Mechanisms of myocardial reperfusion injury

Park, James; Lucchesi, Benedict R.

doi:10.1016/s0003-4975(99)01073-5

Cited by 287 publications

(204 citation statements)

References 21 publications

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“…Platelet products, e.g. TXA 2 and serotonin, may exacerbate microcirculatory spasm, leading to further thrombosis and sluggish coronary flow [4]. (iii) TMP inhibits the L-type Ca 2+ currents in rat ventricular myocytes [30].…”

Section: Discussionmentioning

confidence: 99%

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Tetramethylpyrazine induces heme oxygenase-1 expression and attenuates myocardial ischemia/reperfusion injury in rats

et al. 2006

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The accumulation of oxygen free radicals and activation of neutrophils are strongly implicated as pathophysiological mechanisms mediating myocardial ischemia/reperfusion injury. Heme oxygenase-1 (HO-1) has been reported to play a protective role in oxidative tissue injuries. In this study, the cardioprotective activity of tetramethylpyrazine (TMP), an active ingredient of Chinese medicinal herb Ligusticum wallichii Franchat, was evaluated in an open-chest anesthetized rat model of myocardial ischemia/reperfusion injury. Pretreatment with TMP (5 and 10 mg/kg, i.v.) before left coronary artery occlusion significantly suppressed the occurrence of ventricular fibrillation. After 45 min of ischemia and 1 h of reperfusion, TMP (5 and 10 mg/kg) caused a significant reduction in infarct size and induced HO-1 expression in ischemic myocardium. The HO inhibitor ZnPP (50 lg/rat) markedly reversed the anti-infarct action of TMP.

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Section: Discussionmentioning

confidence: 99%

“…The oxygen free-radical system has been implicated in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury [1,2]. The oxygen radicals are generated by injured myocytes and endothelial cells in the ischemic zone, as well as neutrophils that enter the ischemic zone, and become activated on reperfusion.…”

Section: Introductionmentioning

confidence: 99%

Tetramethylpyrazine induces heme oxygenase-1 expression and attenuates myocardial ischemia/reperfusion injury in rats

et al. 2006

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“…The levels of serum CK-MB were significantly elevated after PCI, but values were still within the normal range, indicating that PCI induced a low-grade injury but not necrosis of the myocardium. The elevation of CK-MB after PCI may be due to a burst of oxygen free radicals, calcium overload, and activation of leukocytes and platelets (Piper et al, 1998;Ambrosio and Tritto, 1999;Park and Lucchesi, 1999). In addition, a limitation of blood flow to heart tissue caused by coronary angioplasty may lead to partial leakage of enzyme from the myocardium.…”

Section: Fig 4 Associations Between P-selectin (A)/mg (B) and Adversmentioning

confidence: 99%

“…However, late restenosis is still quite frequent despite successful angioplasty (Serruys et al, 1988;Pendyala et al, 2008). Another risk is ischemia-reperfusion injury of the myocardium occurring in the immediate stage after successful angioplasty, despite extensive efforts to reduce its incidence (Park and Lucchesi, 1999). Restenosis and ischemia-reperfusion injury of the myocardium may be viewed as multifactorial responses of the vascular tissue to balloon and stent injury and reflow, which include endothelial dysfunction, platelet activation, disorder of electrolytes, and clotting-plasminogen imbalance (Monnink et al, 2003;Bhoday et al, 2006;Ma et al, 2006;Thanyasiri et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Temporal changes in circulating P-selectin, plasminogen activator inhibitor-1, magnesium, and creatine kinase after percutaneous coronary intervention

Ying

Xiang

Lü

et al. 2010

J. Zhejiang Univ. Sci. B

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Abstract:Objective: This study aims to determine the mechanisms underlying restenosis and ischemia-reperfusion injury of the myocardium after percutaneous coronary intervention (PCI). Methods: The present study examined serial changes (5 min, 30 min, 2 h, 6 h, and 24 h after PCI) in circulating P-selectin, plasminogen activator inhibitor-1 (PAI-1), magnesium (Mg), and creatine kinase-myocardial band fraction (CK-MB) levels, which may be associated with restenosis and myocardial injury in patients undergoing PCI. The occurrence rates of major adverse cardiovascular events were collected over a six-month follow-up. Results: PCI induced an early elevation of P-selectin, which correlated positively with the inflation pressure used in the PCI procedure. PCI also caused a significant and sustained decrease in serum Mg in PCI patients, without an effect on PAI-1. An increase in CK-MB was observed in PCI patients, although values were within normal reference range. In addition, elevated P-selectin and decreased Mg measured shortly after the coronary angioplasty procedure were associated with recurrent treatment and heart failure, respectively. Conclusions: Our study demonstrates that PCI induces temporal changes of P-selectin, Mg, and CK-MB, which may be involved in restenosis and ischemia-reperfusion injury. These findings highlight the need for using antiplatelet therapy and Mg to reduce the risks associated with PCI.

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“…The immunoinflammatory system also seems to be involved in such alterations in the reperfusion period by means of arachidonic acid products [17][18][19]. Ventricular fibrillation after the return of coronary circulation is a common event, and it is not often recognized as a problem.…”

Section: -Electromicrography Of Cardiac Muscle -M-mitochondria; G-glymentioning

confidence: 99%

Análise ultra-estrutural do miocárdio usando solução cardioplégica cristalóide com e sem procaína em pacientes submetidos à troca valvar aórtica

Dussin¹,

Moura²,

Gib³

et al. 2008

Rev Bras Cir Cardiovasc

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Análise ultra-estrutural do miocárdio usando solução cardioplégica cristalóide com e sem procaína em pacientes submetidos à troca valvar aórtica Ultrastructural study of the myocardium using cardioplegic crystalloid solution with and without procaine in patients undergoing aortic valve replacement Abstract Objective: The aim of this study was to assess whether the presence of procaine in crystalloid cardioplegic solution increases myocardial protection at the ultra structural level.Methods: Eighteen patients that underwent aortic valve replacement in the Hospital de Clínicas de Porto Alegre over a 10-month period were studied. They were randomly allocated into two groups: group A -eight patients receiving cardioplegia without procaine; group B -ten patients receiving cardioplegia with procaine. Myocardial biopsies were performed in three different periods: 1st -before ischemic arrest, 2nd -at the end of ischemic arrest, and 3rd -15 minutes after reperfusion.Results: The ultra structural analysis comparing the groups in the three moments did not show any statistically significant difference. The mean score in group A at moment I, II and III was 0.1 ± 0.2; 0.4 ± 0.3; 0.4 ± 0.4, and group B 0.2 ± 0.2; 0.4 ± 0.3; 0.7 ± 0.2. Comparative analysis of CK-MB was similar. The spontaneous return to sinus rhythm after aortic declamping in group B occurred in 70% and in group A 12.5% (p=0.024).Conclusion: Both cardioplegic solutions tested were equally effective in myocardial preservation, and we could not demonstrate at the ultrastructural level any benefit when procaine was added. The spontaneous return to sinus rhythm after aortic declamping was significantly greater when procaine was added. 390DUSSIN, LH ET AL -Ultrastructural study of the myocardium using cardioplegic crystalloid solution with and without procaine in patients undergoing aortic valve replacement Bras Cir Cardiovasc 2008; 23(3): 389-395 Rev

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Mechanisms of myocardial reperfusion injury

Cited by 287 publications

References 21 publications

Tetramethylpyrazine induces heme oxygenase-1 expression and attenuates myocardial ischemia/reperfusion injury in rats

Tetramethylpyrazine induces heme oxygenase-1 expression and attenuates myocardial ischemia/reperfusion injury in rats

Temporal changes in circulating P-selectin, plasminogen activator inhibitor-1, magnesium, and creatine kinase after percutaneous coronary intervention

Análise ultra-estrutural do miocárdio usando solução cardioplégica cristalóide com e sem procaína em pacientes submetidos à troca valvar aórtica

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