Enhanced tolerance of the rat myocardium to ischemia and reperfusion injury early after acute myocardial infarction

Pantos, Constantinos; Mourouzis, Iordanis; Dimopoulos, Antonios; Markakis, Konstantinos; Panagiotou, Matthew; Xinaris, Christodoulos; Tzeis, Stylianos; Kokkinos, Alexandros; Cokkinos, Dennis V.

doi:10.1007/s00395-007-0645-4

Cited by 32 publications

(22 citation statements)

References 22 publications

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“…Previous studies suggested that the deletion of Hsp70 is associated with cardiac dysfunction and impaired stress response to I/R ex vivo [20]. In contrast, Hsp70 has been suggested to play a cardioprotection role early after myocardial infarction [31]. In this study, we showed the cardioprotective effect of Hsp70 against I/R injury, and the regulation of caspase-independent apoptosis by Hsp70 in heart in vivo.…”

Section: Discussionsupporting

confidence: 51%

Mitochondria to nucleus translocation of AIF in mice lacking Hsp70 during ischemia/reperfusion

Choudhury

Bae

et al. 2011

Basic Res Cardiol

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Heat shock protein 70 (Hsp70) has been shown to have an anti-apoptotic function, but its mechanism is not clear in heart. In this study, we examined the effect of Hsp70 deletion on AIF-induced apoptosis during ischemia/reperfusion (I/R) in vivo. Although Hsp70 KO and WT mice demonstrated similar amounts of AIF released from mitochondria after I/R surgery, Hsp70 KO mice showed a significantly greater increase in apoptosis, larger infarct size, and decreased cardiac output. There was also a significant fourfold increase in the nuclear accumulation of AIF in Hsp70 KO mice compared with WT mice. Treatment with 4-AN (4-amino-1,8-napthalimide, 3 mg/kg), a potent inhibitor of PARP-1, which is a critical regulator of AIF-induced apoptosis, significantly blocked the release of AIF from mitochondria and the translocation of AIF into the nuclei after I/R in both WT and Hsp70 KO mice. In addition, 4-AN treatment resulted in a significant inhibition of apoptosis, a reduction of infarct size, and attenuated cardiac dysfunction in both WT and Hsp70 KO mice after I/R. The anti-apoptotic function of Hsp70 occurs through the inhibition of AIF-induced apoptosis by blocking the mitochondria to nucleus translocation of AIF. PARP-1 inhibition improves cardiac function by blocking AIF-induced apoptosis.

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Section: Discussionsupporting

confidence: 51%

Mitochondria to nucleus translocation of AIF in mice lacking Hsp70 during ischemia/reperfusion

Choudhury

Bae

et al. 2011

Basic Res Cardiol

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“…during heart surgery and serves as an important prognostic factor in cardiac interventions [1,10,15,18,20]. Furthermore, LDH also has high relevance as a marker for ischemic processes and cell necrosis, both in vitro [9,17,24] and in vivo [2,4,19,23].…”

Section: Discussionmentioning

confidence: 99%

Reduced diagnostic value of lactate dehydrogenase (LDH) in the presence of radiographic contrast media

Franke

Fuhrmann

Mrowietz³

et al. 2010

Clinical Hemorheology and Microcirculation

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Isoforms of the enzyme lactate dehydrogenase (LDH) were found in almost all cells of the organism and an elevated activity of LDH in the circulation is thought to be a clear indicator of elevated cell destruction coinciding with an increased release of components from the cellular cytoplasm, e.g. LDH. Here, we report on an in-vitro examination to test whether radiographic contrast media (RCM) could induce cell destruction followed by an increase in LDH release. The RCM were tested in non-flow cultures of human umbilical venous endothelial cells (HUVEC) of the fourth passage seeded on extracellular matrix and the results were compared to those from control cultures not exposed to contrast media.The examination revealed that the addition of contrast media to the cell culture media supplemented with pooled human serum (HSP) as source of exogenous LDH was followed by a strong decrease in LDH activity both in the absence and presence of HUVEC. Within 1.5 min after the addition of contrast media to the culture medium supplemented with HSP (30% vol of the culture medium were replaced by either of two contrast media, Iodixanol or Iopromide) the LDH activity decreased about 80% compared to the initial values. In contrast, the LDH activity did not change in cell culture media not supplemented with RCM.The partial replacement of HSP supplemented cell culture medium by RCM will cause a dilution of cell culture medium constituents. The decrease of LDH activity, however, was much stronger than the decrease thought to be attributable to the effects of dilution of cell culture medium, so that the role of dilution seems to be a minor one in this case. It has to be assumed that the RCM could interact with the LDH available in the culture medium as well as with the substrates delivered with the measurement system for the assessment of LDH activity, so that both, the amount of LDH and the activities of enzymes involved might be influenced.In the presence of HUVEC a similar effect was observed. Here, a little less strong decrease of LDH activity occurred compared to the decrease in cell culture medium without HUVEC. This was unexpected because a considerable amount of HUVEC were detached after the addition of contrast media and many of these cells were damaged seriously so that a significant amount of endogenous LDH should have been released.These unexpected results make it necessary to re-evaluate those past time examinations focussed on cell damage/destruction in the presence of contrast media, where the measurement of LDH activity was used as indicator or cell vitality and where cell decease rates were correlated to questionable toxic influences. According to the results of the examination reported here it is difficult to uphold the interpretation of recently published findings that contrast media almost exclusively induce cellular apoptosis and not necrosis.

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“…Evidence shows that ischemic contracture and/or hypercontracture profiles of the hearts are very closely related to the functional responses of those hearts to ischemia/reperfusion (I/R) injury [1][2][3]. This relation has also been observed in hearts from hypothyroid and post-infarcted animals, similar to the hearts obtained from healthy animals [4,5]. However, there is no data, to our knowledge, regarding the relation in diabetic hearts.…”

Section: Introductionmentioning

confidence: 93%

Association of Ischemic Contracture, Hypercontracture and Post-Ischemic Recovery in Diabetic Rat Heart

Altunkaynak

Özçeli̇kay

2017

BJMMR

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Objective: Previous studies suggest a relation among ischemic contracture and/or hypercontracture profiles and the functional responses in diseased hearts isolated from hypothyroid and post-infarcted animals. We therefore aimed to find out whether there is a similar relation in the diabetic hearts. Methods: Experiments were performed on Sprague-Dawley rats divided into control and diabetic groups. Diabetes was induced by streptozotocin (45 mg/kg) in citrate buffer (0.1 M, pH:4.5) into the tail vein of the rat. Isolated hearts from control and diabetic rats were subjected to 40-min ischemia followed by 40-min of reperfusion. The left ventricular end-diastolic pressure and left ventricular developed pressure were measured during the experimental protocol. Furthermore, the increase in minimal value of left ventricular pressure during ischemia and the peak value of left ventricular end

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Enhanced tolerance of the rat myocardium to ischemia and reperfusion injury early after acute myocardial infarction

Cited by 32 publications

References 22 publications

Mitochondria to nucleus translocation of AIF in mice lacking Hsp70 during ischemia/reperfusion

Mitochondria to nucleus translocation of AIF in mice lacking Hsp70 during ischemia/reperfusion

Reduced diagnostic value of lactate dehydrogenase (LDH) in the presence of radiographic contrast media

Association of Ischemic Contracture, Hypercontracture and Post-Ischemic Recovery in Diabetic Rat Heart

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