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Страница 1 од 414 резултати
Angiotensin II Type I Receptor Antagonism Attenuates Nicotine-Induced Cardiac Remodeling, Dysfunction, and Aggravation of Myocardial Ischemia-Reperfusion Injury in Rats.
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Increased exposure to nicotine contributes to the development of cardiac dysfunction by promoting oxidative stress, fibrosis, and inflammation. These deleterious events altogether render cardiac myocytes more susceptible to acute cardiac insults such as ischemia-reperfusion (I/R) injury. This study
Differential release of calcitonin gene-related peptide and neuropeptide Y from the isolated heart by capsaicin, ischaemia, nicotine, bradykinin and ouabain.
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The influence of various drugs as well as total ischaemia on the outflow of calcitonin gene-related peptide (CGRP), which is present in sensory nerves, and neuropeptide Y (NPY), which is co-stored with noradrenaline (NA), from the isolated guinea-pig heart, was studied in vitro. Capsaicin exposure
[Protective effects of nicotine on inflammatory cytokines in myocardial ischemia/reperfusion injury in rats].
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OBJECTIVE
To investigate the effect of nicotine on inflammatory cytokines in myocardial ischemia/reperfusion (I/R) injury in rat.
METHODS
Fifty male Sprague-Dawley (SD) rats were divided into five groups by random numbers table (each n=10): sham operation group (S group), I/R group, nicotine 400
The effect of angiotensin (1-7) on survival of random pattern skin flaps with nicotine-induced ischemia in rats.
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OBJECTIVE
The purpose of this study was to reveal the effect of angiotensin (1-7) on survival of random pattern, nicotinized, ischemic flap model in rats.
METHODS
We used female Sprague Dawley rats weighing between 250 and 300 g. The study was performed on 3 groups each of them was consisted of 30
Effect of sildenafil citrate in nicotine-induced ischemia: An experimental study using a rat model.
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Recent experimental and clinical studies have demonstrated the negative effects of nicotine on the viability of skin flaps. Necrotic damage to skin flaps can result in significant complications including delayed wound healing, dehiscence and wound contraction. Phosphodiesterase type 5 inhibitors,
Nicotine patch therapy in smoking cessation reduces the extent of exercise-induced myocardial ischemia.
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OBJECTIVE
We sought to determine the effects of nicotine patch therapy, when used to promote smoking cessation, on myocardial ischemia in patients with coronary artery disease.
BACKGROUND
Nicotine patches substantially increase quit rates among cigarette smokers, but their safety in patients with
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.
Augmented myocardial ischaemia by nicotine--mechanisms and their possible significance.
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1. To study the effect of nicotine on the severity of experimental myocardial ischaemia, Langendorff hearts of rabbits (n=7-12 per group) were subjected to 2 h of low-flow ischaemia followed by 1 h of reperfusion. 2. Infusion of nicotine (100 ng ml(-1)) caused only minor changes in non-ischaemic
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
Effects of nicotine on thromboxane/prostacyclin balance in myocardial ischemia.
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It has been proven that nicotine contributes to cardiovascular diseases, although its precise mechanism of action is still unclear. The purpose of this study is to find how nicotine may complicate myocardial ischemia by affecting the thromboxane/prostacyclin (TXA(2)/PGI(2)) balance. We used four
Acute and chronic effects of nicotine on anastomotic patency following ischemia/reperfusion.
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The effect of nicotine on anastomotic patency was studied using an isogenic rat-knee transplantation model. Animals were divided into experimental and control groups, with experimental animals exposed to either 40 days of twice-daily nicotine injections (Group 1-chronic exposure) or acute nicotine
Antimuscle atrophy effect of nicotine targets muscle satellite cells partly through an α7 nicotinic receptor in a murine hindlimb ischemia model.
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We have recently identified that donepezil, an anti-Alzheimer drug, accelerates angiogenesis in a murine hindlimb ischemia (HLI) model. However, the precise mechanisms are yet to be fully elucidated, particularly whether the effects are derived from endothelial cells alone or from other nonvascular
Nicotine-induced exocytotic norepinephrine release in guinea-pig heart, human atrium and bovine adrenal chromaffin cells: modulation by single components of ischaemia.
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The influence of single components of myocardial ischaemia, such as anoxia, substrate withdrawal, hyperkalemia and extracellular acidosis, on nicotine-induced norepinephrine (NE) release was investigated in the isolated perfused guinea-pig heart, in incubated human atrial tissue and in cultured
Effects of nicotine on blood flow and delayed neuronal death following intermittent transient ischemia in rat hippocampus.
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A cholinergic neural vasodilative response in the cerebral cortex and hippocampus, independent of metabolic vasodilation, was recently demonstrated by activating the nicotinic acetylcholine receptors (nAChRs) via activation of cholinergic neurons originating in the nucleus basalis of Meynert and
Investigation of the Possibility of Using Serum Ischemia Modified Albumin (IMA) as a Novel and Early Marker of the Extent of Oxidative Stress Induced by Various Tobacco Products.
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BACKGROUND
Ischemia Modified Albumin (IMA) is an altered serum albumin that forms under the conditions of oxidative stress and is considered as a biomarker of cardiac ischemia. The objective of this study was to evaluate the ischemia modified albumin (IMA) in the serum of the individuals with
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