Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The experimental rats were randomly divided into three groups: i.e. control group; endotoxic shock group (the model of endotoxic shock was induced by intravenous administration of E. Coli endotoxin, 16 mg/kg); and electroacupuncture (EA) group ("Renzhong" or "Zusanli" acupoint was stimulated for 15 minutes at 1 hr after injection of endotoxin). The experimental rats were decapitated at 75 minutes after injecting endotoxin. Their livers were taken out for cryostat section, and histochemical observation. The results were as follows: 1) The glycogen in the hepatic cells of endotoxic shocked rats were almost completely depleted. The activities of SDH Mg(++)-ATPase and G-6-Pase and 5'-Nase were decreased; especially the activities of 5'-Nase in the biliary canaliculi and sinusoids were apparently reduced. 2) The content of hepatic glycogen in EA group was increased, but some of them was still depleted. The activities of SDH, Mg(++)-ATPase and G-6-Pase were slightly increased as compared with that of the endotoxic shock group. The activity of 5'-Nase was obviously increased after EA. The preliminary results indicated that EA at "Renzhong" or "Zusanli" acupoint of rats with endotoxic shock might play certain role on improving the hepatic metabolism and promoting the membrane transport action.
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PMID:[Histochemical observation of the effect of electroacupuncture on the livers of rats with endotoxic shock]. 875 27

We examined pharmacologically the influence of nitric oxide (NO), guanosine 3':5'-cyclic monophosphate (cyclic GMP), adenine 3':5'-cyclic monophosphate (cyclic AMP), and protein kinase C-linked signaling pathways on relaxation to potassium in aortic segments isolated from rats treated for 6 h with bacterial endotoxin (lipopolysaccharide). Endotoxemia for 6 h was associated with a severe hypotension and vascular hyporeactivity to norepinephrine (NE), and an increase in plasma NO in vivo and aortic NO ex vivo. The NE-induced contraction was attenuated and the potassium-induced relaxation was accentuated in the aorta of rats with endotoxic shock. Ouabain inhibited the potassium-induced relaxation in aortae from normal and endotoxemic rats. 8-Bromo-cyclic GMP significantly enhanced the potassium-induced relaxation in control aortae, whereas 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) abolished this difference between normal and endotoxemic rats. In contrast, inhibition of potassium-induced relaxation was observed in aortae from normal and endotoxemic rats treated with 8-bromo-cyclic AMP or phorbol 12-myristate 13-acetate. Individually, inhibitors of protein kinase A or protein kinase C did not significantly alter relaxation to potassium; however, in combination, these inhibitors significantly potentiated relaxation in aortae from control rats. These results suggest that activity of Na(+)-K(+)-ATPase is enhanced in the vascular bed of animals with endotoxic shock and that this elevation in activity is mediated by NO-cyclic GMP, but not by cyclic AMP-protein kinase A or protein kinase C.
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PMID:Nitric oxide-cyclic GMP contributes to abnormal activation of Na+-K+-ATPase in the aorta from rats with endotoxic shock. 1566 35

During septic shock, muscle produces lactate by way of an exaggerated NaK-adenosine triphosphatase (ATPase)-stimulated aerobic glycolysis associated with epinephrine stimulation possibly through beta2 adrenoreceptor involvement. It therefore seems logical that a proportion of hyperlactatemia in low cardiac output states would be also related to this mechanism. Thus, in low-flow and normal-to-high-flow models of shock, we investigate (1) whether muscle produces lactate and (2) whether muscle lactate production is linked to beta2 adrenergic stimulation and Na+K+-ATPase. We locally modulated the adrenergic pathway and Na+K+-ATPase activity in male Wistar rats' skeletal muscle using microdialysis with nonselective and selective beta blockers and ouabain in different models of rodent shock (endotoxin, peritonitis, and hemorrhage). Blood flow at the probe site was evaluated by ethanol clearance. We measured the difference between muscle lactate and blood lactate concentration, with a positive gradient indicating muscle lactate or pyruvate production. Epinephrine levels were elevated in all shock groups. All models were associated with hypotension and marked hyperlactatemia. Muscle lactate concentrations were consistently higher than arterial levels, with a mean gradient of 2.5+/-0.3 in endotoxic shock, 2.1+/-0.2 mM in peritonitis group, and 0.9+/-0.2 mM in hemorrhagic shock (P<0.05 for all groups). Muscle pyruvate concentrations were also always higher than arterial levels, with a mean gradient of 260+/-40 microM in endotoxic shock, 210+/-30 microM in peritonitis group, and 90+/-10 microM in hemorrhagic shock (P<0.05 for all groups). Despite a decrease in blood flow, lactate formation was decreased by all the pharmacological agents studied irrespective of shock mechanism. This demonstrates that lactate production during shock states is related, at least in part, to increased NaK-ATPase activity under beta2 stimulation. In shock state associated with a reduced or maintained blood flow, an important proportion of muscle lactate release is regulated by a beta2 receptor stimulation and not secondary to a reduced oxygen availability.
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PMID:Increased aerobic glycolysis through beta2 stimulation is a common mechanism involved in lactate formation during shock states. 1832 49