PubMedDate not supplied

The influence of pyridoxine in diabetic peripheral neuropathy.

To determine the role of pyridoxine in the treatment of diabetic peripheral neuropathy, 18 symptomatic diabetic patients were treated with vitamin B6 or placebo in a double-blind controlled study. Only one patient had a low plasma pyridoxal phosphate level at the start of the study. After 4 mo of treatment with pyridoxine hydrochloride (50 mg three times daily) 6 of 9 pyridoxine-treated and 4 of 9 placebo-treated patients noted significant relief from their neuropathic symptoms. There was no difference between the two groups with regard to fasting plasma glucose, motor nerve conduction velocity, or ophthalmologic examination at the beginning or at the conclusion of the study. Our results suggest that vitamin B6 deficiency is not a factor in the etiology of diabetic peripheral neuropathy. Furthermore, treating diabetic peripheral neuropathy with high dose vitamin B6 or placebo results in a similar frequency of symptomatic improvement.

Adult↗