citrulline/blutung

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Systemic L-citrulline prevents cerebral vasospasm in haptoglobin 2-2 transgenic mice after subarachnoid hemorrhage.

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BACKGROUND Nitric oxide (NO) depletion and periadventitial inflammation contribute to the pathogenesis of cerebral vasospasm. L-Citrulline increases L-arginine levels, thereby raising NO synthesis. Transgenic C57Bl6 mice with a haptoglobin (Hp) 2-2 genotype develop more severe vasospasm than

Dexamethasone significantly attenuates sub-arachnoid hemorrhage-induced elevation in cerebrospinal fluid citrulline and leukocytes.

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OBJECTIVE Cerebral vasospasm is a leading cause of death and disability following aneurysmal subarachnoid hemorrhage (SAH). Nitric oxide (NO) is a potent mediator of vasodilation, and citrulline is a known contributor to NO production. The leukocytosis inflammatory response can increase

L-arginine attenuates trauma-hemorrhage-induced liver injury.

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OBJECTIVE Liver injury is common after trauma-hemorrhage for which the underlying mechanism is not clear. Although administration of the essential amino acid L-arginine has been reported to restore the depressed cardiovascular functions and cell-mediated immune responses after trauma-hemorrhage, it

Nitric oxide synthase in acute alteration of nitric oxide levels after subarachnoid hemorrhage.

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OBJECTIVE Subarachnoid hemorrhage (SAH) is associated with acute decreases and subsequent recovery of cerebral nitric oxide (NO) levels, but the mechanisms of these alterations are not known. In this study, we measured NO synthase (NOS) protein and kinetics to determine its involvement in the

Effect of major and minor surgery on plasma levels of arginine, citrulline, nitric oxide metabolites, and ornithine in humans.

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OBJECTIVE To determine the effect of surgical invasiveness on plasma levels of arginine, citrulline, ornithine, and nitric oxide (NO) in humans. BACKGROUND Surgical trauma may have a profound effect on the metabolism of NO. However, human studies reported both increased and decreased NO levels after

Association of an endogenous inhibitor of nitric oxide synthase with cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage.

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OBJECTIVE Delayed cerebral vasospasm after subarachnoid hemorrhage (SAH) may be evoked by the decreased availability of nitric oxide (NO). Increased cerebrospinal fluid (CSF) levels of asymmetric dimethyl-L-arginine (ADMA), an endogenous inhibitor of NO synthase (NOS), have been associated with the

Vasodilation by intrathecal lipopolysaccharide of the cerebral arteries after subarachnoid haemorrhage in dogs.

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To investigate the influence of inducible nitric oxide synthase on cerebral arteries after subarachnoid haemorrhage (SAH) in vivo, lipopolysaccharide (LPS), a major inducer of inducible nitric oxide synthase, was injected intracisternally into control and SAH model dogs. Intracisternal injection of

[Protection of naoyi-an granule in ischemic brain injury secondary to intracerebral hemorrhage in rats].

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OBJECTIVE To explore the protective effect and its mechanism of the traditional Chinese medicine complex, naoyi-an granule(NYAG), on intracerebral hemorrhage(ICH) in rats. METHODS Collagenase-induced ICH rats were used. Inducible nitric oxide synthase(iNOS) activity of ischemic cerebral cortex

Peptidylarginine Deiminase 2 Knockout Improves Survival in Hemorrhagic Shock.

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The peptidylarginine deiminase (PAD) family converts arginine into citrulline through protein citrullination. PAD2 and PAD4 inhibitors can improve survival in hemorrhagic shock (HS). However, the impact of isoform specific PAD inhibition in improving survival has not been studied. In

Is arginine/asymetric dimethylarginine ratio depletion an indicator of insufficient resuscitation in a porcine model of hemorrhage-reperfusion?

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BACKGROUND Hemorrhagic shock leads to a complex cascade of metabolic and hormonal processes that may result in hypoperfusion, end organ damage, and death even when blood pressure is restored. Studies have shown that morbidity and mortality could be attributable to a diminished availability of

The role of nitric oxide in the reversal of hemorrhagic shock by oxotremorine.

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In the present study, the effect of the nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methylester (L-NAME), on the antishock actions of oxotremorine was investigated in rats subjected to hemorrhagic shock under urethane anesthesia. L-citrulline production in the AV3V region, as an indicator

Distinguishing Intracerebral Hemorrhage from Acute Cerebral Infarction through Metabolomics.

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UNASSIGNED Acute cerebral infarction (ACI) and intracerebral hemorrhage (ICH) are potentially lethal cerebrovascular diseases that seriously impact public health. ACI and ICH share several common clinical manifestations but have totally divergent therapeutic strategies. A poor diagnosis can affect

Remediation of hemorrhagic shock-induced intestinal barrier dysfunction by treatment with diphenyldihaloketones EF24 and CLEFMA.

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Gut is very sensitive to hypoperfusion and hypoxia, and deranged gastrointestinal barrier is implicated in systemic failure of various organs. We recently demonstrated that diphenyldihaloketone EF24 [3,5-bis(2-fluorobenzylidene)piperidin-4-one] improves survival in a rat model of hemorrhagic shock.

Association between cerebrospinal fluid levels of asymmetric dimethyl-L-arginine, an endogenous inhibitor of endothelial nitric oxide synthase, and cerebral vasospasm in a primate model of subarachnoid hemorrhage.

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OBJECTIVE Decreased availability of nitric oxide (NO) has been proposed to evoke delayed cerebral vasospasm after sub-arachnoid hemorrhage (SAH). Asymmetric dimethyl-L-arginine (ADMA) inhibits endothelial NO synthase (eNOS) and, therefore, may be responsible for decreased NO availability in cases of

Ornithine transcarbamylase deficiency unmasked because of gastrointestinal bleeding.

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Ornithine transcarbamylase (OTC) is a mitochondrial-matrix enzyme that catalyzes conversion of ornithine and carbamyl phosphate to citrulline, the second step in the urea cycle. The urea cycle is the most important pathway to detoxification of ammonia in human beings. Ornithine transcarbamylase

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