نتایج جستجو برای: reperfusion rat

تعداد نتایج: 305847  

Journal: :international journal of endocrinology and metabolism 2023

Background: The harmful impact of ovariectomy on myocardial ischemia-reperfusion (M/IR) injury has been established in the short term. Objectives: In this study, we aimed to investigate long-term effects M/IR injury. Methods: Two methods involving dorsolateral skin incisions were used induce ovariectomized (OVX) rat model. rats divided into 2 groups: Control and OVX (n = 6). At end hearts isola...

Journal: :American journal of physiology. Heart and circulatory physiology 2001
T Yamamura H Otani Y Nakao R Hattori M Osako H Imamura

Bcl-2 family proteins play a crucial role in the cytoprotective action of insulin-like growth factor-I (IGF-I) by regulating cell death signaling at the mitochondrial level. The present study examined the effect of IGF-I on the expression of Bcl-2 family proteins in the rat heart mitochondria in relation to myocardial protection against ischemia-reperfusion injury. Systemic IGF-I (1 mg) treatme...

2010
Joon Hong Kim Joon Kim Yong-Hyeon Park Kook Jin Cheun Young-Ho Jang

BACKGROUND It was reported that N,N,N'N'-tetrakis-[2-pyridylmethyl]-ethylenediamine (TPEN), a transition metal chelator, confers cardioprotection against myocardial ischemic injury. In this study, we investigated the effect of TPEN targeting reperfusion period in isolated rat hearts. METHODS Langendorff perfused rat hearts were subjected to 30 min of regional ischemia and 2 h of reperfusion. ...

Journal: :jundishapur journal of natural pharmaceutical products 0
mahin dianat department of physiology, physiology research center, faculty of medicine, ahvaz jundishapur university of medical sciences, ahvaz, ir iran mahdi esmaeilizadeh department of physiology, diabetic research center, ahvaz jundishapur university of medical sciences, ahvaz, ir iran; department of physiology, diabetic research center, ahvaz jundishapur university of medical sciences, ahvaz, ir iran. tel: +98-9151131801 mohammad badavi department of physiology, physiology research center, faculty of medicine, ahvaz jundishapur university of medical sciences, ahvaz, ir iran ali reza samarbaf-zadeh department of virology, faculty of medicine, ahvaz jundishapur university of medical sciences, ahvaz, ir iran bahareh naghizadeh department of pharmacology, faculty of medicine, ahvaz jundishapur university of medical sciences, ahvaz, ir iran

background myocardial injury caused by ischemia-reperfusion leads to cardiac dysfunction, tissue injury and metabolic changes. the production of reactive oxygen species (ros) and lipid peroxidation are accompanied by ischemia-reperfusion injury. objectives the aim of this study was to assess the cardio protective potential effects of crocin in comparison with vitamin e on antioxidant capacity i...

Journal: :American journal of physiology. Heart and circulatory physiology 2007
Paul A Townsend Sean M Davidson Samantha J Clarke Igor Khaliulin Christopher J Carroll Tiziano M Scarabelli Richard A Knight Anastasis Stephanou David S Latchman Andrew P Halestrap

Urocortin (UCN) protects hearts against ischemia and reperfusion injury whether given before ischemia or at reperfusion. Here we investigate the roles of PKC, reactive oxygen species, and the mitochondrial permeability transition pore (MPTP) in mediating these effects. In Langendorff-perfused rat hearts, acute UCN treatment improved hemodynamic recovery during reperfusion after 30 min of global...

Journal: :The Journal of pharmacology and experimental therapeutics 2005
Anita Pálfi Ambrus Tóth Gyozo Kulcsár Katalin Hantó Péter Deres Eva Bartha Róbert Halmosi Eszter Szabados László Czopf Tamás Kálai Kálmán Hideg Balázs Sümegi Kálmán Tóth

Blocking poly(ADP-ribosyl)ation of nuclear proteins protects the heart from ischemia-reperfusion injury. In addition, activation of Akt and mitogen-activated protein kinase (MAPK) cascades also plays a pivotal role in the survival of cardiomyocytes during ischemia-reperfusion; however, the potential interplay between these pathways is yet to be elucidated. We therefore tested the hypothesis whe...

2001
JIALIN BAO KAORI SATO MIN LI YOUHE GAO RUHUL ABID WILLIAM AIRD MICHAEL SIMONS MARK J. POST Kaori Sato Min Li Youhe Gao Ruhul Abid William Aird Michael Simons

Bao, Jialin, Kaori Sato, Min Li, Youhe Gao, Ruhul Abid, William Aird, Michael Simons, and Mark J. Post. PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated IkBa degradation. Am J Physiol Heart Circ Physiol 281: H2612–H2618, 2001.— PR-39 inhibits proteasome-mediated IkBa degradation and might protect against ischemia-reperfusion injury. We studied PR-39, ...

Journal: :Circulation 1998
A P Vakeva A Agah S A Rollins L A Matis L Li G L Stahl

BACKGROUND Myocardial ischemia and reperfusion (MI/R)-induced tissue injury involves necrosis and apoptosis. However, the precise contribution of apoptosis to cell death, as well as the mechanism of apoptosis induction, has not been delineated. In this study, we sought to define the contribution of the activated terminal complement components to apoptosis and necrosis in a rat model of MI/R inj...

Introduction: This study was aimed to investigate the effects of postconditioning by natural honey on cardiac arrhythmias in the ischemic isolated rat heart. Methods: Male Wistar rats were divided into four groups then anesthetized by sodium pentobarbital. The animal hearts were removed and quickly mounted on a Langendorff apparatus and perfused under constant pressure by a modified Krebs-H...

2015
Rashmi Arora Sudha Vengurlekar

Apoptosis is a crucial event that can initiate ischaemia-reperfusion induced inflammation and subsequent tissue injury. Myocardial ischaemia reperfusion is associated with activation of intracellular death proteases known as calpains. Myocardial ischaemia was induced in isolated rat heart which was subjected to 30 min ischaemia followed by reperfusion for 120min. The effect of calpain inhibitor...

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