نتایج جستجو برای: transient ischemia

تعداد نتایج: 204291  

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 1997
M Tsuda K Imaizumi T Katayama K Kitagawa A Wanaka M Tohyama T Takagi

To elucidate the molecular mechanisms underlying neuronal death after transient forebrain ischemia, we cloned genes expressed after transient forebrain ischemia in the Mongolian gerbil by a differential display method. A gerbil homolog of rat zinc transporter, ZnT-1, which transports intracellular Zn2+ out of cells, was isolated. Its expression became detectable exclusively in pyramidal neurons...

2004
Kevin Kit Parker James A. Lavelle L. Katherine Taylor Zifa Wang David E. Hansen

Parker, Kevin Kit, James A. Lavelle, L. Katherine Taylor, Zifa Wang, and David E. Hansen. Stretch-induced ventricular arrhythmias during acute ischemia and reperfusion. J Appl Physiol 97: 377–383, 2004; 10.1152/japplphysiol.01235.2001.—Mechanical stretch has been demonstrated to have electrophysiological effects on cardiac muscle, including alteration of the probability of excitation, alteratio...

Journal: :Circulation 1980
E H Schuster B H Bulkley

Whether an acute myocardial infarction due to occlusion of one major coronary artery can cause ischemia in the distribution of a second narrowed coronary artery by the mechanism of collateral interruption (i.e., ischemia at a distance) is not known. To study this, we reviewed 128 consecutively autopsied patients with acute fatal myocardial infarcts and identified 20 patients in whom angina, ass...

Journal: :The Journal of pharmacology and experimental therapeutics 2006
Claudio Storini Luigi Bergamaschini Raffaella Gesuete Emanuela Rossi Diana Maiocchi Maria Grazia De Simoni

We have studied the effect of DX-88, a selective recombinant inhibitor of human plasma kallikrein, in transient or permanent focal brain ischemia (with or without reperfusion, respectively) induced in C57BL/6 mice. Twenty-four hours after transient ischemia, DX-88 administered at the beginning of ischemia (pre) induced a dose-dependent reduction of ischemic volume that, at the dose of 30 microg...

Journal: :physiology and pharmacology 0
hamdollah panahpour ali akbar nekooeian gholam abbas dehghani medicinal & natural products chemistry research center, shiraz university of medical sciences, shiraz, iran

introduction: development of brain edema following focal cerebral ischemia exacerbates primary ischemic injury. blood brain barrier (bbb) opening is an important part of edema named as vasogenic brain edema. in this study, quantitative alterations of bbb permeability is experimentally evaluated using transient focal cerebral ischemia in the rat. methods: two groups of male rats (ischemic and sh...

Journal: :archives of trauma research 0
mohammad ali atlasi anatomical sciences research center, kashan university of medical sciences, kashan, ir iran; anatomical research center, kashan university of medical sciences, kashan, ir iran. tel: +98-9131615603, fax: +98-3615551112سازمان اصلی تایید شده: دانشگاه علوم پزشکی کاشان (kashan university of medical sciences) homayoun naderian anatomical sciences research center, kashan university of medical sciences, kashan, ir iranسازمان اصلی تایید شده: دانشگاه علوم پزشکی کاشان (kashan university of medical sciences) mahdi noureddini physiology research center, kashan university of medical sciences, kashan, ir iranسازمان اصلی تایید شده: دانشگاه علوم پزشکی کاشان (kashan university of medical sciences) esmaeil fakharian trauma research center, kashan university of medical sciences, kashan, ir iranسازمان اصلی تایید شده: دانشگاه علوم پزشکی کاشان (kashan university of medical sciences) abolfazl azami anatomical sciences research center, kashan university of medical sciences, kashan, ir iranسازمان اصلی تایید شده: دانشگاه علوم پزشکی کاشان (kashan university of medical sciences)

results in all groups ischemic changes were apparently observed in hippocampus ca1 neurons. in two-vessel occlusion model, after 3 and 24 hours of reperfusions, ischemic cells accounted for 14.9% and 23.2%, respectively. in four-vessel occlusion model, after 3 and 24 hours of reperfusions, ischemic cells accounted for 7.6% and 44.9% (p < 0.0001), respectively. background an appropriate animal m...

2013
Michael K. Tso R. Loch Macdonald

Subarachnoid hemorrhage and transient global cerebral ischemia result in similar pathophysiological changes in the cerebral microcirculation. These changes include microvascular constriction, increased leukocyte-endothelial interactions, blood brain barrier disruption, and microthrombus formation. This paper will look at various animal and preclinical studies that investigate these various micr...

Journal: :Journal of neuroscience research 2009
Yi-Wen Ruan Zhigang Lei Yuan Fan Bende Zou Zao C Xu

Dendritic spines form postsynaptic components of excitatory synapses in CA1 pyramidal neurons and play a key role in excitatory signal transmission. Transient global ischemia is thought to induce excitotoxicity that triggers delayed neuronal death in the CA1 region. However, the mechanism underlying structural changes of excitatory synapses after ischemia is not completely understood. Here, we ...

Journal: :physiology and pharmacology 0
abedin vakili department and physiological research center, semnan university of medical sciences‎ gholam abbas dehghani department of physiology

introduction: anesthetic agents, blood pressure, arterial ph and blood gases have found to influence on the pathophysiology of experimental stroke. despite, there are very few comparative studies about effects of anesthetic agents in animal model of cerebral ischemia. therefore, in this study, we investigated the effects of chloral hydrate and pentobarbital anesthesia, as comparative study, on ...

2010
Luisa Perasso Carla Emilia Cogo Debora Giunti Carlo Gandolfo Piero Ruggeri Antonio Uccelli Maurizio Balestrino

Although many studies have shown that administration of stem cells after focal cerebral ischemia improves brain damage, very little data are available concerning the damage induced by global cerebral ischemia. The latter causes neuronal death in selectively vulnerable areas, including the hippocampal CA1 region. We tested the hypothesis that intravenous infusion of bone marrowderived stromal ce...

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