Spelling suggestions: "subject:"ischemia reperfusion injury"" "subject:"ischemia reperfusion jnjury""
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The Role of Small Heat Shock Protein 20 and Its Phosphorylation in the Regulation of Cardiac Function and Ischemia/Reperfusion InjuryQian, Jiang 06 August 2010 (has links)
No description available.
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A NOVEL ROLE OF SIRT1 IN SILDENAFIL INDUCED CARDIOPROTECTION IN MICEShalwala, Mona 07 May 2010 (has links)
Phosphodiesterase-5 inhibitor, sildenafil (SIL) protects against myocardial ischemia/reperfusion (I-R) injury. We hypothesized that SIL-induced protection may be mediated through activation of SIRT1, an enzyme which deacetylates proteins involved in cellular stress response. Adult male ICR mice were treated with SIL (0.7mg/kg ip), Resveratrol (RSV) (5mg/kg ip) (positive control), or saline (0.2 ml ip). The hearts were harvested 24 h later and homogenized for SIRT1 activity analysis. Both SIL and RSV increased cardiac SIRT1 activity (P<0.001) as compared to Saline. Adult mouse ventricular cardiomyocytes pre-treated with either SIL or RSV (1µM) in vitro also upregulated SIRT1 activity (P<0.05). SIL also reduced infarct size following 30 min. ischemia and 24 h reperfusion in vivo. Sirtinol (5mg/kg in 10% DMSO, ip), a SIRT1 inhibitor abolished the infarct-limiting effect of SIL and RSV (P<0.001). In conclusion, activation of SIRT1 by SIL plays an essential role in cardioprotection against I-R injury.
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IMPACT OF PHOSPHOINOSITIDES ON REGULATION OF K-ATP BY ATP AND HYDROGEN SULFIDEHendon, Tyler 01 January 2018 (has links)
Hydrogen sulfide (H2S) reduces ischemia reperfusion (IR) injury by stimulating adenosine triphosphate (ATP) sensitive potassium channels (KATP) [1-5]. Demonstrating H2S stimulation is unique to KATP, as other inwardly rectifying potassium (Kir) channels demonstrate inhibition or are unaffected [6]. We recently showed that H2S inhibits Kir2 and Kir3 by decreasing channel sensitivity to phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2 or PIP2) [6]. Here, we test the hypothesis that H2S regulation of Kir6.2, a pore-forming subunit of the KATP channel, is also dependent on PIP2. Using whole-cell patch-clamp we show that H2S increases the activity of Kir6.2 channels expressed in HEK-293 cells. To study the mechanism, we modulated PIP2 levels by expressing a light- activated phosphatase, or by including high levels of a water-soluble PIP2 analog in the patch pipette. The results suggest that H2S augmentation of Kir6.2 channel activity is increased when PIP2 levels are elevated.
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The Effect of Alpha 1-Antitrypsin on Ischemia-Reperfusion Injury in Lung TransplantationGao, Wenxi 20 November 2012 (has links)
Ischemia-reperfusion (IR) injury is a severe complication in lung transplantation characterized by inflammation, alveolar damage, and hypoxemia. Alpha 1-antitrypsin (A1AT), a protease inhibitor, is currently used clinically for the treatment of A1AT deficiency emphysema. A1AT has been shown to have the potential to reduce IR injury through its anti-inflammatory and anti-apoptotic effects. We hypothesized that A1AT will ameliorate IR injury through these effects. We tested A1AT in two models of IR: a cell culture model of simulated lung transplantation and a rat in situ pulmonary ligation model. In cell culture, we found that A1AT exerts its protective effects by inhibiting cell death and inflammatory cytokine release in a dose-dependent manner. In the rat pulmonary ischemia-reperfusion model, we found that A1AT improved lung function by inhibiting apoptosis and inflammation. There is potential for future application of A1AT in the treatment of IR injury in lung transplantation.
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The Effect of Alpha 1-Antitrypsin on Ischemia-Reperfusion Injury in Lung TransplantationGao, Wenxi 20 November 2012 (has links)
Ischemia-reperfusion (IR) injury is a severe complication in lung transplantation characterized by inflammation, alveolar damage, and hypoxemia. Alpha 1-antitrypsin (A1AT), a protease inhibitor, is currently used clinically for the treatment of A1AT deficiency emphysema. A1AT has been shown to have the potential to reduce IR injury through its anti-inflammatory and anti-apoptotic effects. We hypothesized that A1AT will ameliorate IR injury through these effects. We tested A1AT in two models of IR: a cell culture model of simulated lung transplantation and a rat in situ pulmonary ligation model. In cell culture, we found that A1AT exerts its protective effects by inhibiting cell death and inflammatory cytokine release in a dose-dependent manner. In the rat pulmonary ischemia-reperfusion model, we found that A1AT improved lung function by inhibiting apoptosis and inflammation. There is potential for future application of A1AT in the treatment of IR injury in lung transplantation.
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Aging, habitual exercise, and vascular ischemia-reperfusion injuryDeVan, Allison Elizabeth 18 March 2011 (has links)
Ischemia-reperfusion (IR) injury occurs during myocardial infarction and during some cardiovascular surgeries. Animal studies support the role of endurance exercise training in preventing myocardial IR injury and coronary endothelial dysfunction. In human and animal studies, habitual exercise has been shown to attenuate endothelial dysfunction caused by aging and disease. It is unknown; however, if exercise can protect against vascular IR injury in humans and if so, whether these effects persist with advancing age. Using 20 minutes of forearm ischemia and the response of the brachial artery as a noninvasive surrogate model for the heart, the association between the mode of exercise training (endurance versus resistance) and vascular IR injury was examined in young healthy adults in the first study. Endothelial function, as measured by flow-mediated dilation (FMD) in the brachial artery, decreased significantly after forearm ischemia, suggesting that this noninvasive model of the heart produces significant and measureable vascular injury. These measures returned to baseline levels within 30 minutes following ischemia, illustrating the transient nature of this form of IR injury. The magnitude of injury and recovery from ischemia were not significantly different among young sedentary, endurance-trained, and resistance-trained subjects, suggesting that exercise training is not associated with protection from vascular IR injury in a young, healthy population. In the second study, the association between aging, endurance exercise training, and vascular IR injury was studied. Twenty minutes of forearm ischemia was associated with a transient fall in brachial FMD in young and older sedentary and endurance-trained subjects. Young subjects recovered more quickly from IR injury than older subjects. Within 30 minutes of injury, the endothelial function of the young group was back to baseline while blunted endothelial function persisted in older subjects for greater than 45 minutes after injury. There was no association between endurance exercise training and enhanced recovery from IR injury. These findings suggest that aging is associated with delayed recovery from vascular IR injury and that endurance training does not appear to modulate the vascular IR injury responses. / text
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Mechanisms by Which Arachidonic acid Metabolite, Epoxyeicosatrienoic acid Elicit Cardioprotection Against Ischemic Reperfusion InjuryBATCHU, SRI NAGARJUN Unknown Date
No description available.
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Mechanisms of epoxyeicosatrienoic acid-induced cardioprotectionChaudhary, Ketul R Unknown Date
No description available.
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A pathologic role for angiotensin II and endothelin-1 in cardiac remodelling and ischaemia and reperfusion injury in a rat model of the metabolic syndrome /Smith, Wayne. January 2006 (has links)
Thesis (MScMed)--University of Stellenbosch, 2006. / Bibliography. Also available via the Internet.
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Renal ischemia/reperfusion injury in diabetes : experimental studies in the rat /Melin, Jan, January 2002 (has links)
Diss. (sammanfattning) Uppsala : Univ., 2002. / Härtill 4 uppsatser.
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