Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although basal release of cyclic AMP from isolated perfused rat hearts was not measurable, isoprenaline induced substantial release of the nucleotide, suggesting that in vivo the myocardium can contribute to plasma cyclic AMP. Anoxia also increased the amount of cyclic AMP released, but insulin and nicotinate alone or in combination had no effect.
 ...
PMID:The release of adenosine 3':5'-cyclic monophosphate from the isolated perfused rat heart. 17 4

1. The effects of monosaccharides, glycolytic intermediates, metabolic inhibitors and anxia, have been studied on the membrane electrical activity of mouse pancreatic islet cells in vitro using a single intracellular micro-electrode for both voltage recording and current injection. 2. In addition to D-glucose (28mM), D-mannose (16-6mM), and L-leucin (10mM), the substances D-glyceraldehyde (11mM), and acetoacetate (20 mM), induced action potentials in islet cells but other glucos analogues and metabolic intermediates including L-glucose dod not. 3. Mannoheptulose 20 mM), but not D-galactose or 2-deoxy-D-glucose, antagonized the electrical activity induced in islet cells by D-glucose, 28mM. Prior treatment of the cells with mannoheptulose caused them to hyperpolarize and completely prevented the appearance of electrical activity on subsequent exposure to D-glucose. 4. Electrical activity induced by D0glucose 28mM, was progressively inhibited by phloridzin, 10mM, if the cells were exposed to D-glucose and inhibitor simultaneously, and abolished on pretreatment with inhibitor for 30-60 min. Phloridzin also caused depolarization of the islet cells which was independent of extracellular glucose. 5. Anoxia completely blocked the electrical activity induced by glucose but not that evoked by D-glyceraldehyde, L-leucine, tolbutamide or glibenclamide. 6. Iodoacetic acid, 5 mM, rapidly blocked glucose-induced electrical activity whilst that elicited by tolbutamide was relatively resistant to inhibition. 7. The nature and possible location of the glucoreceptor in pancreatic islet cells is discussed in relation to the origin and functional significance of glucose-induced electrical activity and insulin secretion.
 ...
PMID:Pancreatic islet cells: effects of monosaccharides, glycolytic intermediates and metabolic inhibitors on membrane potential and electrical activity. 109 22

Experiments were carried out on dogs using bielectrode probes having as adequate impedancemeter. The probe is introduced via a cranial opening into the grey matter. This gives the following: a low frequency reading which is related to the extra cellular fluid component; a high frequency reading which is related to the total overall liquids; and a proportionality ratio of these liquids in the explored volume. The impedance variations are functions of the nature and intessity of vascular disturbance. Variation of the low frequency impedance (5 kHz) is the most significant. The experimental prodedure consists of: 1) Abrupt and permanent circulatory arrest; 2) Circulatory reduction by haemorrhage followed by recovery (if necessary by means of blood transfusion); 3) Anoxia by CO inhalation, recovery affected by means of O2 inhalation; and 4) Hypoglycemic coma induced by intravenous injection of insulin. The changes in the biochemical state of the cerebral tissue give very large variations of the low frequency impedance. It is these variations which are to constitute the object of this communication.
 ...
PMID:Investigation of electrical impedance variations of dog brain tissue during experimental metabolic disturbances. 111 14

The effects of substrates on the metabolic inhibitor-induced changes in the action potential and contraction of papillary muscles obtained from patients undergoing corrective open-heart surgery were studied. Anoxia produced a marked shortening of the action potential duration and a decrease in the resting potential, rate of rise of action potential, effective refractory period, and contractility. In anoxic muscle, although glucose completely restored the action potential duration, effective refractory period, and resting potential to control levels, it was unable to completely restore the contractility to the control level. Substrate depletion and metabolic inhibitors (iodoacetate, dinitrophenol) produced effects similar to that of anoxia, but at a faster rate. Glucose restored the action potential and, to a lesser extent, contractility to the control level in dinitrophenol-treated muscle but was ineffective in so doing the iodoacetate-treated muscle. Pyruvate, however, was effective in restoring the action potential and contracility in iodoacetate-treated muscle. Pretreatment of the muscle with glucose and, particularly, with glucose plus insulin prevented the combined effects of anoxia and lack of glucose on the action potential and contractility for a prolonged period. These results suggest that intravenous infusion of glucose and insulin before and during surgery might prevent or reduced the effect of anoxia on the electrical and mechanical activity of the heart during open-heart surgery.
 ...
PMID:Cardiac metabolism and electromechanics of human heart. 120 70

Myocardial metabolism in live guinea pigs was investigated by 13C and 31P nuclear magnetic resonance (NMR) at 20.18 and 32.5 MHz, respectively. 13C NMR studies allowed monitoring of myocardial glycogen synthesis during intravenous infusion of D-[1-13C]glucose and insulin. Anoxia resulted in degradation of the labeled glycogen within 6 min and appearance of 13C label in lactic acid. Infusion of sodium [2-13C]acetate resulted in incorporation of label into the C-4, C-2, and C-3 positions of glutamate, reflecting "scrambling" of the label expected from tricarboxylic-acid-cycle activity. 31P NMR spectra of heart in live guinea pigs were obtained continuously in 20.5-sec time blocks during 3 min of anoxia, during subsequent reoxygenation, and, in separate animals, during terminal anoxia. Reversible anoxia resulted in rapid degradation of phosphocreatine (t1/2 = 54.5 +/- 2.5 sec), which recovered fully during reoxygenation. Heart inorganic phosphate increased during anoxia and returned to basal levels after oxygen was restored. During 3 min of anoxia, no significant changes in ATP levels or pH were detected.
 ...
PMID:Carbon-13 and phosphorus-31 nuclear magnetic resonance studies of myocardial metabolism in live guinea pigs. 285 45

1. Regulation of glucose uptake was compared between extensor digitorum longus (EDL) and soleus (Sol) muscles in rats. 2. Insulin stimulated glucose uptake more in EDL than in Sol. 3. Under high concentrations of insulin, the glucose uptake was higher in EDL than Sol. 4. Inhibition of oxidative phosphorylation by anoxia or an uncoupler stimulated glucose uptake more in EDL than in Sol. 5. Anoxia abolished the effect of insulin on glucose uptake in both EDL and Sol. 6. The blocker to glucose transport system reduced glucose uptake more in Sol than in EDL.
 ...
PMID:Regulation of glucose uptake in rat slow and fast skeletal muscles. 290 47

Glucose-insulin-potassium (GIK) given during myocardial ischemia or anoxemia results in improved myocardial function and augments energy reserves of myocardial glycogen (MG). Because many patients with heart disease also have myocardial hypertrophy, our purpose was to examine whether similar elevations in MG can occur in hypertrophic hearts with GIK administration and to study the effect of hypovolemic shock on those MG levels. Mongrel dogs (n = 5) with myocardial hypertrophy underwent serial myocardial biopsies of the left (LV) and right (RV) ventricles, and blood samples were followed by GIK infusion (14.5 ml/kg/hr) for 2 hr. after which the dogs were subjected to 2 hr of hypovolemic shock (mean arterial pressure = 40 mmHg). It was found that after GIK infusion MG was consistently elevated in both RV (.43 +/- .02 to .60 +/- .04 g%) and LV (.63 +/- .07 to .71 +/- .01 g%) and FFA declined (.20 +/- .05 to .05-.01 mEq/liter). The MG responded to hypovolemia by further significant elevations (RV 1.16 +/- .33; LV .82 +/- .17), as did FFA (.38 +/- .21). These results indicate that hypertrophic hearts can indeed respond to GIK infusion by increasing MG in both the RV and LV, as do normal hearts. These hearts then submitted to hypovolemic shock showed a further elevation of MG. The elevated insulin levels post-GIK resulted in suppression of FFA. Thus GIK administration may have a sparing effect on energy stores of the heart during hypovolemic shock, which could have clinical implications in the treatment of patients with hypertrophic myocardia.
 ...
PMID:Response of hypertrophic heart myocardial glycogen to GIK and hypovolemic shock. 294 28

We have examined the possibility that 125I-insulin binding by isolated rat hepatocytes is modulated by cellular ATP levels. To avoid complications due to ATP-dependent internalization of bound insulin, 125I-insulin binding was determined at 10 degrees C; at this temperature, equilibrium binding was achieved after incubation for 4-6 h. When hepatocytes were incubated at 37 degrees C under anaerobic conditions, ATP levels and 125I-insulin binding were both lowered by about 65%. Anoxia inhibited the association of 125I-insulin with the hepatocyte receptor; the dissociation of insulin from hepatocytes was not affected. Cellular ATP levels and 125I-insulin binding were both restored when anaerobic cells were incubated further at 37 degrees C under aerobic conditions. When anaerobic cells were incubated in air at 10 degrees C during the insulin binding assay, 125I-insulin binding recovered completely, but ATP levels were unaffected. The inhibitory effect of anoxia on 125I-insulin binding was not due to any effect on 125I-insulin degradation or on cell viability. We conclude (1) that the ability of hepatocytes to bind insulin can be modulated on a short-term basis in response to the metabolic status of the cell, and (2) that modulation of the liver cell insulin receptor is not a function of cellular ATP levels.
 ...
PMID:Inhibitory effect of anoxia on 125I-insulin binding by rat hepatocytes. 352 46

The effect of various inhibitors on insulin release from pieces of rabbit pancreas incubated in vitro was studied. Insulin release was stimulated by glucose (3mg./ml.), leucine (5mm), tolbutamide (200mug./ml.), ouabain (10mum), a raised extracellular K(+) concentration (60mm) and substitution of the Ca(2+) content of the incubation medium by Ba(2+) (2.5mm). (a) Mannoheptulose (6mg./ml.) inhibited glucose-stimulated insulin release only. (b) Anoxia abolished or inhibited insulin release stimulated by glucose, leucine, tolbutamide and K(+), but had little or no effect on release stimulated by ouabain or Ba(2+). (c) 2,4-Dinitrophenol (0.25mm) abolished or inhibited insulin release stimulated by glucose, ouabain or Ba(2+). (d) Diazoxide (250mug./ml.) abolished or inhibited insulin release stimulated by glucose, leucine, tolbutamide, ouabain or Ba(2+) (0.25 or 1mm). Diazoxide had no effect on insulin release stimulated by Ba(2+) (2.5mm) and potentiated release stimulated by K(+). (e) Adrenaline (1mum) abolished insulin release stimulated by glucose, leucine, tolbutamide, ouabain or Ba(2+). K(+)-stimulated release was inhibited by adrenaline. (f) Tetrodotoxin (1mum) had no effect on insulin release stimulated by glucose, leucine, tolbutamide, ouabain, K(+) or Ba(2+). (g) Nupercaine (1mm) abolished insulin release stimulated by glucose or Ba(2+).
 ...
PMID:The interaction of various inhibitors and stimuli of insulin release studied with rabbit pancreas in vitro. 580 8

Guinea pig heart metabolism was studied in vivo by 13C NMR at 20.18 MHz. High-quality proton-decoupled 13C NMR spectra with excellent signal-to-noise ratios and resolution could be obtained in 6 min. Natural-abundance spectra showed resonances that could be assigned to fatty acids, but glycogen was not seen. During intravenous infusion of D-[1-13C]glucose and insulin, the time course of myocardial glycogen synthesis was followed serially for up to 4 hr. Anoxia resulted in degradation of the labeled glycogen within 6 min and appearance of 13C label in lactic acid. Infusion of sodium [2-13C]acetate resulted in incorporation of label into the C-4, C-2, and C-3 positions of glutamate and glutamine, reflecting "scrambling" of the label expected from tricarboxylic acid cycle activity. Examination of the 31P NMR spectrum of the guinea pig heart in vivo demonstrated no change in the high-energy phosphates during the time periods of the 13C NMR experiments. Our studies indicate that 13C NMR is a unique non-destructive tool for the study of heart metabolism in vivo.
 ...
PMID:In vivo carbon-13 nuclear magnetic resonance studies of heart metabolism. 657 24


1 2 Next >>