Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

GM1 ganglioside injections (i.p.) reduce amphetamine-induced asymmetric rotation in rats 48 h after a partial unilateral transection of the nigrostriatal pathway. We found that this reduction was maximal when rats received their first GM1 injection within 2 h after surgery. Rats injected 4-12 h after surgery, or rats only pretreated with GM1, showed no significant effect on rotation. Striatal membrane Na+,K+-ATPase in rats injected with GM1 0-2 h after hemitransection showed only a 10% loss in activity (versus the untransected hemisphere) as compared to control losses of 38%. The maintenance of membrane Na+,K+-ATPase activity in GM1-treated rats may be one mechanism by which a balance between hemispheres in striatal dopaminergic transmission is preserved, resulting in reduced asymmetric rotation. The observation that there is a critical postsurgical period when GM1 administration results in optimal functional recovery supports our hypothesis that gangliosides are exerting an acute effect on damaged CNS tissue. This acute effect is further evidenced by the reduced loss of membrane Na+,K+-ATPase following injury.
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PMID:Acute effects of GM1 ganglioside: reduction in both behavioral asymmetry and loss of Na+, K+-ATPase after nigrostriatal transection. 301 50

As evidenced by their ability to reduce cerebral edema, exogenous ganglioside administration exerts acute effects on CNS injury processes. We report here that ganglioside (GM1 or AGF2) treatment results in a 52% decrease in mortality 48 hours after the induction of ischemia in gerbils by permanent unilateral ligation of the common carotid artery. By comparing the occluded vs. nonoccluded sides of the brain (cortex and hippocampus) we found a significant loss of membrane Na, K-ATPase activity due to ischemia in control animals, but no such differences were found between the hemispheres of ganglioside-treated gerbils. We hypothesize that gangliosides may be "protecting" membrane function as indicated by these ATPase analyses, reducing local CNS damage at the time of injury (i.e., reduced cell loss, fiber degeneration, membrane failure). By acutely limiting the extent of CNS tissue damage, conditions may be optimized for any subsequent CNS regrowth and functional recovery.
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PMID:Gangliosides (GM1 and AGF2) reduce mortality due to ischemia: protection of membrane function. 302 26

Total ischaemia of loops of dog colon was induced by clamping all afferent arteries and the colonic wall for different periods of time.Net sodium transport across the mucosa is abolished after one hour's ischaemia, but Na(+)-K(+)-ATPase levels in microsomal suspensions from the mucosa only fall significantly after two hours' ischaemia. Studies on the functional and morphological recovery of colons subjected to three hours' ischaemia have disclosed an extremely heterogeneous response among the 24 dogs used. Although all parameters were non-existent 24 hours after the intervention, one colon revealed a morphological and functional recovery one week after the operation, whilst two, three, and three out of six recovered after two, three, and four weeks respectively. There was a good correlation between the functional and macroscopic appearance of these recovered loops, though histologically various degrees of disorganization of the mucosa were observed. Among the loops that had no function, there was also a considerable variation in their microscopic structures. The level of Na(+)-K(+)-ATPase in the mucosa was found to be a faithful indicator of the functional state of the tissue, and could be closely correlated with the morphological findings.
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PMID:Functional and morphological response of the dog colon to ischaemia. 426 58

Short loops of dog small intestine, filled with a buffered glucose solution, were subjected to one hour's total ischaemia by clamping the corresponding mesenteric artery and vein as well as the intestinal wall at each end of the loop. Immediately after the ischaemic period and 24 hours later, their functional capacity, together with that of neighbouring control loops, was determined by studying the absorption of phenylalanine and beta-methyl-glucoside in vitro and by measuring the levels of Na(+)-K(+)-ATPase in the mucosa. The release of lysosomal enzymes after the ischaemia was studied by gauging the levels of acid phosphatase in the venous blood draining the ischaemic loop. The state of the mucosal microcirculation was investigated by injection of indian ink into the mesenteric artery removal of the loop. Immediately after ischaemia, considerable structural damage was observed in the intestinal mucosa, with desquamation of the villous tips, oedema, vascular stasis, and haemorrhagic infiltration in the lamina propria. No dye was observed in the mucosal capillaries. All transport capacity was abolished, but ATPase levels were unchanged. A significant release of lysosomal enzymes into the venous blood was noted. One day later structural and functional recovery was complete, and vascularization of the villous core was restored.
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PMID:The recovery of function and microcirculation in small intestinal loops following ischaemia. 426 59

Impaired cardiac sarcoplasmic reticulum (SR) function, as evidenced by reduced SR Ca2+ uptake rate and decreased SR Ca(2+)-adenosine triphosphatase activity, has been found in postischemic "stunned" myocardium and in hearts subjected to hypothermic arrest. In this study, we compared the effects of retrograde continuous coronary sinus warm blood cardioplegia (WBC) and retrograde intermittent cold blood cardioplegia (CBC) on cardiac SR function and postischemic ventricular functional recovery in pig hearts. Twelve in situ isolated pig hearts supported by cardiopulmonary bypass were subjected to 120 minutes of cardioplegic arrest with either WBC (37 degrees C) or CBC (6 degrees to 10 degrees C), followed by 60 minutes of 37 degrees C reperfusion. Left ventricular global contractile function and coronary blood flow were measured before arrest and during reperfusion. Cardiac SR was isolated from left ventricular biopsy specimens, and 45Ca2+ uptake by SR and SR Ca(2+)-adenosine triphosphatase activity were determined. The recovery of left ventricular global contractile function as indicated by the maximum of the first derivative of left ventricular pressure was significantly improved in the WBC group compared with that of the CBC group (70% versus 46%; p < 0.05). The SR Ca(2+)-adenosine triphosphatase activity was better preserved after 60 minutes reperfusion in WBC compared with CBC (0.31 +/- 0.02 versus 0.20 +/- 0.03 microM Pi/min/mg protein, p < 0.05), and the recovery of SR Ca2+ uptake was significantly improved by WBC compared with CBC (1.15 +/- 0.12 versus 0.83 +/- 0.04 microM Ca2+/min/mg protein; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postischemic deterioration of sarcoplasmic reticulum: warm versus cold blood cardioplegia. 823 90

An increase in intracellular Na+ during ischaemia has been associated with myocardial injury. In this study, we determined whether inhibition of Na+/K+ ATPase activity contributes to this increase and whether Na+/K+ ATPase activity can be maintained by provision of glucose to perfused rat hearts during low flow, 0.5 ml/min, ischemia. We used 31P NMR spectroscopy to determine changes in myocardial energetics and intracellular and extracellular volumes. 23Na NMR spectroscopy, with DyTTHA3- present as a shift reagent, was used to measure changes in intracellular Na+ and 87Rb NMR spectroscopy was used to estimate Na+/K+ ATPase activity from Rb+ influx rates, Rb+ being an NMR-sensitive congener of K+. In hearts provided with 11 mM glucose throughout ischemia, glycolysis continued and ATP was twofold higher than in hearts without glucose. In the glucose-hearts, Rb+ influx rate was threefold higher, intracellular Na+ was fivefold lower at the end of ischemia and functional recovery during reperfusion was twofold higher. We propose that continuation of glycolysis throughout low flow ischemia allowed maintenance of sufficient Na+/K+ ATPase activity to prevent the increase in intracellular Na+ that would otherwise have led to myocardial injury.
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PMID:The role of Na+/K+ ATPase activity during low flow ischemia in preventing myocardial injury: a 31P, 23Na and 87Rb NMR spectroscopic study. 854 87

Ischemia and ischemic stress hormones induce endogenous cardiac protection against ischemia-reperfusion (I/R) injury. Although ischemia and ischemic stress hormones are accompanied by increased [Ca2+], it is unknown whether either opening of the sarcoplasmic reticular ryanodine Ca2+ channel (SR RyR) or inhibition of Ca2+ uptake by the sarcoendoplasmic reticular Ca(2+)-ATPase (SERCA) prior to I/R can similarly induce post-I/R functional protection. To study this, isolated, crystalloid perfused Sprague-Dawley rat hearts were used to assess the effects of inducing a pre-ischemic [Ca2+]i load by either priming the SR RyR with ryanodine (Ry, 5 nM/2 min) or by transient blockade of the SERCA 10 min prior to global I/R (20 min). A pre-ischemic Ca2+ load by either SR RyR activation or SERCA blockade improved post-ischemic myocardial functional recovery (developed pressure, end diastolic pressure, coronary flow, heart rate, and left ventricular creatine kinase activity). We conclude that 1) Ca(2+)-induced myocardial functional protection involves the SR Ca2+ source, 2) a pre-ischemic Ca2+ load induced with either Ry or thapsigargin constructively primes against myocardial I/R injury, and 3) Ca(2+)-induced cardioadaptation to I/R injury may have important therapeutic implications prior to planned ischemic events such as cardiac allograft preservation and cardiac bypass surgery.
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PMID:Constructive priming of myocardium against ischemia-reperfusion injury. 890 38

The motor nerve transplantation (MNT) technique is used to transfer an intact nerve into a denervated muscle by harvesting a neurovascular pedicle of muscle containing motor endplates from the motor endplate zone of a donor muscle and implanting it into a denervated muscle. Thirty-six adult New Zealand White rabbits underwent reinnervation of the left long peroneal (LP) muscle (fast twitch) with a motor nerve graft from the soleus muscle (slow twitch). The right LP muscle served as a control. Reinnervation was assessed using microstimulatory single-fiber electromyography (SFEMG), alterations in muscle fiber typing and grouping, and isometric response curves. Neurofilament antibody was used for axon staining. The neurofilament studies provided direct evidence of nerve growth from the motor nerve graft into the adjacent denervated muscle. Median motor endplate jitter was 13 microsec preoperatively, and 26 microsec at 2 months, 29.5 microsec at 4 months, and 14 microsec at 6 months postoperatively (p < 0.001). Isometric tetanic tension studies showed a progressive functional recovery in the reinnervated muscle over 6 months. There was no histological evidence of aberrant reinnervation from any source outside the nerve pedicle. Isometric twitch responses and adenosine triphosphatase studies confirmed the conversion of the reinnervated LP muscle to a slow-type muscle. Acetylcholinesterase studies confirmed the presence of functioning motor endplates beneath the insertion of the motor nerve graft. It is concluded that the MNT technique achieves motor reinnervation by growth of new nerve fibers across the pedicle graft into the recipient muscle.
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PMID:Motor nerve transplantation. 932 51

Decrease in alveolar oxygen tension may induce acute lung injury with pulmonary edema. We investigated whether, in alveolar epithelial cells, expression and activity of epithelial sodium (Na) channels and Na,K-adenosine triphosphatase, the major components of transepithelial Na transport, were regulated by hypoxia. Exposure of cultured rat alveolar cells to 3% and 0% O2 for 18 h reduced Na channel activity estimated by amiloride-sensitive 22Na influx by 32% and 67%, respectively, whereas 5% O2 was without effect. The decrease in Na channel activity induced by 0% O2 was time-dependent, significant at 3 h of exposure and maximal at 12 and 18 h. It was associated with a time-dependent decline in the amount of mRNAs encoding the alpha-, beta-, and gamma-subunits of the rat epithelial Na channel (rENaC) and with a 42% decrease in alpha-rENaC protein synthesis as evaluated by immunoprecipitation after 18 h of exposure. The 0% O2 hypoxia also caused a time-dependent decrease in (1) ouabain-sensitive 86Rubidium influx in intact cells, (2) the maximal velocity of Na,K-ATPase on crude homogenates, and (3) alpha1- and beta1-Na,K-ATPase mRNA levels. Levels of rENaC and alpha1-Na,K-ATPase mRNA returned to control values within 48 h of reoxygenation, and this was associated with complete functional recovery. We conclude that hypoxia induced a downregulation of expression and activity of epithelial Na channels and Na,K-ATPase in alveolar cells. Subsequent decrease in Na reabsorption by alveolar epithelium could participate in the maintenance of hypoxia-induced alveolar edema.
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PMID:Hypoxia downregulates expression and activity of epithelial sodium channels in rat alveolar epithelial cells. 937 26

Repetitive brief ischemic episodes (ischemic preconditioning, PC) result in transient intracellular acidosis and protect the heart from subsequent ischemic injury, potentially through a protein kinase C (PKC)-dependent mechanism. We hypothesized that repetitive brief acidification of the heart without concomitant ischemia would also protect the heart from ischemic injury via a PKC-dependent mechanism. Isolated rat hearts underwent 30 min of global ischemia following control perfusion (CTL), or after PC or repetitive acidosis (RA), in the presence of absence of chelerythrine, a specific PKC inhibitor. Intracellular pH, PCr and ATP were measured using 31P NMR spectroscopy, while intracellular sodium [Na]i was measured using 23Na spectroscopy. Na,K-ATPase activity was measured prior to ischemia and on reperfusion. Both PC and RA resulted in transient acidification prior to ischemia. Ischemic injury, as assessed by creatinine kinase (CK) release on reperfusion, was reduced in both the PC and RA hearts [63+/-14 and 16+/-4 IU/g dry weight (dw) respectively, v 705+/-72 IU/gdw for control P<0.001], and was associated with improved functional recovery on reperfusion. PC and RA each significantly reduced Na,K-ATPase activity prior to ischemia (8.18+/-0.47 and 7.76+/-0.54 micromol ADP/h/mg protein) when compared to control (11.05+/-0.54 micromol ADP/h/mg protein P<0.05), limited the rate of ATP depletion during ischemia, and resulted in more rapid normalization of [Na]i on reperfusion. Chelerythrine resulted in intermediate CK release in PC and RA hearts (443+/-48 and 375+/-72 IU/gdw, P<0.001 v PC, P<0.01 v control), but did not alter the rate of ATP depletion or [Na]i kinetics in either PC or RA hearts. PC and RA each protect the ischemic heart, having in common ATP preservation during ischemia and more rapid normalization of [Na]i on reperfusion. These effects, not modulated by protein kinase C, are consistent with the hypothesis that ATP preservation during ischemia provides enhanced substrate for sodium efflux via the Na,K-ATPase on reperfusion.
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PMID:Repetitive acidosis protects the ischemic heart: implications for mechanisms in preconditioned hearts. 1032 17


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