Myocardial protective effect and its mechanism of leukocyte-depleted reperfusion in neonatal rabbit hearts

Sawa, Yoshiki; Nakano, Susumu; Shimazaki, Yasuhisa; Nishimura, Motonobu; Kuratani, Tohru; Matsuda, Hikaru

doi:10.1016/0003-4975(94)91919-4

Cited by 14 publications

(6 citation statements)

References 16 publications

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“…WBC‐reduced blood components have been demonstrated to prevent the recurrence of febrile nonhemolytic transfusion reactions, to reduce the risk of alloimmunization to HLAs in selected patients, and to reduce the risk of CMV in selected patients 20,126‐128 . They have also been shown to prevent of postcardiopulmonary bypass lung injury 129‐132 . Many institutions have chosen to use WBC‐reduced blood components, in lieu of the traditional seronegative components, when CMV reduced‐risk components are indicated.…”

Section: Wbc‐reduced Blood Componentsmentioning

confidence: 99%

Guidelines for assessing appropriateness of pediatric transfusion

2002

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Section: Wbc‐reduced Blood Componentsmentioning

confidence: 99%

Guidelines for assessing appropriateness of pediatric transfusion

2002

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“…In addition, it is apparent that dysfunction of endothelial cells may promote the migration of neutrophils and other blood-derived components. 19,[31][32][33] As migration of neutrophils and/or macrophages may be responsible for the development of myocardial reperfusion injury and atherosclerosis, it is critical to maintain the endothelium to prevent cardiovascular disease. Recently, a new concept, that regulation of cell death by apoptosis may be an important determinant of vessel structure, has been postulated.…”

Section: Matsushita Et Al Importance Of Nf-b In Hypoxia-induced Apoptmentioning

confidence: 99%

“…The fact that hypoxia induced endothelial cell death through NF-B activation is extremely important, given that migration of leukocytes/neutrophils plays a pivotal role in the development of myocardial reperfusion injury and atherosclerosis. 19,[31][32][33] Disruption of endothelium in response to hypoxia may be responsible for the pathogenesis of cardiovascular disease. Indeed, the effective blockade of a series of cytokine and adhesion molecule genes during the initial acute phase of reperfusion by in vivo transfection of NF-B decoy ODNs results in a subsequent inhibitory effect on the development of myocardial infarction.…”

Section: Matsushita Et Al Importance Of Nf-b In Hypoxia-induced Apoptmentioning

confidence: 99%

Hypoxia-Induced Endothelial Apoptosis Through Nuclear Factor-κB (NF-κB)–Mediated bcl-2 Suppression

Matsushita

Morishita

Nata

et al. 2000

Circulation Research

165

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The transcription factor nuclear factor-kappaB (NF-kappaB) plays a pivotal role in the coordinated transactivation of cytokine and adhesion molecule genes involved in endothelial activation. Although recent reports have documented the contribution of NF-kappaB to apoptosis, it is still controversial. Especially, the role of NF-kappaB in endothelial apoptosis is largely unknown. Hypoxia significantly induced human aortic endothelial cell death and apoptosis in a time-dependent manner (P<0.01), accompanied by NF-kappaB activation. Decrease in total cell number and increase in apoptotic cells induced by hypoxia were significantly attenuated by NF-kappaB decoy, but not by scrambled decoy, oligodeoxynucleotides (ODNs) (P<0.01). Increase in DNA fragmentation induced by hypoxia was also significantly inhibited by NF-kappaB decoy ODNs as compared with scrambled decoy ODNs (P<0.01). Moreover, transfection of NF-kappaB decoy ODNs resulted in a significant decrease in caspase-3-like activity, which is a common pathway for apoptosis, compared with scrambled decoy ODNs. Importantly, transfection of NF-kappaB decoy ODNs significantly increased protein of bcl-2, an inhibitor of apoptosis, and did not alter bax, a promoter of apoptosis, thereby resulting in a significant increase in the ratio of bcl-2 to bax (P<0.01). bcl-2 mRNA was also decreased by hypoxia, whereas transfection of NF-kappaB decoy ODNs significantly attenuated decrease in bcl-2 mRNA. These results demonstrate that activation of NF-kappaB by hypoxia induced endothelial apoptosis in a bcl-2-dependent manner. The importance of NF-kappaB in endothelial apoptosis was confirmed by the observation that pyrrolidine dithiocarbamate, a potent NF-kappaB inhibitor, prevented endothelial apoptosis, caspase 3-like activity, and bcl-2 downregulation induced by hypoxia. To test this hypothesis in vivo, we transfected NF-kappaB decoy ODNs into rat intact carotid artery after reperfusion injury. Reperfusion injury was associated with a significant increase in endothelial apoptosis at 24 hours, whereas NF-kappaB decoy ODN treatment markedly decreased terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL)-positive endothelial cells at 24 hours after reperfusion (P<0.01). Here, using synthetic double-stranded DNA with high affinity for NF-kappaB as a decoy approach, we demonstrated that activation of NF-kappaB by hypoxia caused aortic endothelial cell death and apoptosis through the suppression of bcl-2. NF-kappaB-mediated endothelial apoptosis induced by hypoxia may be involved in the pathogenesis of endothelial dysfunction observed in cardiovascular ischemic diseases.

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“…[11][12][13] Numerous animal studies demonstrated that, when leukocytes were removed from the circulating blood, reperfusion injury could be ameliorated and better transplant organ preservation/survival obtained. [14][15][16][17][18][19][20][21][22][23][24] Bando et al 18 noted that leukocyte reduction, in a dog model of 'routine' CPB, resulted in a significant reduction in free radical generation and substantially preserved pulmonary function. In a bovine heart-lung transplantation experiment, 21 only 50% of control animals survived transplantation after more than 2 h, compared to 100% of the leukocyte-reduced animals.…”

Section: Leukocyte Reduction In Animal Modelsmentioning

confidence: 99%

Leukocyte reduction in cardiovascular surgery

2001

Perfusion

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Myocardial protective effect and its mechanism of leukocyte-depleted reperfusion in neonatal rabbit hearts

Cited by 14 publications

References 16 publications

Guidelines for assessing appropriateness of pediatric transfusion

Guidelines for assessing appropriateness of pediatric transfusion

Hypoxia-Induced Endothelial Apoptosis Through Nuclear Factor-κB (NF-κB)–Mediated bcl-2 Suppression

Leukocyte reduction in cardiovascular surgery

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