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Biomedical subjects

M Epstein

Publications and source records attributed to M Epstein.

At least 325 records · Page 18Linked to original sources
PubMed1978

Metabolism of arginine by the isolated perfused rat kidney.

In order to evaluate the renal contribution to the metabolism of arginine, we have evaluated its biosynthesis and catabolism in the isolated perfused rat kidney. The kidneys of eight male Sprague-Dawley rats were perfused with Krebs-Ringer-bicarbonate buffer containing albumin and amino acids. Twenty-five muCi of L-[guanidino-14C]arginine or 25 muCi L-[guanidino-14C]citrulline were added to the system and radiochromatograms of the perfusate were obtained at 0, 30, 60, and 90 min. Perfusate levels of urea, creatine, and guanidine derivatives were measured with high-pressure liquid chromatography. During perfusion there was net utilization of arginine and net production of creatine, guanidinoacetic acid (GAA) and guanidinosuccinic acid (GSA). The guanidino carbon of arginine was incorporated by the kidney into urea, creatine GSA, GAA, and guanidinobutyric acid. The production of 14C-labeled urea from L-[guanidino-14C]citrulline was substantially lower than that previously demonstrated in the liver, while that of arginine was approximately 20 times greater. These studies demonstrate the important contribution of the kidney to the synthesis and metabolism of arginine.

Acetates↗
PubMed1978

Volume as a determinant of plasma aldosterone in anephric man.

Previous studies from this laboratory have demonstrated that the redistribution of blood volume and concomitant central hypervolemia induced by water immersion to the neck (NI), produces a prompt and profound suppression of plasma renin activity (PRA) and plasma aldosterone concentration (PA) without concomitant alterations in serum sodium and potassium concentrations. The NI model was utilized to assess the responsiveness of PA to volume expansion in 12 anephric subjects. The patients were studied on 2 occasions, 48 h after their last dialysis: during a seated control study (7 of the patients) and during 3 h of NI (all 12 patients). The conditions of seated posture and time of day were identical. Blood for PRA, PA, and cortisol was obtained at 30-min intervals for 5 h. PRA was undetectable in all patients. NI failed to alter PA. Plasma cortisol declined progressively throughout NI; serum potassium concentration remained unchanged. An identical NI study in normal subjects suppressed PA by 60%. These data demonstrate that when plasma composition and posture are maintained constant, marked central hypervolemia does not alter PA in anephric man. The present findings support the role of the renin-angiotensin system as the prepotent mediator of volume-induced changes in PA.

Adult↗
PubMed1978

Computerization of three-channel thrombelastograph.

A small-size and low-cost microcomputer using an Intel 8080 micro-processer is employed to provide real-time data collection and reduction of a three-channel electronic-readout thrombelastograph (TEG). Computed values of significant clotting parameters are obtained instantly allowing for rapid analysis and monitoring of many patients. Computer hardware was designed to optimize signal sampling rates, processing time and storage.

Analog-Digital Conversion↗
PubMed1978

Familial hyperkalemia, hypertension, and hyporeninemia with normal aldosterone levels. A tubular defect in potassium handling.

A 52-year-old man had hypertension, persistent hyperkalemia, and hyperchloremic metabolic acidosis; renal and adrenal functions were normal. Four other members of the family have the same findings. The patient's plasma aldosterone (PA) level was within normal range, though plasma renin activity (PRA) was undetectable. The ability to conserve sodium with increased endogenous aldosterone levels, and the inability to increase potassium excretion while exogenous mineralocorticoid (fludrocortisone acetate) was administered, indicated a distal tubular defect in potassium handling. Effective reduction of the hyperkalemia by K+ -Na+ exchange resin also corrected the acidosis and the hyperchloremia, suggesting that hyperkalemia may cause metabolic acidosis.

Acidosis↗
PubMed1977

On the relative location of the inhibitor-and calcium-binding sites in bovine trypsin as determined by nuclear magnetic resonance. Possible ambiguities in paramagnetic probe mapping studies.

Possible pitfalls in mapping studies utilizing the nuclear relaxation rates induced by paramagnetic probes are pointed out. In cases in which a distance is sought between a paramagnetic ion and a small molecule (e.g. substrate, inhibitor, etc.), both bound non-covalently to a macromolecule, heterogeneity in the system with respect to the binding of either of them may result in ambiguous conclusions. It is shown that the trypsin-gadolinium (III)-inhibitor system is heterogeneous, as revealed in the dependence of the water and inhibitor proton line-widths upon both the Gd3+ and the enzyme concentrations and in the effects of added Ca2+ on the line-widths. The results imply that in published work (Abbott et al. (1975) Biochemistry 14, 4935) the distance from a weak rather than from the strong metal ion binding site of trypsin (EC 3.4.21.4) may have been determined.

Amidines↗
PubMed1977

Fetal pancreatic glucagon responses in glucose-intolerant nonhuman primate pregnancy.

Rhesus monkey pancreatic alpha-cell function in streptozotoc-induced glucose-intolerant pregnancy is similar to that in normal primate pregnancy. Specifically, basal maternal and fetal plasma glucagon levels equate, and the fetal alpha cell does not respond to the glucagonogenic stimulus of either intravenous alanine or insulin-induced hypoglycemia. This contrasts with the accelerated maturation of the fetal beta cell in glucose-intolerant pregnancy, and does not support the concept of functional coupling of the pancreatic islet by a common glucose-based process. Fetal plasma glucagon levels do increase after L-dopa injection to the fetus. These data indicate that alpha cell unresponsiveness is a function of the glucagon-releasing mechanism rather than inadequate hormonal synthesis.

Alanine↗
PubMed1977

Management of hyperstimulation syndrome.

A case of hyperstimulation syndrome secondary to Pergonal therapy is presented. Successful management was based principally on severe sodium and fluid restriction without the use of volume expanders. The rationale for this therapeutic approach is presented and discussed. Although this iatrogenic disease should be virtually eliminated with the monitoring of daily urinary estrogens, severe hyperstimulation may still occur as a result of laboratory error.

Adult↗
PubMed1977

Evaluation of cerebrospinal fluid production in the development of communicating hydrocephalus.

Diminished absorption of cerebrospinal fluid (CSF) is the most common cause of communicating hydrocephalus. Soon after the absorptive capacity is decreased, the CSF pressure increases, producing ventricular enlargement if the process is not halted. CSF production was measured by ventriculo-cisternal perfusion during and after the production of communicating hydrocephalus, using an atraumatic animal model. Animals with chronic hydrocephalus and normal pressure had normal CSF production. CSF production tended to be lower in animals with increased pressure. When CSF absorption is compromised, decreased CSF production does not appear to be a significant compensatory mechanism.

Acute Disease↗
PubMed1977

Flow system fluorescence polarization measurements on fluorescein diacetate-stained EL4 cells.

We have adapted a multiparameter cell sorter to measure the distribution of fluorescence polarization in cell populations. Measurements carried out on EL4 cells show that the percent polarization of fluorescein fluorescence decreases with increasing fluorescence intensity. This inverse relationship between polarization and intensity is shown both within the cell population and by the average values of the two quantities during both the increase and decrease of fluorescence intensity. The quantitative relation between intensity and polarization is different in hypertonic than in isotonic media. These results suggest that polarization measurements carried out at a fixed time after incubation of cells with fluorescein diacetate, which is converted to fluorescein within the cells, may depend in part on the rate of fluorescein accumulation, and that agents that have been reported to change the polarization of fluorescein in living cells may do so by changing the kinetics of fluorescein accumulation.

Cell Line↗