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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the controversy over whether the neonatal heart is more or less susceptible to global ischemia than the adult heart, the time interval between the onset of ischemia and the beginning of contracture (TIC) was compared in neonatal (n = 6, 3 to 5 days old) and adult (n = 6, 4 to 5 months old) pig hearts. A comparison of the myocardial concentrations (mumol/g wet weight) of ATP, glycogen, lactate, and glucose-6-phosphate (G-6-P) was also done. The anesthetized animals underwent a sternotomy, and control right ventricular myocardial biopsy samples were taken. The heart of each was rapidly excised and placed in a 37 degrees C substrate-free Krebs-Henseleit bath. A compliant balloon was placed in the left ventricle to record pressure changes. Time to onset and peak TIC were recorded and additional proximal right ventricular biopsy samples were taken. Data were recorded as mean +/- SEM. Results demonstrated that neonatal hearts had a significantly shorter (p less than .05) TIC (29.5 +/- 1.7 min) than adult hearts (43.0 +/- 2.9 min) and exhibited more rapid lactate accumulation (2.5 +/- 0.5 to 22.1 +/- 3.0, p less than .001) and an increase in G-6-P (0.07 +/- 0.03 to 0.34 +/- 0.07, p less than .01) with a nonsignificant decline in myocardial glycogen (23.3 +/- 12.1 to 17.4 +/- 4.0, p greater than .05). Our findings indicate that neonatal hearts are more sensitive than adult hearts to global ischemia, which has potential implications for myocardial protection in pediatric cardiac surgery.
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PMID:Relative vulnerability of neonatal and adult hearts to ischemic injury. 366 14

Rabbit eyes, in vivo and in vitro, were exposed to UV-B irradiation at 300 nm, from a mercury arc lamp with an 11 nm bandpass filter. Radiant exposure ranged from 0.1 J/cm2 to 0.5 J/cm2. In vivo, swelling of the cornea resulted over a 12 to 40 hr period, the extent and duration being directly related to exposure. Recovery of normal thickness was complete within four days. Corneas removed at 18 hr after exposure recovered normal thickness during a five hour perfusion period, except for those most heavily exposed. When removed at 42 hr post exposure all corneas thinned to almost normal thickness. SEM showed the endothelial cells of exposed eyes to have either exaggerated villi on the surface and a disorganized mosaic or, after higher exposures, to be devoid of villi and have loose, flap like cell borders and large "blebs." After exposure of isolated corneas mounted for perfusion, swelling again ensued and similar changes were observed in the appearance of the cells, except that "blebs" were not found. No significant changes were observed in the metabolic components ATP, ascorbate and glutathione, nor was there any indication of lipid peroxidation. At higher in vivo exposures, the aqueous humor did show a decrease in ascorbate concentration and an increase in protein content, which probably result from a breakdown of the blood-aqueous barrier. UV-B irradiation may cause or promote changes in the endothelium associated with aging, but the one time radiant exposures of the magnitude used in this study, appear to have no severe or permanently toxic effects.
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PMID:The effects of UV-B irradiation on the corneal endothelium. 366 57

Myocardial exogenous substrate preference was studied under conditions of increased plasma lactate concentration before and after a severe (halving of tissue ATP concentration, sixfold increase in tissue lactate concentration) but reversible (less than 1% necrosis on reperfusion) global ischaemic stress produced by continuous hypothermic electromechanical arrest of the heart of four hours' duration by aortic cross clamping and multidose potassium cardioplegia. Fatty acid oxidation was studied using 1-14C-palmitate under steady state conditions and under similar isovolumic fixed pressure conditions with the heart at a constant rate using a left ventricular intracavitary balloon. Exogenous free fatty acid oxidation during the pre-ischaemic period with an increased lactate concentration (3.9-5.8 mmol . litre-1) was 0.62(0.21) mumol . min-1 X 100 g-1 (mean (SEM)). This represented a mean of 32% of the total carbon dioxide produced in contrast to a post-ischaemia free fatty oxidation rate of 2.67(0.87) mumol . min-1 X 100 g-1, in the presence of even further increased plasma lactate concentrations (8.47-11.17 mmol . litre-1), representing a mean of 82% of the total carbon dioxide output. These data suggest that the substrate preference of the myocardium, under conditions of increased plasma lactate concentration, shifts to greater oxidation of exogenous free fatty acids after ischaemic stress.
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PMID:Exogenous substrate preference of the post-ischaemic myocardium. 371 5

The effect of temperature changes (36-40 degrees C) on the liver function was studied in the isolated perfused pig liver. When compared with control studies no effect was observed on lactate, glucose, bile flow, ATP and energy charge, and the recovery after the changes in temperature was complete. The only significant changes observed regarded the hepatic oxygen uptake and galactose elimination capacity. The increase of 1 degree C resulted in an increase in galactose elimination of 6%, corresponding to a Q10 of 1.98 (SEM 0.12) with an energy of activation of 48 kJ/mol (SEM 4.7). Oxygen uptake was linearly related to galactose elimination (1.75 mol for 1 mole change in galactose elimination). These results indicate that circulatory changes are unimportant within physiological temperature changes. It is concluded that temperature effects on galactose elimination are too small to warrant a correction when used as a clinical test of quantitative liver function.
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PMID:The effect of physiological temperature changes on the galactose elimination capacity of the isolated perfused pig liver. 374 57

When uptake of L-[14C]ascorbic acid ([14C]AA) to various organs in guinea-pigs was studied after intracardiac injection, the adenohypophysis, pars intermedia, and the neurohypophysis had an uptake per milligramme protein which was about half of the uptake to the adrenals. Adrenal uptake was 20 +/- 2.8 pmol mg-1 protein microCi-1 injected. The uptake to the different parts of the hypophysis was considerably higher than the uptake to pancreas, liver, kidney, spleen and other organs. When isolated nerve endings (neurosecretosomes) from ox neurohypophyses were incubated with a medium containing labelled dehydroascorbic acid ([14C]DHA), the uptake was much slower than when the medium contained labelled ascorbic acid. The uptake of [14C]DHA showed a linear dependence on concentration, and was not influenced by addition of Mg2+ and ATP. Addition of Mg2+ + ATP, omission of Ca2+ and Mg2+ or exchange of Na+ in the medium with K+ had no effect on the uptake of ascorbic acid. When isolated secretory granules from ox neurohypophyses were incubated with a medium containing [14C]DHA, uptake was considerably faster than the uptake when they were incubated in a medium containing [14C]AA. The uptake of dehydroascorbic acid was linear with the concentration in the medium and was not changed by addition of Mg2+ ATP. Addition of 10 mM NH4Cl or exchange of 120 mM K+ in the incubation medium with Na+ did not change the uptake of dehydroascorbic acid. The contents of copper, zinc, iron and cobalt were determined in isolated nerve endings (A) and membranes (B) as well as in lysate (C) from isolated neurosecretory granules. The results (in nmol mg-1 protein) were for Cu: (A): 0.25 +/- 0.01 (SEM), (B): 0.67 +/- 0.16, (C): 0.22 +/- 0.06; for Zn: (A): 0.53 +/- 0.13, (B): 6.97 +/- 0.75, (C): 1.8 +/- 0.53; and for Fe: (A): 15.6 +/- 1.9, (B): 6.92 +/- 0.32, (C): 3.15 +/- 0.43. In all preparations the cobalt content was below the detection limit (less than 5 pmol mg-1 protein).
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PMID:Uptake of dehydroascorbic acid and ascorbic acid to isolated nerve terminals and secretory granules from ox neurohypophyses. 381 87

Mouse fetuses homozygous for the lethal cab (cardiac abnormal) mutation are characterized by pleiotropic effects that lead to immediate postnatal death. Mutant fetuses have only 4% of the normal amount of hepatic glycogen and 39% of the normal cardiac glycogen reserve, coupled with lower specific activities of glycogen synthase and phosphorylase. Analysis with the periodic acid-Schiff reagent histochemical stain demonstrated that cab homozygotes also have reduced amounts of structural polysaccharides. One of the most distinctive mutant phenotypic traits is severe prenatal hypoglycemia, with average (+/-SEM) plasma glucose concentrations of 0.35 +/- 0.14 mM in late fetuses compared to 3.47 +/- 0.69 mM in normal littermates. Compromise of glucose transport from dam to fetus or altered cellular glucose utilization was considered as a possible basis for the low extracellular and intracellular (hepatic) levels of glucose in mutants. Transport of the glucose analogue alpha-methyl[14C]glucoside by the placenta of cab homozygotes is normal. However, metabolism of [14C]glucose by mutant cells yields only 20% of the normal amount of 14CO2. This reduced efficiency of glucose metabolism is correlated with lower ATP concentrations in mutant organs. Aberrant glucose utilization may account for the pleiotropic features of the cab syndrome.
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PMID:Prenatal expression of a lethal genetic defect in carbohydrate metabolism in mice. 385 87

The release of vasodilating substances from the vascular endothelium has been postulated to depend on a rise in the level of intracellular free calcium (Cai++). We measured Cai++ in intact monolayers of calf endothelial cells, grown in culture, that were loaded with the fluorescent calcium indicator quin 2. Fluorescence (excitation wavelength 340 nm, emission wavelength 492 nm) was calibrated by raising Cai++ to a maximum with the calcium ionophore ionomycin (0.1 microM) and by lowering it to a minimum with ionomycin plus manganese (0.4 mM), which quenches quin 2 fluorescence completely. Loss of fluorescent dye from the cells was calculated from fluorescence at the isosbestic excitation wavelength (365 nm). Resting Cai++ was 71 +/- 3 (SEM) nM. ATP (adenosine-5'-triphosphate) raised Cai++ dose-dependently and reversibly to 458 +/- 60 nM at a concentration of 10 microM, and at 0.1 mM to values close to those that occurred under ionomycin. ADP (A-5'-PP) and AMP (A-5'-P) had smaller effects with a maximal Cai++ of 287 +/- 72 nM at 30 microM ADP and 176 +/- 17 nM at 0.1 mM AMP. At these concentrations, ADP and AMP attenuated significantly the increase of Cai++ under ATP (10 microM). Adenosine (0.1 or 0.3 mM) and acetylcholine (0.1 to 30 microM) enhanced Cai++ inconsistently, by a maximum of 50 nM. These effects were abolished by theophylline and atropine, respectively. In the absence of extracellular calcium, ATP still raised Cai++, although endothelial responsiveness declined after repetitive stimulations. We conclude that activation of purinergic receptors increases intracellular free calcium in endothelial cells, and that this increase is probably an essential trigger for synthesis of prostacyclin and the labile endothelium-derived relaxant factor.
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PMID:Increased free calcium in endothelial cells under stimulation with adenine nucleotides. 394 90

According to current concepts, soluble phosphatidic-acid phosphatase, converting phosphatidic acid into a diglyceride, is a rate-limiting enzyme in the hepatic biosynthesis of triglycerides. The present paper is the first report on this enzyme in human liver. The enzyme activity was assayed in ammonium sulphate precipitates of cytosol obtained from human liver biopsies. The activity was stimulated by preincubation with alkaline phosphatase and inhibited by Mg-ATP, suggesting that phosphorylation-dephosphorylation may be of some importance for the expression of the activity of the enzyme. When assayed under optimal conditions, the activity obtained in liver biopsies from normal-weight gallstone patients averaged 12.8 +/- 2.0 nmol min-1 (mg protein)-1 (mean +/- SEM) (n = 17). The enzyme activity was slightly higher in liver biopsies from morbidly obese subjects 16.4 +/- 2.8 nmol min-1 (mg protein)-1 (n = 14). The difference between the two groups of subjects was probably in part sex-dependent and was not statistically significant. A similar small and insignificant difference between the two groups of subjects was found when the enzyme activity was assayed in the maximally stimulated state--i.e. after incubation with alkaline phosphate. These findings suggest that an increased capacity of the soluble phosphatidic-acid phosphatase is not of major importance for the increased triglyceride synthesis known to occur in obesity. Other factors (i.e. availability of substrate and cofactors) may be of greater importance.
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PMID:Triglyceride metabolism in human liver: studies on hepatic phosphatidic-acid phosphatase in obese and non-obese subjects. 608 51

The properties of a cell surface nucleoside 5'-triphosphatase have been studied in small, intact, frog skeletal muscles, as a means of distinguishing the enzyme from other adenosine 5'-triphosphatases and of understanding its behaviour in the muscle membrane. The ectoenzyme in situ was shown to be a Ca2+- or Mg2+-activated ATPase liberating 7.5 +/- 0.4 (mean +/- SEM, n = 30) mumol of inorganic phosphate/g of muscle per 20 min, when the muscle was exposed to 2 mM ATP and 2 mM Ca2+ in Ringer's solution. The apparent Km for Mg2+ was 0.74 mM and for Ca2+ was 0.23 mM. A residual ATPase activity (20%) was found in the complete absence of divalent cations suggesting the existence of two ATPase types. A broad specificity toward nucleoside 5'-triphosphates was exhibited by the ecto-ATPase, but there was no nonspecific phosphatase activity. The enzyme was inhibited by La3+ and Cd2+, but was insensitive to ouabain, 2,4-dinitrophenol, oligomycin, and ruthenium red. Thus the ectoenzyme was not a Na+, K+-transport ATPase, was not an ATPase of mitochondrial origin, or a Ca2+-transport enzyme. Insulin had no effect. Inhibition by mersalyl, carbodiimide, and polar and cross-linking nonpolar nitrobenzene derivatives suggested that, for maximum activity, this membrane-bound enzyme required free sulfhydryl groups, certain free carboxyls, and an appreciable degree of hydrophobicity in its microenvironment.
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PMID:Characteristics of skeletal muscle ecto-ATPase in situ. 615 Jul 52

Recent investigations have indicated that cellular rheogenic properties may interfere with the correct estimation of Na+ and amino transport stoichiometry. We have reevaluated the stoichiometry of Na+ and alpha-aminoisobutyric acid (alpha-AIB) cotransport in Ehrlich ascites tumor cells depleted of Na+ and ATP by incubation in Na+-free HEPES-buffered medium (pH 7.2) containing 160 mM K+ and 2.5 microM valinomycin. Transfer of the cells to a medium with 10 mM 22Na+, 10 mM 3H-AIB, and 150 mM K+ resulted in an enhancement of Na+ flux above basal levels, which represents 0.6 of the AIB uptake. Under these conditions the membrane potential, -7.0 +/- 0.1 mV (SEM), does not change with the addition of AIB, -7.3 +/- 0.6 mV (SEM). HgCl2 (10 microM) added to the medium inhibited AIB flux and AIB-stimulated Na+ flux by 45-50% but did not change the coupling ratio. HgCl2 (10 microM) does not inhibit the basal Na+ flux nor does it affect cellular Na+ or K+ content. In physiological medium cotransport is electrogenic. The membrane potential of Ehrlich cells in physiological medium is -22.3 +/- 0.8 mV (SEM) and depolarizes to -16.7 +/- 0.7 mV (SEM) upon addition of AIB. Under these conditions the coupling ratio was highly variable but the ratio of codepression is 0.90 +/- 0.02 (SEM) in the presence of HgCl2 (10 microM). These results are consistent with a model (Smith and Robinson, 1981) in which the stoichiometry is one cosubstrate molecule per molecule of alpha-AIB. We suggest that H+ provides the alternative cosubstrate in this low Na+ environment and that in high Na+ medium the Na+:AIB stoichiometry approaches 1:1.
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PMID:The use of HgCl2 to evaluate the cosubstrate: amino acid transport stoichiometry in Ehrlich ascites tumor cells. 622 Oct 25


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