Aging Reduces the Cardioprotective Effect of Ischemic Preconditioning in the Rat Heart

Fenton, Richard A.; Dickson, Eric W.; Meyer, Theo E.; Dobson, James G.

doi:10.1006/jmcc.2000.1189

Cited by 135 publications

(95 citation statements)

References 11 publications

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“…1 and Table 2). This lack of an age-related decline in ischemic tolerance is at odds with many studies (1,14,22,25) but is in agreement with several others (12,20,21,24,29,35). In addition, two studies (6,32) have reported that aging from immaturity to mature adulthood results in greater I/R injury, but then tolerance improves from adulthood to senescence.…”

Section: Discussionsupporting

confidence: 87%

“…Cardiac function working heart with equal preload, afterload, and heart rate, the enhanced cardioprotection after exercise preconditioning was due to adaptations within the ventricle. Although several reports indicate that aging attenuates or abolishes the improved tolerance to I/R after ischemic preconditioning (1,2,12,20,24,29), those studies focused on the "early" stage of preconditioning, which does not require protein synthesis and lasts only 2-3 h after the preconditioning stimulus (5,19). In this regard, Abete et al (1) reported that a 6-wk swimming program restored the effectiveness of ischemic preconditioning in aged Wistar rats.…”

Section: Discussionmentioning

confidence: 99%

“…For example, several studies conclude that HSP70 expression after heat stress is impaired in the heart of aged animals (for a review, see Ref. 30), and the cardioprotective benefits induced by ischemic preconditioning are attenuated or abolished with age (2,12,20,24,29). Thus the purpose of this study was to determine the effect of age on exercise-induced protection against I/R and on changes in cardioprotective proteins.…”

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confidence: 99%

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Exercise improves postischemic function in aging hearts

Starnes

Taylor

Park

2003

American Journal of Physiology-Heart and Circulatory Physiology

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.-Exercise improves cardioprotection against ischemiareperfusion in young animals but has not been investigated in older animals, which represent the population most likely to suffer an ischemic event. Therefore, we sought to determine the effects of aging on exercise-induced cardioprotection. Young, middle-aged, and old (4, 12, and 21 mo old) male Fischer 344 rats ran 60 min at 70-75% of maximum oxygen consumption. Twenty-four hours postexercise, isolated perfused working hearts underwent 22.5 min of global ischemia and then 30 min of recovery (reperfusion). Compared with sedentary rats (n ϭ 8-9 rats/group), recovery of function (cardiac output ϫ systolic pressure) improved after exercise (n ϭ 9 rats/group) by 40% at 4 mo, 78% at 12 mo, and 59% at 21 mo. Exercise increased inducible heat shock protein 70 expression 105% at 4 mo but only 27% at 12 mo and 24% at 21 mo. Catalase activity progressively increased with age (P Ͻ 0.05) and was increased by exercise at 4 mo (26%) and 21 mo (19%). Manganese superoxide dismutase activity was increased by exercise only at 21 mo (45%). No exerciserelated change in any antioxidant enzyme was observed at 12 mo. We conclude that exercise can enhance cardioprotection regardless of age, but the cardioprotective protein phenotype changes with age.

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Exercise improves postischemic function in aging hearts

Starnes

Taylor

Park

2003

American Journal of Physiology-Heart and Circulatory Physiology

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“…The effect of aging on PC is unclear. Some studies [27,28,29] but not others [30] support the concept that the early PC response is absent in old animals. Aging abolishes the late phase of ischemia-induced PC in mice [31] but not the late phase of opioid-induced late PC in rats [32].…”

Section: Cox-2 Involvement In Pcmentioning

confidence: 99%

The late phase of preconditioning and its natural clinical application—gene therapy

Bolli

Tang

et al. 2007

Heart Fail Rev

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There is little doubt that the discovery of ischemic preconditioning (PC) has been one of the fundamental milestones in the field of ischemic biology in the past 20 years. The purpose of this article is to review the pathophysiology and molecular basis of the late phase of myocardial PC. The exploitation of late PC for the development of novel gene therapy strategies aimed at inducing a permanently preconditioned cardiac phenotype (prophylactic cardioprotection) will also be discussed. Deciphering the mechanism of late PC has not only conceptual interest but also a considerable therapeutic implications, since transfer of the genes that underlie late PC would be expected to replicate the salubrious effects of this response of the heart to stress.

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“…The aging heart is more susceptible to the damage induced by myocardial infarction, and most of the studies suggest that cardioprotection with ischemic or pharmacological conditioning becomes less effective (Boengler, Schulz, & Heusch, 2009; Fenton, Dickson, Meyer, & Dobson, 2000; Przyklenk, Maynard, Darling, & Whittaker, 2008; Schulman, Latchman, & Yellon, 2001). mPTP is thought to be a key factor in these processes, and the mechanism responsible for this loss of effectiveness may result from an activation of mPTP.…”

Section: Evidence For the Involvement Of Mptp Opening In Age‐associatmentioning

confidence: 99%

Mitochondria and aging: A role for the mitochondrial transition pore?

2018

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SummaryThe cellular mechanisms responsible for aging are poorly understood. Aging is considered as a degenerative process induced by the accumulation of cellular lesions leading progressively to organ dysfunction and death. The free radical theory of aging has long been considered the most relevant to explain the mechanisms of aging. As the mitochondrion is an important source of reactive oxygen species (ROS), this organelle is regarded as a key intracellular player in this process and a large amount of data supports the role of mitochondrial ROS production during aging. Thus, mitochondrial ROS, oxidative damage, aging, and aging‐dependent diseases are strongly connected. However, other features of mitochondrial physiology and dysfunction have been recently implicated in the development of the aging process. Here, we examine the potential role of the mitochondrial permeability transition pore (mPTP) in normal aging and in aging‐associated diseases.

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Aging Reduces the Cardioprotective Effect of Ischemic Preconditioning in the Rat Heart

Cited by 135 publications

References 11 publications

Exercise improves postischemic function in aging hearts

Exercise improves postischemic function in aging hearts

The late phase of preconditioning and its natural clinical application—gene therapy

Mitochondria and aging: A role for the mitochondrial transition pore?

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