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The effect of intravenous magnesium sulfate infusion on serum levels of sodium and potassium in patients with aneurysmal subarachnoid hemorrhage.

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Abnormal serum sodium levels are frequently observed among patients with aneurysmal subarachnoid hemorrhage (SAH) and may worsen cerebral edema or mass effect. Low serum potassium levels (hypokalemia) are also common among patients with aneurysmal SAH and are associated with prolonged QT interval

Role of ATP-sensitive potassium channels and inflammatory response of basilar artery smooth muscle cells in subarachnoid hemorrhage of rabbit and immune-modulation by shikonin.

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OBJECTIVE

To investigate the role of inflammatory response, oxidative damage and changes of ATP-sensitive potassium channels (sK_ATP) in basilar artery (BA) smooth muscle cells (SMCS) of rabbits in subarachnoid hemorrhage (SAH) model.

METHODS

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Attenuation of basilar artery spasm after experimental subarachnoid hemorrhage in rabbit by potassium channel activator cromakalim--a preliminary result.

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Cerebral vasospasm associated with aneurysmal subarachnoid hemorrhage (SAH) remains a major complication in patients suffering from SAH. Regulation of membrane potential of arterial smooth muscle through activation or inhibition of potassium (K+) channel activity provides an important mechanism to

Subarachnoid hemorrhage and the role of potassium channels in relaxations of canine basilar artery to nitrovasodilators.

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This study was designed to determine the effect of subarachnoid hemorrhage (SAH) on potassium (K+) channels involved in relaxations of cerebral arteries to nitrovasodilators. The effects of K+ channel inhibitors on relaxations to 3-morpholinosydnonimine (SIN-1) and sodium nitroprusside (SNP) were

Spectrum of altered reactivity of isolated cerebral arteries following subarachnoid haemorrhage--response to potassium, pH, noradrenaline, 5-hydroxytryptamine, and sodium loading.

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The circular contractile responses to various stimuli have been measured in segments of cerebral arteries (both middle cerebral and basilar) taken from dogs either 3 or 7 days following the cisternal injection of autologous blood under anaesthesia. The maximum contractile response to

Systemic administration of the potassium channel activator cromakalim attenuates cerebral vasospasm after experimental subarachnoid hemorrhage.

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OBJECTIVE Cerebral vasospasm is a primary complication after aneurysmal subarachnoid hemorrhage (SAH). Recent evidence indicates that the activation of potassium (K+) channels may be of benefit in relieving spastic constriction. The present study examined the effects of systemic administration of a

Serum potassium and sodium levels after subarachnoid haemorrhage.

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BACKGROUND Many studies have demonstrated that subarachnoid haemorrhage (SAH) is associated with hyponatraemia but associations with potassium levels are less well studied. There is a clear physiological link between sodium and potassium and abnormal potassium levels that can lead to dangerous

Serum glucose/potassium ratio as a clinical risk factor for aneurysmal subarachnoid hemorrhage.

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OBJECTIVE Aneurysmal subarachnoid hemorrhage (SAH) can result in poor outcomes, and biomarkers for predicting poor prognosis have not yet been established. The aim of this study was to clarify the significance of the serum glucose/potassium ratio for predicting the prognosis of aneurysmal

Serum Glucose and Potassium Ratio as Risk Factors for Cerebral Vasospasm after Aneurysmal Subarachnoid Hemorrhage.

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Cerebral vasospasm is associated with poor prognosis in patients with aneurysmal subarachnoid hemorrhage (SAH), and biomarkers for predicting poor prognosis have not yet been established. We attempted to clarify the relationship between serum glucose/potassium ratio and cerebral

Calcium and potassium channels in experimental subarachnoid hemorrhage and transient global ischemia.

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Healthy cerebrovascular myocytes express members of several different ion channel families which regulate resting membrane potential, vascular diameter, and vascular tone and are involved in cerebral autoregulation. In animal models, in response to subarachnoid blood, a dynamic transition of ion

Higher brain extracellular potassium is associated with brain metabolic distress and poor outcome after aneurysmal subarachnoid hemorrhage.

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BACKGROUND Elevated brain potassium levels ([K+]) are associated with neuronal damage in experimental models. The role of brain extracellular [K+] in patients with poor-grade aneurysmal subarachnoid hemorrhage (aSAH) and its association with hemorrhage load, metabolic dysfunction and outcome has not

Reactivity of rabbit basilar artery to alterations in extracellular potassium and calcium after subarachnoid hemorrhage.

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Hemolysis of periarterial clots after subarachnoid hemorrhage may liberate large quantities of K+ into the vicinity of cerebral blood vessels and possibly change their sensitivity to endogenous vasoactive agents. The current study examined the influence of subarachnoid hemorrhage on the sensitivity

Expression and function of inwardly rectifying potassium channels after experimental subarachnoid hemorrhage.

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Cerebral vasospasm after subarachnoid hemorrhage (SAH) is because of smooth muscle contraction, although the mechanism of this contraction remains unresolved. Membrane potential controls the contractile state of arterial myocytes by gating voltage-sensitive calcium channels and is in turn primarily

Temporal profile of potassium channel dysfunction in cerebrovascular smooth muscle after experimental subarachnoid haemorrhage.

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The pathogenesis of cerebral vasospasm after subarachnoid haemorrhage (SAH) involves sustained contraction of arterial smooth muscle cells that is maximal 6-8 days after SAH. We reported that function of voltage-gated K+ (KV) channels was significantly decreased during vasospasm 7 days after SAH in

Influence of experimental subarachnoid hemorrhage on nicotine-induced contraction of the rat basilar artery in relation to nicotinic acetylcholine receptors, calcium, and potassium channels.

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BACKGROUND Cigarette smoking is associated with symptomatic vasospasm after subarachnoid hemorrhage (SAH). METHODS Rat basilar arteries of a normal group and SAH groups (1 hour, 2 days, and 1 week) were removed from the brain and cut into spiral preparations. RESULTS A central nervous system (CNS)

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