2000
DOI: 10.1097/00024382-200013010-00012
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Myocardial Reperfusion: Leukocyte Accumulation in the Ischemic and Remote Non-Ischemic Regions

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Cited by 8 publications
(7 citation statements)
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“…On the other hand, reperfusion leads to further cardiomyocyte injury (lethal reperfusion injury), with effects ranging from activation of ROS to increases in Ca 2+ overload or stimulation of the inflammatory cascade and can have deleterious effects on the already injured myocardium [56,57]. The main culprits of this action are believed to be the leukocytes [58], as well as endothelial cells that are activated by various proinflammatory cytokines (IL-6, IL-8, TNF-α) and the complement system (C5a/C5b mainly) [59]. Lastly, various adaptations of the I/R protocol have been investigated (involving pre-and post-conditioning) and have shown to protect from the I/R injury, with anti-inflammatory effects forming the basis of this protective action.…”
Section: And Wound Healingmentioning
confidence: 99%
“…On the other hand, reperfusion leads to further cardiomyocyte injury (lethal reperfusion injury), with effects ranging from activation of ROS to increases in Ca 2+ overload or stimulation of the inflammatory cascade and can have deleterious effects on the already injured myocardium [56,57]. The main culprits of this action are believed to be the leukocytes [58], as well as endothelial cells that are activated by various proinflammatory cytokines (IL-6, IL-8, TNF-α) and the complement system (C5a/C5b mainly) [59]. Lastly, various adaptations of the I/R protocol have been investigated (involving pre-and post-conditioning) and have shown to protect from the I/R injury, with anti-inflammatory effects forming the basis of this protective action.…”
Section: And Wound Healingmentioning
confidence: 99%
“…This multifactorial "no-reflow" phenomenon is the consequence of severe ischemic damage to the microvasculature, 22 resulting in its obstruction at the moment of reperfusion 23 from capillary compression by myocardial edema, 24 myocardial ischemic contracture, 25 direct ischemic microvascular injury with endothelial cell swelling, 26 and an increased vasomotor tone. 27 Microvascular obstruction by erythrocyte and leukocyte plugging 28 or platelet aggregation 29 also seems to participate in the development of no-reflow, which influences infarct size and CBF during reperfusion. 30 In our study, the CBF and peak hyperemia CBF during reperfusion were lower in the animals with a decreased ABP than in animals with a stable ABP during reperfusion.…”
Section: Reperfusion Injury and Postischemic Cbfmentioning
confidence: 99%
“…The role of the circulating neutrophil in reperfusion injury has been the subject of much investigation. It is well‐documented that leukocyte accumulation is enhanced preferentially in areas of ischemia/reperfusion (I/R) 3–6 . The addition of neutrophils during reperfusion following cardiac ischemia has shown increases in myocyte injury 7,8 as well as diminished contractile function 9,10 .…”
Section: Introductionmentioning
confidence: 99%