Biomedical subjects

E R Levin

Publications and source records attributed to E R Levin.

At least 55 records · Page 3Linked to original sources

PubMed1991

[Elaboration of a quantitative method of evaluation of disease severity in patients with ventricular disorders of cardiac rhythm].

Mathematical approaches to the evaluation of the severity of the pathological process were used to develop an objective quantitative method to assess the severity of ventricular arrhythmias. The method is highly informative and reliable. It may be useful in the control of the efficacy of antiarrhythmic therapy and in the application of a differential approach to choice of therapy strategy for the patients.

Adult↗

PubMed1991

[Etatsizin efficacy in patients with ventricular tachycardias. The results of intracardiac electrophysiological research].

As many as 30 patients with different pathologies of the cardiovascular system and paroxysms of ventricular tachycardias were examined. According to the ultrasonography data, an ejection fraction was not lower than 35% in all the patients. It has been shown by electrophysiological studies that intravenous injection of ethacizine in a dose of 0.6 +/- 0.1 mg/kg prevented induction of ventricular tachycardia in 66.7% of patients. In 16.7% of patients, the drug exerted an arrhythmogenic effect that showed up by a decrease of the cycle of tachycardia. Oral administration of ethacizine in the daily dose 100 or 150 mg prevented tachycardia induction by endocardial stimulation in 20.8% of patients. The arrhythmogenic effect of the drug was recorded in 12.5% of patients. The action of ethacizine when administered by both routes was accompanied by a significant elongation of the P--Q interval, QRS complex and of the cycle of ventricular tachycardia. Continuous administration of ethacizine in the daily dose 150 mg to patients with a positive antiarrhythmic drug action (according to the electrophysiological data) prevented paroxysms of ventricular tachycardia, with the observation period being 2 to 6.5 years.

Adolescent↗

PubMed1991

[The diagnosis and possibilities for the anti-arrhythmia treatment of malignant ventricular disorders of the heart rhythm].

Altogether 130 patients with malignant ventricular disorders of cardiac rhythm were examined to demonstrate a possibility of obtaining the diagnostically significant data with the aid of Holter's monitoring of the ECG in 89.2%, with the aid of bicycle ergometry exercise tests in 72.3%, and by means of an electrophysiological examination of the heart in 82.5% of the above-indicated group of patients. The drug testing with the use of invasive and noninvasive techniques of monitoring the action of antiarrhythmic drugs given per os makes it possible to choose effective therapy on an individual basis. The long-term use of such therapy may prevent ventricular tachycardia relapses and noticeably enhance the patients' survival. Severe organic pathology of the heart associated with a decrease of its pump function seen in the majority of patients with malignant ventricular disorders of cardiac rhythm refractory to pharmacotherapy restricts, in a considerable number of cases, the potentialities of drastic surgical treatment because of the risk of operative death. To improve the disease prognosis of these patients, it is necessary that other methods of nonmedicamentous treatment may be used, requiring a less scope of surgical intervention, such as implantation of a cardioverter-defibrillator.

Adolescent↗

PubMed1990

Natriuretic peptide receptors in cultured rat diencephalon.

To characterize the type of cell expressing natriuretic peptide receptors in the brain and the nature of these receptors, we conducted studies in primary cultured glial and neuronal cells derived from fetal rat diencephalon. The glial predominant cultures (95% of total cells and glial fibrillary acidic protein positive) expressed nearly a 10-fold greater specific binding of the natriuretic peptides to cell surface receptors compared with the neuron-predominant cultures. Scatchard analysis of binding studies with 125I-atrial natriuretic peptide (ANP) and 125I-brain natriuretic peptide (BNP) revealed a single class of receptors with dissimilar affinities (0.25 +/- 0.09 and 0.74 +/- 0.07 nM, respectively, n = 3 experiments p less than 0.01) but similar numbers of binding sites for both peptides (93 and 88 fmol/mg of protein, respectively). Cross-linking of 125I-ANP and BNP to cultured glia followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography identified distinct bands at either approximate Mr 130,000, or 102,000 and 66,000, corresponding to two high molecular weight (B) receptors and one low molecular weight (C) receptor described in other tissues. Different subtypes of astrocytes appeared to express different B receptors. Binding and cross-linking of radiolabeled ANP or BNP were competitively inhibited equally by unlabeled ANP or BNP, indicating that ANP and BNP probably bind the same receptors. The glial cultures functionally expressed a receptor(s) with guanylate cyclase activity; BNP was less potent than ANP in stimulating cGMP at lower concentrations. These results indicate that both high and low molecular weight natriuretic peptide receptors are expressed in astrocyte-predominant cultures from the fetal diencephalon and suggest that glia participate in several actions of ANP which are probably mediated through this area of the brain.

Animals↗

PubMed1989

Decreased atrial natriuretic factor receptors and impaired cGMP generation in glomeruli from the cardiomyopathic hamster.

To determine a possible basis for the decreased action of atrial natriuretic factors (ANF) in congestive heart failure, we compared the cardiomyopathic hamster (CMH) in frank congestive failure, and the age-matched, normal, F1B strain of Golden Syrian Hamsters. Scatchard analysis of competitive binding studies revealed two classes of glomerular receptors. The CMH exhibited decreased binding overall and a markedly decreased number of high affinity receptors but comparable receptor affinity compared to the F1B. In contrast, the low affinity receptor population in the CMH had a much greater affinity compared to the F1B while receptor number was similar. Plasma ANF levels were substantially elevated in the CMH compared to the F1B and in-vitro generation of cGMP was significantly lower in the CMH. Such abnormalities could contribute to the resistance to ANF in this disease.

Animals↗

PubMed1989

Central nervous system mediated vasodepressor action of atrial natriuretic factor.

Administration of 20, 4 or 2.5 micrograms/kg of atriopeptin III (AT III) into the fourth ventricle of the brain of spontaneously hypertensive rats produced a 13, 14 and 7 mm Hg decrease in MAP respectively, while 1 microgram/kg had no effect on MAP and was significantly different from 20 or 4 micrograms/kg (p less than 0.025). In contrast, injection of AT III 20 micrograms/kg into the lateral ventricle did not produce a change in MAP. To examine an interaction of AT III with the opioidergic system, the opiate antagonist, naloxone HCl, 10 micrograms, was given by ICV injection 10 minutes prior to AT III, and significantly prevented the depressor response to AT III (p less than 0.025 compared with AT III alone). Injection of specific anti-sera to beta-endorphin failed to prevent the AT III-induced depressor response. Our results demonstrate that AT III can act within the central nervous system to decrease the MAP of rats, most likely at a locus in proximity to the fourth ventricle of the brain. Further, an interaction with the central opioidergic nervous system underlies the central effects of AT III.

Animals↗

PubMed1989

Atrial natriuretic factor: neuromodulator of the central nervous system regulation of blood pressure.

Extensive examination in the mammalian brain for the presence of atrial natriuretic factors (ANF) has revealed both peptide and receptors specifically distributed throughout the central nervous system. High concentrations of ANF have been found in several hypothalamic nuclei, septal areas, the anteroventral third ventricular area (AV3V), and the median eminence, whereas moderate concentrations have been detected in the circumventricular organs and several brainstem nuclei. The receptors for ANF have been found in moderate to high concentrations in the olfactory lobe, AV3V region, and several circumventricular organs (subfornical organ, organum vasculosum of the lamina terminalis) as well as the nucleus tractus solitarius, median eminence, and choroid plexus. These findings suggest a role for ANF in modulating fluid and electrolyte balance, and blood pressure in this compartment, analogous to the proposed actions of this peptide hormone in the periphery. To determine whether ANF might function as a neuromodulator of blood pressure, we administered ANF via fourth ventricular injection into the brain of hypertensive (SHR) and normotensive rats (WKY). Atrial natriuretic factor caused a moderate and significant decrease in mean arterial blood pressure in both strains. The action of ANF appeared to be mediated by activating the central alpha 2-adrenergic nervous system, probably through the release of catecholamines. Further, a dependence on the secretion and action of an endogenous opioid was probably involved; heart rate was unaffected in these studies. Experiments from other laboratories indicate that central ANF may modulate the pressor effects of centrally acting angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Atrial natriuretic factor-induced vasodepression occurs through central nervous system.

To characterize the blood pressure and heart rate effects of atrial natriuretic peptide (ANP) in the brain, we administered 20 micrograms/kg of atriopeptin III in 5 microliters of 0.9 normal saline into the fourth ventricle of awake, freely moving, spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. ANP produced a 13 +/- 1 mmHg decrease in mean arterial blood pressure (MAP) in the SHR (P less than 0.001 vs. base line or saline control, n = 10) and a 9 +/- 2 mmHg decrease in the WKY (P less than 0.02). Heart rate did not change significantly in response to ANP. To determine whether an interaction with the adrenergic nervous system played a role in the effects of ANP, we administered 100 ng yohimbine HCL, an alpha 2-antagonist, by intracerebroventricular injection, 45 min before ANP and completely prevented the ANP-induced decrease in MAP. In contrast, 100 ng intracerebroventricular prazosin, an alpha 1-adrenergic antagonist, had no significant influence on the MAP effect induced by ANP. A third group of SHR was pretreated with intracerebroventricular 6-OH dopamine to deplete central catecholamines or with saline. The rats pretreated with 6-OH dopamine (n = 6) had no significant response to ANP, which was administered 9 days later. This was significantly different from the saline-pretreated control group (n = 6), which responded with a 19 +/- 3 mmHg decrease in MAP (P less than 0.025). These studies indicate that the administration of ANP into the fourth ventricle of the brain decreases the MAP of rats through an interaction with the central alpha 2-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Atrial natriuretic factor is detectable in human cerebrospinal fluid.

To determine whether atrial natriuretic factor (ANF) is detectable in human cerebrospinal fluid (CSF), I measured ANF in CSF samples obtained from subjects undergoing myelography for various neurological disorders. Immunoreactive ANF, measured by RIA, ranged from undetectable (less than 9.7) to 36 pmol/L. All measurable samples diluted in parallel in the RIA. Reverse phase high pressure liquid chromatography and subsequent RIA confirmed the presence of ANF, with most of the immunoreactivity eluting at the position of standard human ANF-(99-126). Simultaneous plasma ANF levels were measured in most individuals and the plasma concentrations were less than those in CSF; most of the immunoreactivity in plasma also eluted at the position of human ANF-(99-126). Thus, ANF is present in CSF in substantial amounts in some subjects with neurological disorders. Further, the CSF levels exceeded the circulating plasma ANF levels in most subjects. These results suggest that ANF in CSF is at least partially derived from production in the brain and/or is concentrated in the CSF.

Adult↗

PubMed1988

[Study of the comparative anti-arrhythmic effectiveness of allapinin, ethacizine and mexitil in patients with ventricular disorders of cardiac rhythm].

A double blind randomized cross-over study was conducted to analyze antiarrhythmic activity of the new Soviet drugs allapinin , ethacizine in comparison with mexitil. Altogether 33 patients with ventricular disorders of cardiac rhythm of high gradations after Lown B. were investigated including patients with paroxysmal ventricular tachycardia. The authors managed to establish and compare the group antiarrhythmic efficacy and safety of each drug, and to assess a degree of selective efficacy of each of them.

Aconitine↗

PubMed1988

[Programmed endocardiac stimulation of the right ventricle in patients with various forms of ventricular disorders of the heart rhythm: the results and their significance].

An intracardiac electrophysiologic study of 73 patients, including those without ventricular arrhythmias, those with chronic ventricular ectopic activity of varying levels, and those with paroxysmal or nonparoxysmal ventricular tachycardia, has identified specific electrophysiologic phenomena that may be used as criteria for the diagnosis of paroxysmal ventricular tachycardias and assessment of the effect of anti-arrhythmic drugs at electrophysiologic testing.

Arrhythmias, Cardiac↗

PubMed1987

Studies of the penetration of the blood brain barrier by atrial natriuretic factor.

The atrial natriuretic factors (ANF) have been detected in various areas of the brain. To determine whether circulating blood borne ANF could contribute to the ANF content in the central nervous systems we examined the ability of ANF-99-126 or ANF-102-126 to penetrate the blood brain barrier. Carotid artery injections of [3H] inulin with [125I] ANF in anesthetized rabbits resulted in a comparably minimal brain uptake index (BUI) for each labeled substance as measured in cerebral cortex extracts. Injection of [3H] HOH and [125I] ANF resulted in a mean BUI in cortex of 4.9 +/- .6 (SEM)% for ANF relative to triated water; this low uptake was not significantly saturable. The BUI ratio for ANF/HOH in olfactory bulb was somewhat higher though still low, at 7.0 +/- 9%, possibly reflecting the high density of ANF receptors in this structure. Infusion of [125I] ANF into the carotid artery of anesthetized rabbits resulted in little radioactivity being detected in the cerebrospinal fluid. Infusion of unlabeled ANF, which raised plasma levels as high as 26.3 ng/ml, resulted in little change in CSF levels. Our results demonstrate that the uptake of ANF into the brain is minimal and supports the idea that local synthesis of ANF predominantly accounts for the brain pool of this peptide.

Animals↗

PubMed1987

[Long-term intracardiac electrophysiological research on patients with paroxysmal ventricular tachycardias: a prospective method for the choice and evaluation of the effectiveness of anti-arrhythmia treatment].

Fifteen patients with paroxysmal ventricular tachycardia (PVT) were subjected to prolonged intracardiac electrophysiologic investigation (EPI) combined with tests of a variety of antiarrhythmic agents. One to 4 (2 +/- 0.3) agents were found to be capable of preventing ventricular tachycardia in response to endocardial stimulation in 93.3% of cases. Subsequent antiarrhythmic treatment by a drug thus selected prevented ventricular tachycardia paroxysms in all patients: there were no recurrent paroxysms in 10 (71.4%) patients, while tachycardiac attacks grew much less frequent, as compared to the pretreatment situation, and could be easily controlled by an additional dose of the drug in 4 (28.6%). Prolonged intracardiac EPI is a highly efficient method of individual assessment of drugs' antiarrhythmic effect that allows a timely and correct choice of treatment capable of reliable prevention of paroxysms.

Adolescent↗

PubMed1986

The in vitro effects of endogenous opiates on natural killer cells, antigen-specific cytolytic T cells, and T-cell subsets.

In concert with the known effects of stress on immune function, we examined a possible neurohumoral connection. The endogenous opiates beta-endorphin, dynorphin, and methionine-enkephalin were assessed for their in vitro effects on human natural killer cell activity, antigen-specific cytolysis, and numbers and ratios of T cells and T-cell subsets. Preincubation with beta-endorphin, an opiate released into the circulation during various stresses, caused a 50% reduction in natural killer cell activity. All endogenous opiates significantly decreased antigen-specific cytolysis. Inhibition of cytolysis in vitro was not mediated through an alteration of T-cell subsets or inhibition of T-cell soluble factors (interleukin 2). The direct effects of these opiates on cytolytic T-cell and natural killer cell function may provide a link between stress and disease susceptibility.

Cytotoxicity, Immunologic↗

PubMed1986

Endogenous opioid modulation of pancreatic hormone secretion: studies in dogs.

The role of endogenous opioid peptides in the modulation of secretion of hormones from the endocrine pancreas was studied in dogs. In response to insulin-induced hypoglycemia, plasma glucagon secretion significantly increased, followed by an increase in plasma somatostatin immunoreactivity. Pretreatment with the opiate antagonist, naloxone, prevented the somatostatin response but had no effect on the augmented glucagon secretion. Neither the degree of hypoglycemia nor recovery from the induced glucose nadir were affected by naloxone. Arginine Hcl administration resulted in prompt increases in immunoreactive glucagon and insulin secretion, as well as a rise in serum glucose. Pretreatment with naloxone failed to affect any of these responses. Our results suggest that endogenous opioid peptides mediate the somatostatin response following hypoglycemia-induced glucagon secretion.

Animals↗

PubMed1986

Treatment of gynecomastia with tamoxifen: a double-blind crossover study.

Benign asymptomatic or painful enlargement of the male breast is a common problem, postulated to be due to an increased estrogen/testosterone ration or due to increased estrogenic or decreased androgenic stimulation via estrogen or androgen receptor interactions. Treatment at present consists of analgesic medication or surgery. However, treatment directed against the preponderance of estrogenic stimulation would seem to represent a more specific form of therapy. In the present double-blind crossover study, one-month courses of a placebo or the antiestrogen tamoxifen (10 mg given orally bid) were compared in random order. Seven of ten patients experienced a decrease in the size of their gynecomastia due to tamoxifen (P less than 0.005). Overall, the decrease for gynecomastia for the whole group was significant (P less than 0.01). There was no beneficial effect of placebo (P greater than 0.1). Additionally, all four patients with painful gynecomastia experienced symptomatic relief. There was no toxicity. The reduction of breast size was partial and may indicate the need for a longer course of therapy. A followup examination was performed in eight out of ten patients nine months to one year after discontinuing placebo and tamoxifen. There were no significant changes from the end of the initial study period except for one tamoxifen responder who developed a recurrence of breast tenderness after six months, and one nonresponder who demonstrated an increase in breast size and a new onset of tenderness after ten months. Therefore, antiestrogenic treatment with tamoxifen may represent a safe and effective mode of treatment for selected cases of cosmetically disturbing or painful gynecomastia.

Administration, Oral↗

PubMed1986

Endogenous opioid peptides: do they mediate the acute antihypertensive action of clonidine in humans?

The involvement of endogenous opioid peptides in the antihypertensive action of acutely administered clonidine, a centrally acting adrenergic agonist, was studied in humans. Eight hypertensive subjects received clonidine 0.2 mg orally, naloxone 8 mg i.v. followed by a 0.13 mg/min infusion, and both drugs together on separate days. Clonidine resulted in a significant decrease in mean blood pressure, which was not affected by concomitant treatment with naloxone. Naloxone alone or with clonidine caused significant elevations in plasma aldosterone, not mediated by increased plasma renin activity. Plasma beta-endorphin was not increased after clonidine administration. In humans, the antihypertensive effects of acute clonidine administration do not appear to be mediated by the release or action of endogenous opioids.

Adult↗

PubMed1986

Partitioning of erythrocytes from spontaneously hypertensive and Wistar-Kyoto rats.

The charge-associated and non-charge-associated (probably lipid-related) surface properties of erythrocytes from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY), from which SHR were originally derived, were studied by cell partitioning in dextran-polyethylene glycol aqueous phase systems. A major difference was found in the surface charge-associated and lipid-related properties of red blood cells from SHR and WKY: the cells from WKY had the higher partition ratio in both charge-sensitive and non-charge-sensitive phases. No difference in partitioning could be found between any two SHR nor between any two WKY. The SHR and WKY erythrocytes showed the same difference when compared with one another even when rats had the same blood pressure. When red blood cells from SHR with different blood pressure were compared, there still was no difference in their surface properties. These results suggest that the differences in both charge-associated and lipid-related surface properties of erythrocytes from SHR and WKY are strain-specific (i.e., genetic) but that there is no correlation, reflected by partitioning, between red blood cell surface properties and the degree of the rats' hypertension.

Animals↗