Time-course of cardiac troponin I release from isolated perfused rat hearts during hypoxia/reoxygenation and ischemia/reperfusion

Bertinchant, Jean-Pierre; Polge, Anne; Robert, E; Sabbah, Nadia; Fabbro‐Peray, Pascale; Poirey, Sophie; Laprade, Michel; Pau, Bernard; Juan, Jean-Marie; Balì, Jean-Pierre; Coussaye, Jean-Emmanuel de La; Dauzat, M.

doi:10.1016/s0009-8981(99)00029-7

Cited by 12 publications

(10 citation statements)

References 25 publications

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“…cTnI peaked 1 min after reperfusion but did not return to baseline values and cTnI concentrations in the effluent increased throughout the reperfusion period by using isolated and Langendorff-perfused rat hearts model [31]. cTnI degradation during (I/R) involves both cleavage of cTnI and cross-linking between the troponin complex elements.…”

Section: Discussionmentioning

confidence: 99%

“…One study explained that treatment with DITPA attenuates the acute inflammatory response following myocardial ischemia by reducing inflammatory mediators, IL-6 [31]. Another study revealed that inflammatory cytokines were inversely correlated with serum concentrations of thyroid hormones during pediatric cardiac surgery [40], so the treatment with DITPA might result in reducing levels of TNF- α and IL-1 β in cardiac tissues.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Thyroid Hormone Analogue and a Leukotrienes Pathway-Blocker on Reperfusion Injury Attenuation after Heart Transplantation

2013

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Background. Global myocardial ischemia reperfusion injury after heart transplantation is believed to impair graft function and aggravate both acute and chronic rejection episodes. Objectives. To assess the possible protective potential of MK-886 and 3,5-diiodothyropropionic acid DITPA against global myocardial ischemia reperfusion injury after heart transplantation. Materials and Methods. Adult albino rats were randomized into 6 groups as follows: group I sham group; group II, control group; groups III and IV, control vehicles (1,2); group V, MK-886 treated group. Donor rats received MK-886 30 min before transplantation, and the same dose was repeated for recipients upon reperfusion; in group VI, DITPA treated group, donors and recipients rats were pretreated with DITPA for 7 days before transplantation. Results. Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF-α, IL-1β, and ICAM-1 and plasma level of cTnI (P < 0.05). Morphologic analysis showed that both MK-886 and DITPA markedly improved (P < 0.05) the severity of cardiac injury in the heterotopically transplanted rats. Conclusions. The results of our study reveal that both MK-886 and DITPA may ameliorate global myocardial ischemia reperfusion injury after heart transplantation via interfering with inflammatory pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Thyroid Hormone Analogue and a Leukotrienes Pathway-Blocker on Reperfusion Injury Attenuation after Heart Transplantation

2013

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“…In the isolated heart model, both ischemia and reperfusion induce the release of cardiac enzymes [16][17][18]20 . However, though important, the results shown are inconsistent and illustrate the lack of standardization between different assays and/or sensitivity of the methods used.…”

Section: Discussionmentioning

confidence: 99%

“…Despite the popularity of the use of isolated rat heart preparations in studies of ischemia-reperfusion injury, many different protocols have been employed with variations in the duration of ischemia 15,16 and the degree of the metabolic disturbance 17,18 , making it difficult to compare the severity of the protocols. Additionally, most of these studies did not use angiotensin-I in the perfusate, hindering any conclusions about the effects of ACE inhibition.…”

Section: Introductionmentioning

confidence: 99%

Efeitos da angiotensina-I e isquemia na recuperação funcional em corações isolados

Oliveira

Kucharski

et al. 2011

Arq. Bras. Cardiol.

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“…The nature of these pathophysiological processes resulting in troponin release are still being defined, but they likely represent a spectrum from cell death and frank necrosis with myofilament disruption to less severe and likely transient changes in the integrity and permeability of the sarcolemma membrane [15][16][17].…”

Section: Mechanisms Of Troponin Releasementioning

confidence: 99%

Perspective on the clinical application of troponin in heart failure and states of cardiac injury

Bass¹,

Patterson²

2009

Heart Fail Rev

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The ability to measure the appearance of cardiac specific forms of troponin in the blood represents a major advance in the clinical assessment of patients with many types of cardiovascular disease, especially acute coronary syndromes. In this review we focus on the utility of troponin in heart failure where this biomarker has emerged as an independent predictor of prognosis providing information beyond clinical assessment and measurement of b-type natriuretic peptides. The novel clinical role of troponin in a variety of states associated with myocardial injury, including chemotherapy and patients with cardiovascular risk factors, is discussed.

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Time-course of cardiac troponin I release from isolated perfused rat hearts during hypoxia/reoxygenation and ischemia/reperfusion

Cited by 12 publications

References 25 publications

Effects of Thyroid Hormone Analogue and a Leukotrienes Pathway-Blocker on Reperfusion Injury Attenuation after Heart Transplantation

Effects of Thyroid Hormone Analogue and a Leukotrienes Pathway-Blocker on Reperfusion Injury Attenuation after Heart Transplantation

Efeitos da angiotensina-I e isquemia na recuperação funcional em corações isolados

Perspective on the clinical application of troponin in heart failure and states of cardiac injury

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