hemorrhage/nicotine

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Risk factors of duodenal ulcer bleeding: the role of smoking and nicotine.

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Several studies have shown that cigarette smoking affects duodenal ulcer (DU) recurrence. To verify any correlation between smoking and complications of ulcer disease, we studied 33 DU smokers, 16 DU ex-smokers and 87 DU non-smokers for up to 48 months, recording age, sex, family history of ulcer,

Nicotine replacement therapy in patients with aneurysmal subarachnoid hemorrhage: Systematic review of the literature, and survey of Canadian practice.

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Tobacco smoke increases the risk of aneurysmal subarachnoid hemorrhage (SAH), as well as complications such as vasospasm. Most patients presenting with aneurysmal SAH smoke, and many survivors continue to smoke after discharge. Neurosurgeons often hesitate to use nicotine replacement therapy (NRT)

Influence of experimental subarachnoid hemorrhage on nicotine-induced contraction of the rat basilar artery in relation to arachidonic acid metabolites signaling pathway.

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BACKGROUND Smoking is one of the most important risk factors for cerebral circulatory disorders. The purpose of this study was to investigate the influence of experimental subarachnoid hemorrhage (SAH) on nicotine-induced contraction (arachidonic acid metabolites) in the basilar arteries of

The reversal of experimental hemorrhagic shock induced by nicotine and dimethylphenylpiperazinium is adrenal-dependent.

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In a rat model of volume-controlled hemorrhagic shock causing the death of all control animals within 30 min, the intravenous injection of either nicotine (50 micrograms/kg) or dimethylphenylpiperazinium (DMPP) (0.5 micrograms/kg) produced a rapid and sustained reversal of the shock condition, with

Effects of the experimental subarachnoid hemorrhage on the eicosanoid receptors in nicotine-induced contraction of the rat basilar artery.

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BACKGROUND Smoking is one of the most important risk factors for subarachnoid hemorrhage (SAH). The purpose of this study was to investigate the influence of experimental SAH and arachidonic acid metabolites on nicotine-induced contraction in the rat basilar artery. METHODS Rats were killed at 1

Adrenocorticotropin release is not involved in the nicotine-induced reversal of hemorrhagic shock in anesthetized rats.

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In a model of volume-controlled hemorrhagic shock causing the death of all control animals within 30 min, the intravenous injection of nicotine produced a rapid, sustained and dose-dependent restoration of cardiovascular and respiratory functions, with 60 and 100% survival 2 h after the

Nicotine reverses hemorrhagic shock in rats.

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Cholinergic mechanisms are currently thought to play an essential role in blood pressure homeostasis. Here we show that, in urethane-anaesthetized rats bled to severe hemorrhagic shock, the i.v. administration of nicotine 0.2-50 micrograms/kg causes a prompt, sustained and dose-dependent improvement

Smoking and non-smoking tobacco as risk factors in subarachnoid haemorrhage.

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OBJECTIVE Swedish snuff is a particular form of non-smoking tobacco with high nicotine content. It is unknown whether this form of tobacco is a risk factor similar to smoking for suffering subarachnoid haemorrhage (SAH). In the present study we report our finding concerning smoking and snuff as risk

Nicotine promotes angiogenesis in mouse brain after intracerebral hemorrhage

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Here we examined the effect of nicotine on angiogenesis in the brain after intracerebral hemorrhage (ICH), as angiogenesis is considered to provide beneficial effects on brain tissues during recovery from injury after stroke. Nicotine was administered to C57BL/6 mice suffering from

Viral hemorrhagic septicemia virus glycoprotein production in tobacco.

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Viral hemorrhagic septicemia virus (VHSV) causes mortality in numerous marine and freshwater fish species resulting in heavy losses in fish farming. The glycoprotein gene of VHSV was fused with the cholera toxin B subunit (CTB) and expressed transiently in leaf tissues of Nicotiana benthamiana via

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)

Effects of tobacco dose and length of exposure on delayed neurological deterioration and overall clinical outcome after aneurysmal subarachnoid hemorrhage.

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OBJECTIVE The association between smoking and intracranial aneurysms is now well recognized. However, the relationship between tobacco use and outcome after aneurysmal subarachnoid hemorrhage (SAH) is not as well understood and published results are contradictory. The purpose of this study is to

Nicotine replacement therapy after subarachnoid hemorrhage is not associated with increased vasospasm.

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OBJECTIVE A significant number of patients with aneurysmal subarachnoid hemorrhage are active smokers and at risk for acute nicotine withdrawal. There is conflicting literature regarding the vascular effects of nicotine and theoretical concern that it may worsen vasospasm. The literature on the

Transdermal nicotine replacement therapy in cigarette smokers with acute subarachnoid hemorrhage.

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BACKGROUND We evaluated the safety of nicotine replacement therapy (NRT) in active smokers with acute (aneurysmal) subarachnoid hemorrhage (SAH). METHODS A retrospective observational cohort study was conducted in a prospectively collected database including all SAH patients admitted to an 18-bed

Therapeutic effect of nicotine in a mouse model of intracerebral hemorrhage.

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Intracerebral hemorrhage (ICH) resulting from the leakage of blood into the brain parenchyma triggers severe tissue damage involving neurodegeneration and inflammation. Increasing lines of evidence indicate that the stimulation of central nicotinic acetylcholine receptors affords neuroprotection

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