Changes in Ischemic Tolerance and Effects of Ischemic Preconditioning in Middle-aged Rat Hearts

Tani, Masato; Suganuma, Yukako; Hasegawa, Hiroshi; Shinmura, Ken; Hayashi, Yujiro; Guo, Xiao Dong; Nakamura, Yoshiro

doi:10.1161/01.cir.95.11.2559

Cited by 102 publications

(60 citation statements)

References 33 publications

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“…The efficacy of IPC has been reported to be decreased or lost in senescent patients (2,28) and in aged animals (1,40). We have also found that myocardial ischemic tolerance begins to decrease and that IPC is impaired in middle-aged (12 mo old) rats (46).…”

Section: Effect Of Cr On Myocardial Ischemia-reperfusion Injury and Ipcsupporting

confidence: 53%

“…Rats of 52 wk of age were anesthetized with an intraperitoneal injection of pentobarbital sodium (40 mg/kg). Hearts were excised quickly and perfused with modified Krebs-Henseleit buffer gassed with 95% O 2-5% CO2 at 37°C according to the Langendorff procedure (42,45,46). The coronary perfusion pressure was maintained at 70 mmHg.…”

Section: Methodsmentioning

confidence: 99%

“…Pacing was turned off during global ischemia and turned on 10, 20, and 30 min after reperfusion to measure the recovery of LV function. Indexes of LV function [LV systolic pressure (LVSP); LV developed pressure (LVDP; equal to LVSP Ϫ LVEDP); and LV peak positive and negative dP/dt] were recorded as previously described (42,45,46).…”

Section: Methodsmentioning

confidence: 99%

“…In addition, several experimental and clinical investigations have addressed the issue of whether IPC occurs in aged hearts (1,2,28,40,46). The efficacy of IPC has been reported to be decreased or lost in senescent patients (2,28) and in aged animals (1,40).…”

Section: Effect Of Cr On Myocardial Ischemia-reperfusion Injury and Ipcmentioning

confidence: 99%

“…Hearts from senescent animals are more susceptible to ischemia than those from young animals (7,20,45). Recently, a number of investigators have demonstrated that the cardioprotective effect of ischemic preconditioning (IPC) is impaired in aged animals (1,2,28,40,46). Aging also loses the cardioprotection afforded by postconditioning (8).…”

mentioning

confidence: 99%

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Impact of 6-mo caloric restriction on myocardial ischemic tolerance: possible involvement of nitric oxide-dependent increase in nuclear Sirt1

Shinmura

Tamaki

Bolli

2008

American Journal of Physiology-Heart and Circulatory Physiology

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114

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Ischemic tolerance decreases with aging, and the cardioprotective effect of ischemic preconditioning (IPC) is impaired in middle-aged animals. We have demonstrated that short-term caloric restriction (CR) improves myocardial ischemic tolerance in young and old animals via the activation of adiponectin-AMP-activated protein kinase (AMPK)-mediated signaling. However, it is unknown whether prolonged CR confers cardioprotection in a similar manner. Furthermore, little is known regarding the myocardial expression of silent information regulator 1 (Sirt1; which reportedly mediates various aspects of the CR response) with prolonged CR. Thus, 6-mo-old male Fischer-344 rats were randomly divided into ad libitum (AL) and CR groups. Six months later, isolated perfused hearts were subjected to 25 min of global ischemia followed by 120 min of reperfusion with or without IPC. CR improved the recovery of left ventricular function and reduced infarct size after ischemiareperfusion and restored the IPC effect. Serum adiponectin levels increased, but myocardial levels of total and phosphorylated AMPK did not change with prolonged CR. Total levels of Sirt1 did not change with CR; however, in the nuclear fraction, CR significantly increased Sirt1 and decreased acetyl-histone H3. Eleven rats from each group were given N-nitro-L-arginine methyl ester in their drinking water for 4 wk before death. In these hearts, chronic inhibition of nitric oxide synthase prevented the increase in nuclear Sirt1 content by CR and abrogated CR-induced cardioprotection. These results demonstrate that 1) prolonged CR improves myocardial ischemic tolerance and restores the IPC effect in middle-aged rats and 2) CR-induced cardioprotection is associated with a nitric oxidedependent increase in nuclear Sirt1 content. aging; myocardial ischemia; nutrition; preconditioning; reperfusion injury; silent information regulator 1

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Section: Effect Of Cr On Myocardial Ischemia-reperfusion Injury and Ipcsupporting

confidence: 53%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Effect Of Cr On Myocardial Ischemia-reperfusion Injury and Ipcmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Impact of 6-mo caloric restriction on myocardial ischemic tolerance: possible involvement of nitric oxide-dependent increase in nuclear Sirt1

Shinmura

Tamaki

Bolli

2008

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

114

View full text Add to dashboard Cite

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Myocardial Preconditioning in the Experimental Model: A New Strategy to Improve Myocardial Protection

Rosenkranz¹,

Feng²,

Li³

2003

Myocardial Protection

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Oxidative stress resistance through blocking Hsp60 translocation followed by SAPK/JNK inhibition in aged human diploid fibroblasts

Lee

Bhattarai

Kim

et al. 2008

Cell Biochemistry & Function

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The stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) pathway is a well-known senescence-related stress activated protein kinase. Multiple environmental stresses induce programmed cell death, such as apoptosis. Normal human diploid fibroblast (HDF) cells have a limited life span in vitro, halting proliferation after a fixed number of cell divisions. Aged passage HDF showed resistance to oxidative stress involving heat shock proteins (Hsp60) through a mechanism involving the translocation of Hsp60 from the mitochondria to the cytosol. The present study showed that the translocation of Hsp60 from the mitochondria to the cytosol followed by high levels of p-SAPK/JNK activation as a result of oxidative stress was observed in the young cells only. The inhibition of SAPK/JNK activation by SP600125 under oxidative stress almost completely blocked the translocation of Hsp60 in both young and aged cells. This suggests that aged HDF cells are resistant to oxidative stress by blocking the translocation of Hsp60 from the mitochondria to the cytosol followed by SAPK/JNK inhibition. Overall, the mechanism of resistance by oxidative stress in aged cells is induced by blocked of the translocation of Hsp60 followed by SAPK/JNK inactivation.

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Changes in Ischemic Tolerance and Effects of Ischemic Preconditioning in Middle-aged Rat Hearts

Abstract: These results indicate that hearts became more vulnerable to ischemia with age and that the beneficial effects of preconditioning were reversed in middle-aged rat hearts.

Cited by 102 publications

References 33 publications

Impact of 6-mo caloric restriction on myocardial ischemic tolerance: possible involvement of nitric oxide-dependent increase in nuclear Sirt1

Impact of 6-mo caloric restriction on myocardial ischemic tolerance: possible involvement of nitric oxide-dependent increase in nuclear Sirt1

Myocardial Preconditioning in the Experimental Model: A New Strategy to Improve Myocardial Protection

Oxidative stress resistance through blocking Hsp60 translocation followed by SAPK/JNK inhibition in aged human diploid fibroblasts

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