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)

The purpose of this experiment is to study the role of arginine vasopressin (AVP) in acute cerebral ischemic edema in Mongolian gerbils. The results show that intracerebroventricular injection (ICV) of AVP exacerbates acute ischemic brain edema, while ICV of AVP antiserum significantly decreases the ischemic brain edema. Nimodipine (calcium antagonist) cannot block this role of AVP in brain edema. In addition, the cortical Na(+)-K+ ATPase activity is significantly decreased, while the cAMP content of ischemic cortex and hypothalamus and the cGMP content of the hypothalamus are markedly increased after AVP ICV. These suggest that AVP may play an important role in the pathophysiologic process of ischemic brain edema by inhibiting the Na(+)-K+ ATPase activity of the cerebral cell membrane and the AVP receptors mediated by cAMP and cGMP.
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PMID:Mechanism of action of arginine vasopressin on acute ischemic brain edema. 165 29

Sodium-potassium adenosine triphosphatase (ATPase) enzyme was determined in the brain tissue of 11 patients with head injury and 6 control patients. Patients with head injury included in this study were selected from two categories: (a) patients in deep coma due to severe head injury [Glasgow Coma Scale (GCS) less than 8; 6 cases]; (b) patients with depressed skull fractures with dural tears who were conscious and able to give an adequate verbal response (GCS greater than 10; 5 cases). The level of the enzyme was significantly reduced in comatose patients with severe head injury as compared to the controls (P less than 0.001) or to conscious patients with depressed fractures (P less than 0.001). In the group of conscious patients with depressed fractures, the enzyme level was no different from that of the controls (P = 0.4215). All comatose patients with severely reduced enzyme levels subsequently died, whereas those with depressed fractures with normal enzyme levels survived. The relationship between a low enzyme level and brain edema in severe head injury is discussed.
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PMID:The prognostic value of the brain sodium-potassium ATPase enzyme concentration in head injury. 165 53

During partial ischemia, sodium and potassium ions exchange across the blood-brain barrier, resulting in a net increase in cations and brain edema. Since this exchange is likely mediated by specific transporters such as Na,K-ATPase in the capillary endothelium and because brain capillary Na,K-ATPase activity is stimulated by increased extracellular potassium in vitro, this study was designed to determine if the rate of blood to brain sodium transport is increased in ischemic tissue having an elevated interstitial fluid potassium concentration ([K]ISF) in vivo. Sprague-Dawley rats were studied between 2-3 h after occlusion of the right middle cerebral artery. To identify where cortical tissue with an elevated [K]ISF could be sampled for transport studies, the regional pattern of cerebral blood flow and [K]ISF was obtained in a group of 17 rats using hydrogen clearance and potassium-selective microelectrode techniques. We observed severely elevated [K]ISF (greater than 10 mM) when CBF was less than 20 ml 100 g-1 min-1 and mildly elevated levels at CBF between 20-45 ml 100 g-1 min-1. In a second group of seven rats, permeability-surface area products (PS products) for 22Na and [3H]alpha-aminoisobutyric acid ([3H]AIB) were determined in ischemic cortex with elevated [K]ISF and in nonischemic cortex. The PS products for AIB were similar in both tissues (2.2 +/- 0.7 and 2.1 +/- 0.4 microliters/g/min) while the PS products for sodium was significantly increased in the ischemic tissue (1.5 +/- 0.2 and 2.4 +/- 1.1 microliters/g/min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood to brain sodium transport and interstitial fluid potassium concentration during early focal ischemia in the rat. 184 10

Using in vitro techniques, we have shown that astrocytes do not increase the ouabain-sensitive Na(+)-K(+)-ATPase activity in cerebral endothelial cells. However, malignant astrocytoma cells when co-cultured with cerebral endothelial cells significantly enhance ouabain-sensitive Na(+)-K(+)-ATPase activity in cerebral endothelial cells. Also, Na(+)-K(+)-ATPase activity in cerebral endothelial cells co-cultured with malignant astrocytoma cells is inhibited by corticosteroids to the same degree as ouabain. These results suggest that brain edema associated with malignant glioma may in part be due to an increase in ouabain-sensitive Na(+)-K(+)-ATPase activity at the blood-brain barrier and that the antiedema effects of corticosteroids may be due to a reduction in the activity of this enzyme.
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PMID:Glioma cell influence on cerebral endothelial cell Na(+)-K(+)-ATPase. 216 68

Triethyltin (TET) salt intoxication provokes a myelinic vacuolisation associated with a white matter cerebral edema. The central nervous system disturbances accompanying these phenomena (Na-K-ATPase activity, neurological symptoms, water and sodium cerebral content) can be counteracted by drugs used in age-related brain failure; consequently, TET intoxication could be suggested as an experimental model for studying the aging process. The aim of the present study is to follow-up the biogenic amine concentrations in different brain areas of TET treated rats, knowing that modifications of cerebral amines exist throughout the aging process. The following results are obtained: the cerebral water content of the TET treated rats is significantly increased, confirming the existence of a brain edema. Monoamine concentrations are significantly decreased, specifically noradrenaline (in hypothalamus, mesencephalon, cerebellum); serotonin (in striatum, hypothalamus, mesencephalon); dopamine only in hypothalamus; these are accompanied by an increase of the metabolites 5 HIAA (in striatum and mesencephalon) and HVA (striatum). These modifications are compared to those occurring in physiological aging, and hypothetical mechanisms are reviewed. We conclude that TET intoxication must not be considered as a pathophysiological model of brain aging, but may be considered as a useful pharmacological tool for studying experimental drugs liable to counteract brain age-induced disturbances.
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PMID:Effect of triethyltin chloride on the central aminergic neurotransmitters and their metabolites: relationship with pathophysiology of aging. 241 71

Among a number of biochemical disturbances occurring in the acute phase of brain insults, the destruction of membrane phospholipids and its consequences on the function of membrane-bound proteins is likely to be one of the most important. In the cryogenic type of injury which is classically considered as a relevant animal model of brain contusive lesions in human traumatology, the initial attack of membranes could consist in a peroxidative damage triggered by blood ferrous compounds. This in turn would lead to an activation of phospholipase A2. As a consequence of phospholipid disruption a number of enzymes involved in energy production within the mitochondria are severely impaired. Nevertheless, the level of available ATP within the cell remains normal and even higher than normal. This paradoxical findings suggests that energy utilization is even more lowered than energy production. In fact, the Na+-K+-ATPase activity which normally utilizes approximately 70% of the total amount of cellular energy is severely reduced. We assume that Na+-K+-ATPase impairment is directly responsible for the retention of intracellular Na+ accompanied by osmotically driven water, though admittedly other biochemical disturbances, including tissue acidosis and liberation of excitatory amino-acids, would contribute to the same result. Lastly, a striking feature of these biochemical events is the early activation of those enzymes necessary for phospholipid resynthesis. This should mean that repair processes are at work immediately after the insult allowing resumption of Na+-K+-ATPase function, clearing up of brain edema and restoration of cation exchanges essential for brain work.
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PMID:Membrane damage in acute brain trauma. 254 38

Glucocorticoids have a well-known clinical effect on brain edema and intracranial hypertension, but the mechanism of action is still poorly understood. In the present report the effect of beta-methasone on choroid plexus transport and CSF formation was studied. Following 5 days of daily treatment with betamethasone the CSF production rate in rabbits was reduced by 43% as measured by ventriculo-cisternal perfusion with radioactive inulin. Accordingly, the transport capacity in the choroid plexus, measured in terms of choline uptake and accumulation in vitro, and the activity of Na+--K+-ATPase decreased in both rabbit (in the lateral ventricles by 31 and 31%, respectively) and rat (by 16 and 24%, respectively). Thus, the demonstrated influence of glucocorticoids on these functions of the choroid plexus seem to be important components in their therapeutic effect on intracranial hypertension.
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PMID:Corticosteroid action on choroid plexus: reduction in Na+-K+-ATPase activity, choline transport capacity, and rate of CSF formation. 255 68

Results of our consecutive study on the pathogenic mechanism underlying ischemic brain edema are summarized in this paper. Pertinent findings are as follows: (1) there is a close correlation between the influxes of water and sodium following ischemia; (2) the edema fluid can be regarded as the ultrafiltrate of serum; (3) there is a significant increase in the brain content of HETEs following ischemia; (4) the lipoxygenase activity of brain microvessels is increased following ischemia; (5) the lipoxygenase activity as well as the Na+, K+-ATPase activity of brain microvessels are enhanced by a hydroperoxide, 15-HPETE; (6) inhibition of Na+, K+-ATPase of brain microvessels by intraarterial infusion of ouabain resulted in a significant decrease in edema formation; and (7) not the cyclooxygenase, but the lipoxygenase pathway seems to be involved in the enhancement of microvessel Na+, K+-ATPase. Lipoxygenase(s) and Na+-K+-ATPase of brain microvessels, the activities of which are enhanced by an increased level of free radicals and/or hydroperoxides, may play a significant role in the occurrence of ischemic brain edema.
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PMID:The role of free radicals and eicosanoids in the pathogenetic mechanism underlying ischemic brain edema. 266 83

Following cryogenic lesions of the brain in the rabbit, ictal activity appears within min with a maximum at 2 h. Brain edema increases rapidly between 2-4 h with a maximum at 8 h. The glutamate concentration reaches 209% of control in the perilesional area at 2 h and the time course of glutamate/GABA ratio parallels the time course of epileptic activity. The impairment of Na+-K+-ATPase activity (rise of KMapp for K+) in the glial fraction coincides with the increase of edema. A positive correlation is found between the total amount of ictal activity and the total amount of edema in individual animals, suggesting that epilepsy may enhance edema formation.
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PMID:Relationship between epileptic activity and edema formation in the acute phase of cryogenic lesion. 284 Jun 11

The effects of 15-hydroperoxyarachidonic acid (15-HPAA) on Na+, K+- and Mg+-ATPase activities in the blood-brain barrier (BBB) were examined using rat brain microvessels (MV). 15-HPAA markedly stimulated these ATPase activities in MV at low concentrations whereas the synaptosomal Na+, K+-ATPase activity was inhibited in a dose-dependent manner. Further neurochemical analysis revealed that this stimulatory effect of 15-HPAA in MV was not due to a simple detergent-like action of the compound on the membranes but rather to stimulation of the phospholipase A2 and lipoxygenase activity within MV. In addition, it was shown that free radical reactions were involved in the mechanism. Since such anti-edema drugs as 1,2-bis(nicotinamido)propane were proved to be potent suppressors of the enhanced ATPase activity, further speculations on the role of this effect for ischemic brain edema are offered.
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PMID:Enhancement of ATPase activity by a lipid peroxide of arachidonic acid in rat brain microvessels. 299 34


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