Postischemic Reperfusion Injury Can Be Attenuated by Oxygen Tension Control

Kaneda, Tomoya; Ku, Kwansong; Inoue, Takehiro; Onoe, Masahiko; Oku, Hirosuke

doi:10.1253/jcj.65.213

Cited by 48 publications

(32 citation statements)

References 17 publications

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“…Among various interventions aimed at reducing the deleterious effects of reperfusion, several authors used modifications of the conditions of reperfusion (33). Limiting Ca 2ϩ overload, scavenging oxygen-derived free radicals, reducing arterial PO 2 , or applying a transient acidosis in the early minutes of reperfusion can improve functional recovery after an ischemic insult (8,10,24,27). In the present study, we reported that low-pressure reperfusion reduced infarct size and improved functional recovery after a prolonged global normothermic ischemia in the rat heart.…”

Section: Discussionmentioning

confidence: 99%

Low-pressure reperfusion alters mitochondrial permeability transition

Bopassa

Martineau

Gateau-Roesch

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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We hypothesized that low-pressure reperfusion may limit myocardial necrosis and attenuate postischemic contractile dysfunction by inhibiting mitochondrial permeability transition pore (mPTP) opening. Male Wistar rat hearts (n = 36) were perfused according to the Langendorff technique, exposed to 40 min of ischemia, and assigned to one of the following groups: 1) reperfusion with normal pressure (NP = 100 cmH(2)O) or 2) reperfusion with low pressure (LP = 70 cmH(2)O). Creatine kinase release and tetraphenyltetrazolium chloride staining were used to evaluate infarct size. Modifications of cardiac function were assessed by changes in coronary flow, heart rate (HR), left ventricular developed pressure (LVDP), the first derivate of the pressure curve (dP/dt), and the rate-pressure product (RPP = LVDP x HR). Mitochondria were isolated from the reperfused myocardium, and the Ca(2+)-induced mPTP opening was measured using a potentiometric approach. Lipid peroxidation was assessed by measuring malondialdehyde production. Infarct size was significantly reduced in the LP group, averaging 17 +/- 3 vs. 33 +/- 3% of the left ventricular weight in NP hearts. At the end of reperfusion, functional recovery was significantly improved in LP hearts, with RPP averaging 10,392 +/- 876 vs. 3,969 +/- 534 mmHg/min in NP hearts (P < 0.001). The Ca(2+) load required to induce mPTP opening averaged 232 +/- 10 and 128 +/- 16 microM in LP and NP hearts, respectively (P < 0.001). Myocardial malondialdehyde was significantly lower in LP than in NP hearts (P < 0.05). These results suggest that the protection afforded by low-pressure reperfusion involves an inhibition of the opening of the mPTP, possibly via reduction of reactive oxygen species production.

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Section: Discussionmentioning

confidence: 99%

Low-pressure reperfusion alters mitochondrial permeability transition

Bopassa

Martineau

Gateau-Roesch

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…Many attempts to reduce the extent of myocardial reperfusion injury have been made over the past decades, [9][10][11][12][13][14][15] with most of these efforts directed at lowering the risk posed by certain injurious factors and potentiating various aspects of cardioprotection relating to ischemic duration, oxygen free radicals, pro-inflammatory cytokines, preconditioning, and oxygen tension control. In addition, Minatoguci et al reported that caspase-dependent DNA fragmentation, which is present in infarcted myocytes, did not have an infarct-size reducing effect.…”

Section: Discussionmentioning

confidence: 99%

Participation of Caspase-3-Like Protease in Necrotic Cell Death of Myocardium During Ischemia-Reperfusion Injury in Rat Hearts.

Naka

Sawa

Nishimura

et al. 2003

Circ J

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This experimental study was designed to determine if caspase-3-like protease is activated during a short period of ischemia - reperfusion (I-R) that did not induce apoptosis, and whether protease-3-protease inhibitor could prevent myocardial I-R injury, especially necrotic cell death. The subjects were 20 isolated rat hearts; 10 were pretreated for 20 min with 100 micromol/L of the protease-3-protease inhibitor, peptide antagonist Asp-Glu-Val-Asp-CHO (DEVD) (Group D), and compared with the 10 no-pretreated hearts (Group C). The hearts were then subjected to 20, 30, 45, and 60 min of normothermic global ischemia followed by 30 min of reperfusion. Caspase-3-like protease was significantly elevated after 45 min and 60 min in ischemic hearts. Group D had reduced levels of caspase-3-like protease activity after 45 min and 60 min (302+/-58%, 378+/-69% of pre-ischemic control, respectively), as compared with Group C (542+/-74%, 689+/-85%, respectively) (p<0.05, p<0.05, respectively). Histological analysis also demonstrated a decrease in cellular damage in Group D, as the count ratio of necrotic cells with total cardiomyocytes was 38%, as compared with 78% in the control group (p<0.05). Caspase-3-like protease participated in I-R injury in rat hearts and inhibition of this protease resulted in a reduction of necrotic cell death.

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“…We reported recently that maintaining a more physiologic PO2 during reperfusion following ischemia attenuates reperfusion injury. 19 The mechanism of reperfusion injury is, in part, attributed to calcium overload 2,3 and there is experimental evidence of calcium pump dysfunction in reperfusion injury. 3,20 Although calcium antagonists were initially designed as antianginal agents, they were found to preserve the ischemic myocardium 8,9 and have been tested extensively in regard to myocardial protection.…”

Section: Discussionmentioning

confidence: 99%