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hypotension/phosphatase
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Alterations in hepatic 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase and glucose-6-phosphatase gene expression after hemorrhagic hypotension and resuscitation.
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The mRNA abundance of several hepatic glycolytic and gluconeogenic enzymes and blood hormone concentrations were determined in hemorrhagic hypotension-induced rats before and after resuscitation with lactated Ringer's. Northern blot analysis of total liver RNA after 30 min of hemorrhage showed
Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension.
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The thiazide-sensitive NaCl cotransporter (NCC) of the renal distal convoluted tubule (DCT) controls ion homeostasis and arterial BP. Loss-of-function mutations of NCC cause renal salt wasting with arterial hypotension (Gitelman syndrome). Conversely, mutations in the NCC-regulating WNK kinases or
Deficiency of mitogen-activated protein kinase phosphatase-1 results in iNOS-mediated hypotension in response to low-dose endotoxin.
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Mitogen-activated protein kinase phosphatase-1 (MKP-1) is essential in limiting the proinflammatory response to lipopolysaccharide (LPS). We hypothesized that Mkp-1(-/-) mice would respond to low-dose LPS with a fall in blood pressure due to augmented expression of inducible nitric oxide (NO)
[Activity of acid and alkaline phosphatases, of certain transaminases and of lactate dehydrogenase in the plasma of dogs with prolonged hypovolemic hypotension and during the recovery period].
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MAP kinase phosphatase 1 controls innate immune responses and suppresses endotoxic shock.
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Septic shock is a leading cause of morbidity and mortality. However, genetic factors predisposing to septic shock are not fully understood. Excessive production of proinflammatory cytokines, particularly tumor necrosis factor (TNF)-alpha, and the resultant severe hypotension play a central role in
Inducible nitric-oxide synthase expression is regulated by mitogen-activated protein kinase phosphatase-1.
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Inducible nitric-oxide (NO) synthase (iNOS) plays a critical role in the eradication of intracellular pathogens. However, the excessive production of NO by iNOS has also been implicated in the pathogenesis of septic shock syndrome. Previously, we have demonstrated that mice deficient in
Effects of dexamethasone and surgical hypotension on hepatic morphologic features and enzymes of dogs.
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Effects of corticosteroids and surgical stress on hepatic morphologic features and enzymes were studied in 18 mature dogs of mixed breeding: group 1, control (n = 3); group 2, dexamethasone (n = 5); group 3, dexamethasone and surgery (n = 5); and group 4, surgery (n = 5). Dexamethasone (2.2 mg/kg of
MAP kinase phosphatase-1, a critical negative regulator of the innate immune response.
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Mitogen-activated protein (MAP) kinase cascades are crucial signal transduction pathways in the regulation of the host inflammatory response to infection. MAP kinase phosphatase (MKP)-1, an archetypal member of the MKP family, plays a pivotal role in the deactivation of p38 and JNK. In vitro studies
[Change in phosphatase and acid cathepsin activity in the dog cerebral cortex in terminal states].
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Acid phosphatase, alkaline phosphatase and acid cathepsin activity increased in the subcellular fraction of the grey matter of dog brain in proportion to the duration of compression ischemia, particularly in the postmitochondrial supernatant. An increase in the alkaline phosphatase and of the acid
Effects of hemorrhagic hypotension on cerebral blood flow and perfused capillaries in newborn pigs.
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We examined the effect of hemorrhagic hypotension on cerebral blood flow and perfused capillaries in newborn pigs, 2-10 days old. Cerebral blood flow was measured by using radioactive microspheres, perfused capillaries were determined by infusing a plasma marker, fluorescein isothiocyanate (FITC) -
Losartan-induced hypotension leads to tau hyperphosphorylation and memory deficit.
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Recent studies have reported a correlation between dementia and low blood pressure. How hypotension is associated with the increased risk of Alzheimer's disease (AD) remains unclear. Here we show that one month treatment of losartan, an angiotensin II type 1 (AT1) receptor antagonist, causes chronic
Changes in plasma levels of lysosomal and non lysosomal enzymes during hemorrhagic hypotension.
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In a study of 4-hr hemorrhagic hypotension in dogs, the plasma levels of the lysosomal enzymes, cathepsin (CATH) and acid phosphatase (AP) showed early and progressive increases in activity. The plasma levels of the intestinal fraction of alkaline phosphatase (IAkP) and aspartate aminotransferase
Liver function following hypovolemic hypotension in rats anaesthetized with halothane or enflurane.
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Rats which had approximately 25-30% of their calculated blood volume removed were exposed to halothane (1%) or enflurane (2%) in 33% oxygen for 30 min. Hepatic function was evaluated by determining, at various time intervals, serum activities of glutamic-oxalacetic and glutamic-pyruvic transaminase,
Profound arterial hypotension in dogs: brain electrical activity and organ integrity.
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To determine whether non-invasive measurement of brain electrical activity can predict ischemic brain damage, we recorded the electroencephalogram (EEG) and somatosensory- (SEP) and auditory- (AEP) evoked potentials before, during, and after trimethaphan-induced profound arterial hypotension in
Effect of tepoxalin on renal function and hepatic enzymes in dogs exposed to hypotension with isoflurane.
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OBJECTIVE
To evaluate the possible renal and hepatic toxicity of tepoxalin in dogs exposed to hypotension during isoflurane anesthesia.
METHODS
Prospective, randomized experimental study.
METHODS
Twenty adult mixed-breed dogs, weighing 18.8 ± 2.8 kg.
METHODS
The animals received 10 mg kg(-1)
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