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Biomedical subjects

R Gelfand

Publications and source records attributed to R Gelfand.

At least 19 recordsLinked to original sources
PubMed2005

Optimization of oxygen tolerance extension in rats by intermittent exposure.

Optimization of oxygen tolerance extension by intermittent exposure was studied in groups of 20 rats exposed to systematically varied patterns of alternating oxygen and normoxic breathing periods at 4.0, 2.0, and 1.5 ATA. Oxygen periods of 20, 60, and 120 min were alternated with normoxic intervals that provided oxygen-to-normoxia ratios of 4:1, 2:1, 1:1, and 1:3. In general, median survival times had nearly linear relationships to increasing normoxic intervals with oxygen period held constant. Exceptions occurred at 4.0 and 2.0 ATA where a 5-min normoxic interval was too short for adequate recovery even with a 20-min oxygen period, and an oxygen period of 120 min was too long even with a normoxic interval of 30 min. These exceptions did not occur at 1.5 ATA. Survival time for many intermittent exposure patterns was equivalent to that for continuous exposure to an oxygen pressure definable as a time-weighted average of the alternating oxygen and normoxia periods. However, this predictive method underestimated the degree of protection achieved by several of the intermittent exposure patterns, especially those performed at 4.0 ATA. Results provided guidance for selection of intermittent exposure patterns for direct evaluation in humans breathing oxygen at 2.0 ATA. Definition of intermittent exposure patterns and conditions that produced prominent gains in oxygen tolerance can also facilitate the performance of future experiments designed to study potential mechanisms for oxygen tolerance extension by intermittent exposure. Heat shock and oxidation-specific stress proteins that are induced by exposure to oxidant injury are suggested for emphasis in such investigations.

Animals↗
PubMed1999

Effects of prolonged oxygen exposure at 1.5, 2.0, or 2.5 ATA on pulmonary function in men (predictive studies V).

As part of a study of human organ O2 tolerance, lung flow-volume and spirometric measurements were performed repeatedly before, during, and after continuous O2 exposures at 1.5, 2.0, and 2.5 ATA for average durations of 17.7, 9.0, and 5.7 h, respectively (effects of O2 breathing at 3.0 ATA for 3.5 h were reported previously; J. M. Clark, R. M. Jackson, C. J. Lambertsen, R. Gelfand, W. D. B. Hiller, and M. Unger. J. Appl. Physiol. 71: 878-885, 1991). Additional measurements of pulmonary mechanical function, gas exchange, and alveolar inflammatory cells were obtained before and after O2 exposure. Rates of pulmonary symptom development and lung volume reduction increased progressively with elevation of O2 pressure. Average rates of vital capacity reduction over a useful range of O2 pressures provided a valuable general description of pulmonary O2 tolerance in humans. However, the existence of multiple pulmonary effects of O2 toxicity and the complexity of their interactions require awareness that deviations from the average relationships may occur in different individuals or under varying conditions of O2 exposure and subsequent recovery. The associated pulmonary function deficits may represent responses to a composite of direct and indirect effects of O2 poisoning, along with related consequences and subsequent reactions to those effects.

Acid-Base Equilibrium↗
PubMed1998

Hypoxic ventilatory sensitivity in men is not reduced by prolonged hyperoxia (Predictive Studies V and VI).

Potential adverse effects on the O2-sensing function of the carotid body when its cells are exposed to toxic O2 pressures were assessed during investigations of human organ tolerance to prolonged continuous and intermittent hyperoxia (Predictive Studies V and VI). Isocapnic hypoxic ventilatory responses (HVR) were determined at 1.0 ATA before and after severe hyperoxic exposures: 1) continuous O2 breathing at 1.5, 2.0, and 2.5 ATA for 17.7, 9.0, and 5.7 h and 2) intermittent O2 breathing at 2.0 ATA (30 min O2-30 min normoxia) for 14.3 O2 h within 30-h total time. Postexposure curvature of HVR hyperbolas was not reduced compared with preexposure controls. The hyperbolas were temporarily elevated to higher ventilations than controls due to increments in respiratory frequency that were proportional to O2 exposure time, not O2 pressure. In humans, prolonged hyperoxia does not attenuate the hypoxia-sensing function of the peripheral chemoreceptors, even after exposures that approach limits of human pulmonary and central nervous system O2 tolerance. Current applications of hyperoxia in hyperbaric O2 therapy and in subsea- and aerospace-related operations are guided by and are well within these exposure limits.

Adult↗
PubMed1996

Relationship of 133Xe cerebral blood flow to middle cerebral arterial flow velocity in men at rest.

Cerebral blood flow (CBF) was measured by 133Xe clearance simultaneously with the velocity of blood flow through the left middle cerebral artery (MCA) over a wide range of arterial PCO2 in eight normal men. Average arterial PCO2, which was varied by giving 4% and 6% CO2 in O2 and by controlled hyperventilation on O2, ranged from 25.3 to 49.9 mm Hg. Corresponding average values of global CBF15 were 27.2 and 65.0 ml 100 g min-1, respectively, whereas MCA blood-flow velocity ranged from 42.8 to 94.2 cm/s. The relationship of CBF to MCA blood-flow velocity over the imposed range of arterial PCO2 was described analytically by a parabola with the equation: CBF = 22.8 - 0.17 x velocity + 0.006 x velocity2 The observed data indicate that MCA blood-flow velocity is a useful index of CBF response to change in arterial PCO2 during O2 breathing at rest. With respect to baseline values measured while breathing 100% O2 spontaneously, percent changes in velocity were significantly smaller than corresponding percent changes in CBF at increased levels of arterial PCO2 and larger than CBF changes at the lower arterial PCO2. These observed relative changes are consistent with MCA vasodilation at the site of measurement during exposure to progressive hypercapnia and also during extreme hyperventilation hypocapnia.

Adult↗
PubMed1995

Human tolerance and physiological responses to exercise while breathing oxygen at 2.0 ATA.

Multiple physiological functions were monitored in ten men who performed two 30-min periods of 150-W ergometer exercise during 120-min exposures to O2 at 2.0 ATA. There were no convulsions or electroencephalographic manifestations of increased excitability. Sequential measurements of peripheral visual fields, pulmonary mechanical function, mental performance, and cardiovascular function during the resting recovery after each of the two exercise periods were not detectably altered from pre-exercise control values. Pre- and post-exposure measurements of visual acuity, accommodation, pupil diameter, visual cortical activity, and retinal electrical activity also revealed no significant differences. While CNS symptoms were absent, average arterial PCO2 rose by about 5 mm Hg during both exercise periods. This finding was confirmed in six subjects who performed four 6-min periods of continuous exercise at 50, 100, 150, and 200 W while breathing O2 at 2.0 ATA. Average arterial PCO2 rose nearly linearly from 34.3 mm Hg at rest to 44.0 mm Hg at 200 W. Arterial PCO2-related increments in brain blood flow and PO2 may explain part or all of the known detrimental influence of exercise on CNS O2 tolerance.

Atmospheric Pressure↗
PubMed1991

Pulmonary function in men after oxygen breathing at 3.0 ATA for 3.5 h.

As a pulmonary component of Predictive Studies V, designed to determine O2 tolerance of multiple organs and systems in humans at 3.0-1.5 ATA, pulmonary function was evaluated at 1.0 ATA in 13 healthy men before and after O2 exposure at 3.0 ATA for 3.5 h. Measurements included flow-volume loops, spirometry, and airway resistance (Raw) (n = 12); CO diffusing capacity (n = 11); closing volumes (n = 6); and air vs. HeO2 forced vital capacity maneuvers (n = 5). Chest discomfort, cough, and dyspnea were experienced during exposure in mild degree by most subjects. Mean forced expiratory volume in 1 s (FEV1) and forced expiratory flow at 25-75% of vital capacity (FEF25-75) were significantly reduced postexposure by 5.9 and 11.8%, respectively, whereas forced vital capacity was not significantly changed. The average difference in maximum midexpiratory flow rates at 50% vital capacity on air and HeO2 was significantly reduced postexposure by 18%. Raw and CO diffusing capacity were not changed postexposure. The relatively large change in FEF25-75 compared with FEV1, the reduction in density dependence of flow, and the normal Raw postexposure are all consistent with flow limitation in peripheral airways as a major cause of the observed reduction in expiratory flow. Postexposure pulmonary function changes in one subject who convulsed at 3.0 h of exposure are compared with corresponding average changes in 12 subjects who did not convulse.

Adult↗
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

A compartmental model to quantitate in vivo glucose transport in the human forearm.

Glucose transport is a critical step in the control of glucose disposal that, until presently, has not been quantitated in vivo in humans. We have employed the perfused forearm and euglycemic insulin-clamp techniques in combination with a dual-tracer injection to measure basal and insulin-mediated glucose transport in six normal subjects. L-[3H]glucose, which is not transported, was used to trace extracellular glucose kinetics; 3-O-[14C]-methyl-D-glucose, transportable but not metabolizable, was used to monitor glucose movement across the cell membrane. After bolus intra-arterial injection of the two tracers, plasma samples were obtained every 15-30 s for 10 min from a deep forearm vein to determine the washout curves. A linear compartmental model was developed that accounts for blood flow heterogeneity. It consists of three parallel, two-compartment chains merging into the sampling compartment to which cellular compartments are appended. A priori identifiability analysis was performed. The uniquely identifiable parameterization includes the transport rate constants of glucose into and out of the cell. The model was identified using nonlinear least-squares parameter estimation. Transport parameters are estimated with very good precision, and their reproducibility is satisfactory. The model also allows the estimation of the mean arteriovenous transit times of both the extracellular and the transported tracer. The compartmental model provides a novel approach to investigate glucose transport in vivo in humans.

3-O-Methylglucose↗
PubMed1986

Comparison of the sensitivity and specificity of the CA19-9 and carcinoembryonic antigen assays in detecting cancer of the pancreas.

In this study, we determined the sensitivity and specificity of the new serum assay CA19-9 in detecting adenocarcinoma of the pancreas and compared the results with those of the serum assay to carcinoembryonic antigen (CEA). Thirty-seven patients with biopsy-proven adenocarcinoma (14 patients with resectable disease and 23 patients with unresectable disease) were compared with 157 controls (48 patients with benign pancreatic disease, 34 patients with nonpancreatic sources of abdominal pain, 58 patients with benign jaundice, 7 patients with nonpancreatic malabsorption, and 10 patients with renal failure on dialysis). It was determined that a cutoff of 75 U/ml enhanced the diagnostic efficiency (sensitivity + specificity) of CA19-9 over the manufacturer's recommended cutoff of 37 U/ml. The sensitivity of CA19-9 (greater than 75 U/ml) in detecting cancer was greater than that of CEA (greater than 5 ng/ml) (86.5% vs. 48.4%) (p less than 0.01, McNemar test). The sensitivity of CA19-9 was 78.6% in resectable and 91.3% in unresectable disease. The specificity of CA19-9 was also greater than CEA (92.5% vs. 87.3%), although this difference was not statistically significant. The higher the CA19-9 or CEA level, the greater the specificity of either assay; at CA19-9 levels greater than 600 U/ml and CEA levels greater than 20 ng/ml the specificity is approximately 99%. The combination of an elevated CA19-9 level (greater than 75 U/ml) and an elevated CEA level (greater than 5 ng/ml) also enhanced specificity to 99%. It is concluded that CA19-9 used alone is superior to CEA used alone in detecting cancer of the pancreas and that the combination of mild elevations of both assays improves their specificity. Although the CA19-9 marker can be elevated with other intraabdominal adenocarcinomas (e.g., gastric, biliary, or colonic), CA19-9, together with CEA, will be useful to the clinician in differentiating benign from malignant pancreatic processes and in alerting the clinician to the possible presence of an intraabdominal neoplasm in the proper clinical setting.

Adenocarcinoma↗
PubMed1984

Tranylcypromine vs nortriptyline vs placebo in depressed outpatients: a controlled trial.

This study was designed to compare the therapeutic and adverse effects of tranylcypromine (a monoamine oxidase inhibitor), nortriptyline (a tricyclic antidepressant), and placebo. A total of 122 depressed outpatients randomly assigned to double-blind treatment with one of these agents completed the 4-week protocol. Treatment groups were balanced for proportions of endogenous versus nonendogenous depressions, defined according to the Research Diagnostic Criteria; however, nonendogenous depressions outnumbered endogenous depressions by such a large proportion (4:1) that meaningful statistical comparisons were limited to the nonendogenous group. In this group, both active drugs proved more effective than placebo, with little differences between the two active drugs except in the areas of side effects and of differential sensitivity of the outcome scales to a given drug. It was concluded that tranylcypromine, a drug which has received relatively little use and study in recent years, represents an effective and reasonably safe treatment for nonendogenous depression, although significant advantages over tricyclics with this disorder remain to be demonstrated.

Adolescent↗
PubMed1983

Abnormal involuntary movements in patients on long-acting neuroleptics.

Two hundred and thirty eight patients (144 males, 94 females) on long-acting neuroleptics; mainly fluphenazine decanoate, were surveyed and evaluated for abnormal involuntary movements and associated risk factors. A highly significant correlation was found between the three scales used in the evaluation. The prevalence rate for the transient, acute extrapyramidal syndrome was 37.38%, while that of tardive dyskinesia was 57%. Half of the tardive dyskinesia cases were of minimal severity. Most of these were located in orofacial region. Tardive dyskinesia was more frequent in younger patients but more severe in older age groups. Other associated risk factors were tremors and rigidity, and use of antiparkinsonien drugs. Tardive dyskinesia is a common abnormal involuntary movement in patients on long-acting neuroleptic. Early recognition of TD in this population could help in planning for its prevention by the use of minimum effective dose of medication.

Adolescent↗
PubMed1983

Human respiration at rest in rapid compression and at high pressures and gas densities.

Ventilation (V), end-tidal PCO2 (PACO2), and CO2 elimination rate were measured in men at rest breathing CO2-free gas over the pressure range 1-50 ATA and the gas density range 0.4-25 g/l, during slow and rapid compressions, at stable elevated ambient pressures and during slow decompressions in several phases of Predictive Studies III-1971 and Predictive Studies IV-1975. Inspired O2 was at or near natural O2 levels during compressions and at stable high pressures; it was 0.5 ATA during decompressions. Rapid compressions to high pressures did not impair respiratory homeostasis. Progressive increase in pulmonary gas flow resistance due to elevation of ambient pressure and inspired gas density to the He-O2 equivalent of 5,000 feet of seawater was not observed to progressively decrease resting V, or to progressively increase resting PACO2. Rather, a complex pattern of change in PACO2 was seen. As both ambient pressure and pulmonary gas flow resistance were progressively raised, PACO2 at first increased, went through a maximum, and then declined towards values near the 1 ATA level. It is suggested that this pattern of PACO2 change results from interaction on ventilation of 1) increase in pulmonary resistance due to elevation of gas density with 2) increase in respiratory drive postulated as due to generalized CNS excitation associated with exposure to high hydrostatic pressure. There may be a similar interaction between increased gas flow resistance and increase in respiratory drive related to nitrogen partial pressure and the narcosis resulting therefrom.

Adult↗
PubMed1983

Breathing patterns during submaximal and maximal exercise in elite oarsmen.

Continuous breath-by-breath measurements of ventilatory parameters were performed during submaximal and maximal treadmill exercise in 21 highly conditioned oarsmen. Average maximum values of O2 uptake, minute ventilation (VI), tidal volume (VT), and respiratory frequency (f) were 6.60 l/min (73.5 ml X kg-1 X min-1), 200 l/min, 3.29 l, and 62 breaths/min, respectively. During the transition from moderate to heavy submaximal exercise, VT and f increased progressively. At near-maximal to maximal work loads, VT plateaued and then decreased slightly, while f continued to increase. Increase in f at the start of exercise was achieved predominantly by an abrupt decrease in expiratory duration (TE) with an equally abrupt, but much smaller, decrease in inspiratory duration (TI). During the transition from submaximal to maximal exercise, both TE and TI decreased progressively. Although f appeared to be entrained by stepping rate in a few subjects, the dominant trend during submaximal to maximal exercise was characterized by a relatively small increase in stepping rate with a much larger increment in f. Our data are consistent with the conclusion that exercise breathing patterns are determined by many interacting factors that vary at different work loads, in different individuals, and are probably also influenced by physical conditioning and previous experience.

Adult↗
PubMed1981

Circadian variation in plasma prolactin, gonadotropins, and testosterone in diabetic male patients with and without impotence.

The circadian variation in plasma levels of prolactin, gonadotropins, testosterone, and glucose were studied in 10 young diabetic male patients. Four patients were asymptomatic without sexual dysfunction and six patients had organic impotence. The results of this study indicate that diurnal levels of luteinizing hormone, follicle-stimulating hormone, prolactin, and testosterone are similar in diabetic patients with and without impotence. During the nocturnal period, a sleep-related increase in plasma prolactin levels was noted in diabetic patients without impotence. In diabetic patients with impotence, plasma prolactin levels were similar during the diurnal and nocturnal periods. These results further support previous findings that diabetic patients with organic impotence do not have abnormal gonadotropin and testosterone levels.

Adult↗