brain ischemia/nicotina

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Chronic nicotine exposure inhibits 17beta-estradiol-mediated protection of the hippocampal CA1 region against cerebral ischemia in female rats.

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Nicotine addiction in women increases the risk of ischemic stroke. Importantly, women who smoke and use hormone replacement therapy/oral contraceptives greatly increase their risk of coronary heart disease and ischemic stroke as compared to nonsmoking women who use occasionally oral contraceptives.

Chronic nicotine exposure exacerbates transient focal cerebral ischemia-induced brain injury.

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Tobacco smoking is a risk factor contributing to the development and progression of ischemic stroke. Among many chemicals in tobacco, nicotine may be a key contributor. We hypothesized that nicotine alters the balance between oxidant and antioxidant networks leading to an increase in brain injury

Chronic nicotine induces hypoxia inducible factor-2α in perinatal rat adrenal chromaffin cells: role in transcriptional upregulation of KATP channel subunit Kir6.2.

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Fetal nicotine exposure causes impaired adrenal catecholamine secretion and increased neonatal mortality during acute hypoxic challenges. Both effects are attributable to upregulation of ATP-sensitive K(+) channels (K(ATP) channels) and can be rescued by pretreatment with the blocker, glibenclamide.

Brain death following ingestion of E-cigarette liquid nicotine refill solution

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Background: The use of electronic cigarettes (e-cigarettes) is very common worldwide. To date, an increase of nicotine intoxication following an accidental or intentional ingestion/injection of refill solution (e-liquid) has been

Oral contraceptives and nicotine synergistically exacerbate cerebral ischemic injury in the female brain.

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Oral contraceptives (OC) and smoking-derived nicotine (N) are known to synergistically increase the risk and severity of cerebral ischemia in women. Although it has been known for some time that long-term use of OC and nicotine will have an increased risk of peripheral thrombus formation, little is

Nicotine alters the expression of molecular markers of endocrine disruption in zebrafish.

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Nicotine, a drug of abuse, has been reported to have many adverse effects on the developing nervous system. In rodents, chronic nicotine exposure inhibits estrogen-mediated neuroprotection against cerebral ischemia in females suggesting that nicotine could disrupt endocrine targets. Zebrafish have

Severe Neurological Nicotine intoxication by e-cigarette liquids: Systematic Literature Review

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Electronic cigarettes are a popular, easily purchased, alternative source of nicotine that is considered safer than conventional tobacco. However, Intentional or accidental exposure to e-liquid substances, mainly nicotine, can lead to serious, potentially fatal toxicity. Emergency and critical care

A Case Report of Successful Kidney Donation After Brain Death Following Nicotine Intoxication.

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Nicotine intoxication is a rare cause of death and can lead to brain death after respiratory arrest and hypoxic-ischemic encephalopathy. To our knowledge, no previous reports regarding organ donation after nicotine intoxication have been described. We present a successful case of kidney donation

Perinatal nicotine exposure alters AKT/GSK-3β/mTOR/autophagy signaling leading to development of hypoxic-ischemic sensitive phenotype in rat neonatal brain.

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Maternal cigarette smoking is a major perinatal insult that contributes to an increased risk cardiovascular and neurodevelopmental diseases in offspring. Our previous studies have revealed that perinatal nicotine exposure reprograms a sensitive phenotype in neonatal hypoxic-ischemic encephalopathy

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

Coronary vascular response to the cerebral ischemia reflex.

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Most centrally mediated sympathoexcitatory reflexes produce increases in arterial pressure, heart rate, and peripheral vascular resistance, including coronary vasoconstriction. Cerebral ischemia also causes large increases in arterial pressure and peripheral vasoconstriction but with modest or

Assessment of endothelial function in patients with initial manifestations of chronic cerebral ischemia

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Over the last decade, the number of patients with cerebrovascular diseases in Ukraine has grown by 1.5 times. This negative trend is based on the significant increase of vascular risk factors - arterial hypertension, dyslipidemia, sedentary lifestyle, excessive weight/obesity, diabetes

Nicotine-induced neuroprotection against ischemic injury involves activation of endocannabinoid system in rats.

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Nicotine has been reported to exert certain protective effect in the Parkinson's and Alzheimer's diseases. Whether it has a similar action in focal cerebral ischemia was unclear. In the present study, rats received either an injection of (-)-nicotine hydrogen tartrate salt (1.2 mg/kg, i.p.) or the

Inhibition of miRNA-210 reverses nicotine-induced brain hypoxic-ischemic injury in neonatal rats.

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Maternal tobacco use in pregnancy increases the risk of neurodevelopmental disorders and neurobehavioral deficits in postnatal life. The present study tested the hypothesis that perinatal nicotine exposure exacerbated brain vulnerability to hypoxic-ischemic (HI) injury in neonatal rats through

Mito-Tempo prevents nicotine-induced exacerbation of ischemic brain damage.

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Nicotine may contribute to the pathogenesis of cerebrovascular disease via the generation of reactive oxygen species (ROS). Overproduction of ROS leads to brain damage by intensifying postischemic inflammation. Our goal was to determine the effect of Mito-Tempo, a mitochondria-targeted antioxidant,

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