Search PubMed⌕ Search

Biomedical subjects

J H Kramer

Publications and source records attributed to J H Kramer.

At least 91 records · Page 5Linked to original sources
PubMed1988

Neurobehavioral and psychosocial functioning of women exposed to high altitude in mountaineering.

The effects of chronic hypoxemia upon cognition and behavior were studied in women exposed to high altitude in mountaineering. Neuropsychological tests and psychosocial and physiological questionnaires were given to eight women before, during, and immediately after a Himalayan climb to 20,500 feet. Cognitive functioning remained relatively intact with only two significant decrements, complex abstract reasoning and word-finding ability. Significant changes were found on all psychosocial and physiological questionnaires. Feelings of acceptance of others and anxiety declined significantly. Physical symptoms were greatest during the first five days of ascent. Subjects' self-ratings of mental functioning were significantly better after the expedition than either before or during the climb. Self-assessments were correlated with emotions and physical symptoms, not with actual performances on the test battery. It is suggested that complex cognitive tasks and psychosocial functioning be studied in more detail as these were more influenced by exposure to high altitude in mountaineering.

Adult↗
PubMed1987

Identification of free radicals in myocardial ischemia/reperfusion by spin trapping with nitrone DMPO.

The spin trapping ESR technique was applied to investigate oxygen-derived radicals in ischemic and post-ischemic rat hearts. Using 5,5'-dimethyl-l-pyrroline-N-oxide, carbon-centered radicals were identified during ischemia and oxy-radical adducts (superoxide anion radical, O.-2 and hydroxyl radicals, .OH) in post-ischemic rat heart. The formation of these spin adducts was inhibited by superoxide dismutase, suggesting that superoxide plays a role in the adducts' formation. The results demonstrate that oxygen derived free radicals are important byproducts of abnormal oxidative metabolism during myocardial ischemic and reperfusion injuries.

Animals↗
PubMed1987

Sensory and cognitive evoked potentials in a case of congenital hydrocephalus.

We studied auditory and visual evoked potentials in D.W., a patient with congenital stenosis of the cerebral aqueduct. Head CT scans revealed marked hydrocephalus with expanded ventricles filling more than 80% of the cranium and compressing brain tissue to less than 1 cm in thickness. Despite the striking neuroanatomical abnormalities, however, the patient functioned well in daily life and was attending a local community college at the time of testing. Evoked potentials provided evidence of preserved sensory processing at cortical levels. Pattern reversal visual evoked potentials had normal latencies and amplitudes. Brain-stem auditory evoked potentials (BAEPs) showed normal wave V latencies. Na and Pa components of middle-latency AEP had normal amplitudes and latencies at the vertex, although amplitudes at lateral electrodes were larger than at the midline. In contrast to the normal sensory responses, long-latency auditory evoked potentials to standard and target tones showed abnormal P3 components. Standard tones (probability 85%), evoked N1 components with normal amplitudes (-3.7 microV) and latencies (103 msec), but also elicited large P3 components (17 microV, latency 305 msec) that were never observed following frequent stimuli in control subjects. Target stimuli (probability 15%) elicited P3s in D.W. and controls, but P3 amplitudes were enhanced in D.W. (to more than 40 microV) and the P3 showed an unusual, frontal distribution. The results are consistent with a subcortical source of the P300. Moreover, they suggest that the substitution of controlled for automatic processes may help high-functioning hydrocephalics compensate for abnormalities in cerebral structure.

Adult↗
PubMed1987

Spin-trapping evidence that graded myocardial ischemia alters post-ischemic superoxide production.

The spin trapping agent 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) was used to investigate oxy-radical production in post-ischemic rat hearts previously exposed to 20, 30, or 40 minutes of global ischemia. A hydroxyl spin adduct (DMPO-OH) was identified in coronary effluent during the initial seconds of reperfusion by Electron Spin Resonance (ESR) Spectroscopy. The intensity of the ESR signal in post-ischemic effluent increased as ischemic duration was prolonged; however, regardless of the duration of ischemia, maximal spin adduct detection occurred 3 minutes after initiation of reperfusion. Superoxide dismutase inhibited the formation of DMPO-OH, suggesting that superoxide anion was initially generated and is the principle source for the production on the hydroxyl adduct. Our investigations indicate that superoxide anion is produced during the early moments of reperfusion and that its production in the post-ischemic heart is related to the severity of ischemia.

Animals↗
PubMed1987

Spin trapping of oxygen and carbon-centered free radicals in ischemic canine myocardium.

Oxygen free radical injury has been postulated to occur during myocardial ischemia. We have used Electron Spin Resonance and Spin Trapping techniques to directly demonstrate the production of carbon-centered (R.) and oxygen-centered lipid radical (RO.) in ischemic canine heart. In addition, venous effluent from the ischemic region showed that conjugated dienes (lipid peroxidation products) increased with ischemic duration. Our results suggest that the formation of the oxygen-centered and carbon-centered lipid radical species during ischemia are a consequence of oxy-radical peroxidation of myocardial membrane lipids.

Animals↗
PubMed1986

Potentiation of free radical-induced lipid peroxidative injury to sarcolemmal membranes by lipid amphiphiles.

The effects of naturally occurring lipid amphiphiles on free radical-mediated peroxidative injury in isolated canine sarcolemma were studied. Highly enriched canine myocytic sarcolemmal membranes were preincubated for 10 min at 37 degrees C with or without different amphiphilic lipids before the addition of a free radical-generating system consisting of dihydroxyfumarate and Fe3+-ADP. Lipid peroxidation, assayed as malondialdehyde formation, was catalyzed linearly up to 40 min in the control samples. Pretreatment of the sarcolemma with palmitoyl-CoA, palmitoylcarnitine, or lysophosphatidylcholine accelerated the initial rates (20 min) of peroxidation in a concentration-dependent manner (10-100 microM) and achieved maximal stimulation (240%, 160%, and 210%, respectively, of controls) at 50 microM concentrations of each of these amphiphiles. However, free fatty acids, CoA, and carnitine were without effect. These promoting effects of the amphiphiles persisted over a wide pH range (pH 6.0-7.8) and exhibited additive effects when lower levels of different amphiphiles were combined together. Associated with the accelerated rates of peroxidation produced by palmitoyl-CoA and palmitoylcarnitine were greater losses in the activity of sarcolemmal (Na,K)-ATPase. Since all three kinds of amphiphilic lipids accumulate during ischemia, this study suggests a novel mechanism of potentiation of sacolemmal membrane injury when free radicals are present.

Animals↗
PubMed1985

Effect of tolbutamide on myocardial energy metabolism of the ischemic heart.

The oral hypoglycemic agent tolbutamide has been found to protect the ischemic myocardium against irreversible mechanical failure. The possibility that this salutary effect of tolbutamide was related to its ability to alter energy metabolism was examined in ischemic rat hearts perfused with 5 mM glucose, 5mM acetate and 2.5 units/l insulin. In the presence of 0.6 mM tolbutamide, coronary flow and oxygen consumption were unaltered; however, glucose utilization was stimulated by 30%, glycogenolysis was enhanced by 23%, and the drop in ATP content was reduced by 17% after 30 min, of low-flow perfusion. This elevation in glycolytic flux occurred without a parallel rise in the production of inhibitory metabolites; lactate production was unaltered and tissue lactate/pyruvate ratio decreased. Pyruvate dehydrogenase flux measurements reveal that the mechanism by which tolbutamide increases glycolysis without increasing lactate production is by promoting the entry of pyruvate into the mitochondria. The basis for the observed stimulation of anaerobic metabolism and pyruvate oxidation and how this contributes to the increase in ATP content and benefits the ischemic heart is discussed.

Adenosine Triphosphate↗
PubMed1985

Buccofacial apraxia without aphasia due to a right parietal lesion.

Buccofacial praxis in right-handers is thought to be mediated by the left hemisphere. We present the case of a right-handed man without family history of sinistrality who exhibited a buccofacial apraxia following a unilateral right parietal infarction. Other findings such as intact language, visuospatial impairment, and hemi-inattention are more characteristic of right posterior lesions.

Apraxias↗
PubMed1985

Inhibition of sarcolemmal Na+-K+-ATPase by palmitoyl carnitine: potentiation by propranolol.

Native sarcolemma (SL) from adult canine cardiac myocytes (Na+-K+-ATPase activity 74.2 +/- 3.0 mumol X mg-1 X h-1) was preincubated (10 min, 37 degrees C, pH 7.2) with 1) 20-600 microM palmitoyl carnitine, 2) 250 nM-2.5 mM propranolol, or 3) 20-600 microM palmitoyl carnitine plus propranolol at various concentrations (0.0, 0.025, 0.25, 0.5, 1.0, and 2.5 mM); after preincubation, Na+-K+-ATPase activity was assayed. Palmitoyl carnitine alone (series 1) had no effect on ATPase activity over the range of 20-400 microM but was inhibitory (30%) at 600 microM. Propranolol alone (series 2) did not alter ATPase activity at any concentration. When SL membranes were exposed to both palmitoyl carnitine and propranolol (series 3), a dose-dependent inhibition of ATPase activity was observed. The inhibitory effect was not reversed by 3.0% bovine serum albumin. Propranolol concentrations greater than 0.025 mM significantly inhibited the activity of SL exposed to palmitoyl carnitine (above 150 microM). Palmitoyl carnitine and propranolol do not have to be added simultaneously to produce combined inhibition. Activity was inhibited 50% when SL were pretreated with 100 microM palmitoyl carnitine followed by addition of 2.5 mM propranolol no inhibition occurred if preincubation conditions were reversed. Thus exposure of SL to propranolol and reported physiological levels of palmitoyl carnitine leads to irreversible inhibition of the Na+-K+-ATPase, which may be due to the combined membrane-perturbant actions of these amphipathic agents.

Alamethicin↗
PubMed1985

Perturbations of sarcolemmal and microsomal enzymes by amphiphilic lipids and drugs.

Sarcolemmal (SL) and microsomal (MC) membranes were prepared from adult canine cardiocytes. SL Na+, K+-ATPase (2.35 mumole/min per mg) was enriched 117-fold over the homogenate and MC rotenone-insensitive NADH cytochrome c reductase (RINCR) was enriched 41-fold. Preincubation of SL with 50 microM arachidonyl-CoA (20:4 CoA) stimulated Na+, K+-ATPase almost 2-fold; 250 microM 20:4 CoA inhibited the enzyme by 85%. However, RINCR was inhibited 80% by only 0.2 microM 20:4 CoA. Thus, each of these myocardial lipid-dependent enzymes showed a different sensitivity to perturbation by lipid amphiphiles. In further experiments, SL preincubated with 50 microM 20:4 CoA + 2.5 mM propranolol (which had no effect alone) exhibited a synergistic inhibition of the Na+, K+-ATPase: The enzymatic activity declined 8.5-fold when compared to sarcolemma treated with 50 microM 20:4 CoA alone. Thus, the presence of lipid amphiphiles may result in greater inhibition of the Na+, K+-ATPase when propranolol is present in the membrane.

Acyl Coenzyme A↗
PubMed1984

Differential sensitivity of canine cardiac sarcolemmal and microsomal enzymes to inhibition by free radical-induced lipid peroxidation.

Sarcolemmal and microsomal membranes prepared from adult canine cardiac myocytes (sarcolemmal Na+, K+-ATPase = 71.8 mumol/mg per hr and microsomal rotenone-insensitive NADH cytochrome c reductase = 114 mumol/mg per hr) were each preincubated at 37 degrees C in the presence of a free radical generating system consisting of dihydroxyfumarate and Fe -ADP; loss of the Na+, K+-ATPase and reductase activities, as well as the associated increases in lipid peroxidation, measured by malondialdehyde formation, were temporally correlated in both systems. The ATPase was inhibited 70% when the malondialdehyde was 71 nmol/mg protein at 20 minutes and 90% when malondialdehyde was 138 nmol/mg protein at 90 minutes. Inhibition of reductase activity occurred more gradually, displaying a 27% loss of activity when malondialdehyde reached 34 nmol/mg protein at 20 minutes and 60% with a malondialdehyde value of 67 nmol/mg protein at 90 minutes. The greater susceptibility of the sarcolemma to free radical-induced membrane damage may be due to the higher content of unsaturated fatty acids in this membrane, compared to microsomes.

Animals↗
PubMed1983

Potentiation of the actions of insulin by taurine.

Taurine was found to mediate several changes in myocardial metabolism. In the absence of insulin, only oxygen consumption was significantly elevated by taurine; however, in the presence of 2.5 U/L insulin the amino acid caused the stimulation of glycolysis and glycogenesis, as well as oxygen utilization. These effects of taurine were shown to be dependent on insulin concentration, suggesting a link between the two substances. Measurements of key metabolic intermediates revealed that taurine stimulated glycolysis by enhancing flux through phosphofructokinase. Similarly, it was shown that glycogenesis was promoted because of the increase in glycogen synthase I and decrease in phosphorylase alpha activity. Several possible mechanisms for the observed changes are discussed.

Animals↗
PubMed1983

Cardiac sarcolemmal Na+-K+-ATPase: combined effects of propranolol and arachidonyl CoA.

Sarcolemma from adult canine cardiac myocytes (Na+-K+-ATPase activity 71.8 +/- 3.4 mumol . mg protein-1 . h-1) was preincubated (10 min at 37 degrees C, pH 7.2) with 1) 5-250 microM arachidonyl CoA, 2) 2.5 nM- 2.5 mM propranolol, 3) 5-250 microM arachidonyl CoA plus 2.5 mM propranolol or 4) 2.5 nM-2.5 mM propranolol plus 50 microM arachidonyl CoA; after preincubation the Na+-stimulatable activity was assayed. Arachidonyl CoA alone (50 microM, expt 1) elicited maximum stimulation (89% above control), whereas concentrations greater than 125 microM were inhibitory. Preincubation with propranolol alone (expt 2) had no significant effect on activity. However, when membranes were pretreated with both arachidonyl CoA and 2.5 mM propranolol (expt 3) activity was significantly inhibited. Preincubation with concentrations of propranolol greater than 25 microM were required to reverse the stimulatory effect of 50 microM arachidonyl CoA (expt 4). Propranolol and arachidonyl CoA do not have to be present simultaneously to produce an inhibitory effect. Activity was greatly inhibited (87%) when membranes were preincubated with 100 microM arachidonyl CoA followed by addition of 2.5 mM propranolol; no inhibition was observed if preincubation conditions were reversed. These data suggest that propranolol-induced inhibition of the Na+-K+-ATPase is reversible but becomes irreversible when sarcolemma is pretreated with the fatty acyl CoA, either prior to or during propranolol preincubation.

Acyl Coenzyme A↗
PubMed1983

Effect of tolbutamide on myocardial energy metabolism.

Exposure of rat hearts perfused with 5 mM glucose and 5 mM acetate to tolbutamide led to a dramatic stimulation in glucose utilization and glycolytic flux. This effect was concentration dependent, with the largest response occurring at a tolbutamide concentration of 0.6 mM. Measurement of tissue glycogen content revealed that the higher concentrations of tolbutamide also enhanced glycogenolysis, indicating that the increase in glycolysis was caused by an increase in both glucose consumption and glycogen mobilization. On the basis of the determination of key metabolic intermediates, it was concluded that the stimulation of anaerobic metabolism was mediated by an activation of both phosphofructokinase and phosphorylase. The observed increase in glycolytic flux was associated with a rise in lactate production; however, the most pronounced effect of the drug was the stimulation of glucose oxidation. Thus the percentage of oxygen used in the oxidation of glucose was dramatically increased. Calculations also revealed that the contribution of glucose to overall ATP production rose from 8% in the absence of tolbutamide to about 30% in the presence of the sulfonylurea.

Adenine Nucleotides↗