Prenatal diet determines susceptibility to cardiac ischaemia–reperfusion injury following treatment with diethylmaleic acid and N-acetylcysteine

Elmes, M; McMullen, Sarah; Gardner, David; Langley‐Evans, Simon C.

doi:10.1016/j.lfs.2007.10.022

Cited by 17 publications

(17 citation statements)

References 32 publications

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“…Furthermore, changes in cardiac MnSOD gene expression are linked to functional outcomes, since reductions in MnSOD gene expression are closely matched by reductions in enzyme activity during congestive heart failure in rodents (10). It is also well established that reduced antioxidant defenses in the heart leave it vulnerable to augmented ischemia-reperfusion injury (6,7). Therefore, the findings of impaired MnSOD gene expression in the present study highlight the potential susceptibility of the heart to reduced antioxidant defenses following growth restriction at a much later age of life.…”

Section: Discussionmentioning

confidence: 99%

Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner

Wadley

McConell

Goodman

et al. 2013

Physiological Genomics

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Section: Discussionmentioning

confidence: 99%

Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner

Wadley

McConell

Goodman

et al. 2013

Physiological Genomics

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“…In addition, recent work indicates that prenatal exposure to hypoxia or cocaine inhibit the infarct-sparing effects of ischemic preconditioning later in adult life by a mechanism involving irreversible fetal reprogramming of protein kinase C epsilon expression (561, 626). A large number of studies have provided evidence that adult animals that were exposed to hypoxia, glucocorticoids or maternal low protein diet or obesity in fetal life demonstrate an increased susceptibility to I/R in the early postnatal period (108a, 211a, 211b, 268a, 268b, 327a, 390a, 491a, 491b, 626, 626a, 626b, 660, 675b, 676a, 782, 863a, 864a, 864b, 864c). These results support the notion that a fetus developing in adverse conditions becomes an adult who is susceptible to enhanced I/R injury.…”

Section: Fetal Programming Transgenerational Inheritance and Suscepmentioning

confidence: 99%

Ischemia/Reperfusion

Kalogeris

Baines

Krenz

et al. 2016

Comprehensive Physiology

648

565

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Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload). Cell volume regulatory mechanisms are also disrupted by the lack of ATP, which can induce lysis of organelle and plasma membranes. Reperfusion, although required to salvage oxygen-starved tissues, produces paradoxical tissue responses that fuel the production of reactive oxygen species (oxygen paradox), sequestration of proinflammatory immunocytes in ischemic tissues, endoplasmic reticulum stress, and development of postischemic capillary no-reflow, which amplify tissue injury. These pathologic events culminate in opening of mitochondrial permeability transition pores as a common end-effector of ischemia/reperfusion (I/R)-induced cell lysis and death. Emerging concepts include the influence of the intestinal microbiome, fetal programming, epigenetic changes, and microparticles in the pathogenesis of I/R. The overall goal of this review is to describe these and other mechanisms that contribute to I/R injury. Because so many different deleterious events participate in I/R, it is clear that therapeutic approaches will be effective only when multiple pathologic processes are targeted. In addition, the translational significance of I/R research will be enhanced by much wider use of animal models that incorporate the complicating effects of risk factors for cardiovascular disease.

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“…Elmes et al [20] found impaired recovery of left ventricular developed pressure after an ischemia-reperfusion injury. Pretreatment of the adult rats with N-acetylcysteine improved recovery following the ischemic injury [21] . N-acetylcysteine enhances the antioxidant capacity of the heart by increasing glutathione production, which is then available to react with, and detoxify, endogenously produced hydrogen peroxide.…”

Section: Discussionmentioning

confidence: 91%

“…Previous studies utilizing the STZ rat model of gestational diabetes have shown that maternal and fetal blood levels of 8-isoprostaglandin F 2alpha , a sensitive marker for lipid peroxidation, are significantly increased above control levels [19] . Enhanced susceptibility to oxidative stress in adult offspring programmed by exposure to an adverse intrauterine environment has been demonstrated using a maternal low-protein diet method of intrauterine stress [20,21] . Elmes et al [20] found impaired recovery of left ventricular developed pressure after an ischemia-reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

“…N-acetylcysteine enhances the antioxidant capacity of the heart by increasing glutathione production, which is then available to react with, and detoxify, endogenously produced hydrogen peroxide. Thus, improvement of cardiac function with supplemental N-acetylcysteine suggested that enhancing the intrinsic antioxidant status of the cardiac tissues could attenuate the greater ischemia-reperfusion injury in the programmed hearts [21] .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Programming of Adult Cardiovascular Disease following Exposure to Late-Gestation Hyperglycemia

Agoudemos¹,

Reinking²,

Koppenhafer³

et al. 2011

Neonatology

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Background: In utero exposure to hyperglycemia is becoming increasingly prevalent as the number of women entering pregnancy with type II diabetes, or developing gestational diabetes, increases. Both animal studies and epidemiologic investigations have found cardiovascular abnormalities in adult offspring of hyperglycemic mothers (OHM). Objective: We hypothesized that adult OHM would have abnormal cardiac function in vivo and increased susceptibility to ischemia. Methods: Pregnant rats were made diabetic on day 12 of gestation. Serum glucose was monitored twice daily and insulin provided to maintain serum glucose at 200–400 mg/dl. Offspring were fostered to normal mothers after birth. Adult OHM were studied at 8–10 months of age with echocardiography to assess in vivo cardiac function and isolated hearts to determine the response to ischemia. Results: Echocardiography found significant diastolic dysfunction in male OHM compared to male controls. In isolated hearts, baseline cardiac function and left ventricular compliance was significantly diminished in male OHM compared to controls. Ischemia caused a significant decline in heart function in controls and female OHM, while function in male OHM remained unchanged. Conclusions: Adult male OHM demonstrate programmed cardiac dysfunction. Given the growing number of pregnancies complicated by hyperglycemia, additional assessment of cardiac function of adults born to diabetic mothers may be warranted.

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Prenatal diet determines susceptibility to cardiac ischaemia–reperfusion injury following treatment with diethylmaleic acid and N-acetylcysteine

Cited by 17 publications

References 32 publications

Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner

Growth restriction in the rat alters expression of metabolic genes during postnatal cardiac development in a sex-specific manner

Ischemia/Reperfusion

Programming of Adult Cardiovascular Disease following Exposure to Late-Gestation Hyperglycemia

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