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  • inflammation
  • These indicate that lipoxin A4 mitigates postresuscitation myocardial IRI in which anti-inflammation and suppression of NF-κB activation may play an important role. (springer.com)
  • cTnI
  • Some inflammatory factors (IL-1β, IL-6, TNF-α, and IL-10), NF-κB p65, infarct ratios, apoptotic index, cardiac troponin I (cTnI), hemodynamic and myocardial structures were measured or observed in different groups. (springer.com)
  • induce
  • However, when persistent or too intense, ERs will induce and activate ER proapoptosis fators such as CHOP, caspase-12, This study aimed to elucidate Ischaemic postconditioning (IPO) whether attenuates I/R injury by suppressing ER stress-induced apoptosis. (bmj.com)
  • pathophysiology
  • In this article, the pathophysiology of myocardial lRI and the emerging therapeutic strategies for protecting the heart from its detrimental effects are reviewed. (jci.org)
  • The pathophysiology and molecular mechanisms of reperfusion injury are complex and, regarding diagnosis, individual diagnostic techniques have been proposed but without a proper assessment of the relative values of these methods. (ebook-dl.com)
  • pretreatment
  • Rat cardiomyocytes were exposed to hypoxia-reoxygenation injury after pretreatment with dimethyl sulfoxide (vehicle), necrosis inhibitor (NecX), antioxidant (vitamin C) or apoptosis inhibitor (Z-VAD-fmk). (ahajournals.org)
  • inhibitor
  • Effect of a neutrophil elastase inhibitor (ONO-5046 Na) on ischemia/reperfusion injury using the left-sided heterotopic canine heart transplantation model," Journal of Heart and Lung Transplantation , vol. 20, no. 8, pp. 889-896, 2001. (hindawi.com)
  • hearts
  • The hearts were subjected to global ischaemia for 30 min followed by 60 min reperfusion. (bmj.com)
  • Hearts treated by IPO were subjected to 10 s episodes of 6 alternate myocardial ischaemia/reperfusion applied at the end of the 30 min ischaemic period. (bmj.com)
  • Isolated rat hearts in a Langendorff-preparation (n=9) were arrested by infusion of HTK cardioplegic solution and subjected to 30 min global ischemia followed by 60 min reperfusion (controls). (springer.com)
  • The CK release during the first 30 min of reperfusion was reduced from 312 ± 41 U·g −1 in control hearts to 195 ± 40 and 206 ± 37 U·g −1 in sevoflurane and desflurane treated hearts. (springer.com)
  • Isolated perfused guinea pig hearts were subjected to 30 min ischemia and 4 h reperfusion (control = CTL, n = 8). (springer.com)
  • However, the effects of the CAA0225 in in vivo hearts during ischaemia-reperfusion are unknown. (bmj.com)
  • Isolated male rat hearts, subjected to global ischemia of 25 minutes, were reperfused with low flow with or without sivelestat followed by a full flow reperfusion. (duhnnae.com)
  • vivo
  • We hypothesised that using CAA0225 in an in vivo mouse model of ischaemia-reperfusion would identify the role cathepsin-L plays during ischaemia-reperfusion. (bmj.com)
  • MICROVASCULAR OBSTRUCTION
  • Cardiac MRI analysis revealed a significant relationship between postCreperfusion effector T cell kinetics and microvascular obstruction (MVO), a component of I/R injury, raising the possibility of a mechanistic link. (bl.uk)
  • PI3K
  • Several studies have indicated that the PI3K/Akt signaling pathway plays a key role in cardiac protection against I/R injury ( 16 , 17 ). (scielo.br)