carbenoxolone/hemorrhage

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[The role of gap-junction in suspended animation for hemorrhagic shock with brain injury: experiment with rats].

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OBJECTIVE To investigate the role of gap-junction in suspended animation for hemorrhagic shock with brain injury. METHODS Twenty-four SD rats were made into models of uncontrolled hemorrhagic shock and occlusion of bilateral common carotid arteries and randomly divided into 3 equal groups:

Effects of gap junctional blockers on cerebral vasospasm after subarachnoid hemorrhage in rabbits.

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The role of gap junctional communication in the coordination of vascular behavior has been well established experimentally. The aim of this study was to investigate whether the gap junctional blockers would inhibit cerebral vasospasm after experimental subarachnoid hemorrhage (SAH). We used the

Role of gap junctions in early brain injury following subarachnoid hemorrhage.

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Gap junction inhibition has been demonstrated to reverse the vascular contraction that follows experimental subarachnoid hemorrhage. This study hypothesizes that the use of established gap junction inhibitors: octonal and carbenoxolone, to interrupt cell to cell communication will provide

Effect of gap junction inhibition on intracerebral hemorrhage-induced brain injury in mice.

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It has been reported that gap junction contributes to ischemic brain injury and gap junction inhibitors improve neurological outcome in ischemic brain injury models. In the present study, we investigated the effects of gap junction inhibitor, carbenoxolone, on mortality, neurological deficits and

Carbenoxolone inhibits TRPV4 channel-initiated oxidative urothelial injury and ameliorates cyclophosphamide-induced bladder dysfunction.

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Carbenoxolone (CBX) is a clinically prescribed drug for the treatment of digestive ulcer and inflammation. It is also a widely used pharmacological inhibitor of several channels in basic research. Given that the overactivity of several channels, including those inhibitable by CBX, underlies bladder

Pannexin-1 is involved in neuronal apoptosis and degeneration in experimental intracerebral hemorrhage in rats.

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Pannexins serve an important role in the regulation of extracellular neuronal regenerative currents and cellular signal transduction of glial cells; however, the effects of pannexins in various cerebrovascular diseases have not been reported. The present study focused on the expression and influence

Esculine, ranitidine and carbenoxolone: different modes of action on gastric mucosa.

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1. This study was designed to determine the antiulcerogenicity of esculine in various types of experimentally induced gastric ulcers in which the appearance of lesions is due to an ischemic process: cold-restraint stress and pylorus-ligated induced ulcers. 2. In the first experimental model,

[Peptic ulcer: new aspects of conservative therapy].

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In spite of the large number of preparations, medical therapy of peptic ulcer disease has long been unsatisfactory. Antacids, anticholinergics and diet neither accelerate healing of ulcers nor prevent recurrences. Carbenoxolone affects only gastric ulcers, while some medications exhibit substantial

The pathophysiology of acute gastric ulcer development in normotensive and hypertensive rats: A comparative study

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Although gastric ulcers and hypertension are diseases that affect a large part of the population, the association of these comorbidities is still poorly studied. Therefore, the present study investigated the response of normotensive (NTR) and spontaneously hypertensive (SHR) rats to gastric ulcers

Inhibitory effect of gap junction blockers on cerebral vasospasm.

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OBJECTIVE The gap junction is important in the propagation of dilation/constriction signals along vessels for coordinated behavior in control of vascular tone. The authors hypothesized that gap junctions might play a role in cerebral vasospasm following subarachnoid hemorrhage (SAH). The aims of the

Role of pannexin 1 in Clostridium perfringens beta-toxin-caused cell death.

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Beta-toxin produced by Clostridium perfringens is a key virulence factor of fatal hemorrhagic enterocolitis and enterotoxemia. This toxin belongs to a family of β-pore-forming toxins (PFTs). We reported recently that the ATP-gated P2X7 receptor interacts with beta-toxin. The ATP-release channel

Protease-activated receptor 2 and bradykinin-mediated vasodilation in the cerebral arteries of stroke-prone rats.

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Protease-activated receptor 2 (PAR(2)) expression is up-regulated during vascular injury associated with edema. PAR(2) and bradykinin subtype 2 receptor (B(2)) expression and function were assessed in relation to hypertensive encephalopathy (HE) and cerebral hemorrhage (CH) in middle cerebral

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