Preconditioning with cromakalim improves long-term myocardial preservation for heart transplantation

Kirsch, Matthias; Baufreton, Christophe; Fernandez, Christine; Brunet, Séverine; Pasteau, Fabien; Astier, A.; Loisance, D

doi:10.1016/s0003-4975(98)00357-9

Cited by 17 publications

(7 citation statements)

References 27 publications

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“…Glibenclamide administered alone did not prolong cardiac allograft survival, whereas combined with aprikalim it prolonged cardiac allograft survival. This result is similar to Kirsch's report 16 that preconditioning with cromakalim (a K + channel opener) modestly improved long-term myocardial preservation for heart transplantation, whereas glibenclamide did not abolish the effects of cromakalim. The K + ATP channel inhibitor, gliclazide, prolonged cardiac allograft survival compared to control group, but the mechanism remains unknown.…”

Section: Discussionsupporting

confidence: 90%

Prolongation of rat heart allograft survival with K+ATP-dependent channel modulators

et al. 1999

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Controversies exist regarding the immunoregulatory properties of K(+) ATP channel modulators. We investigated the effects of aprikalim, a K(+) ATP-dependent channels activator, and glibenclamide and gliclazide, two inhibitors of K(+) ATP-dependent channels, on the prolongation of heart allograft survival in the rat. Nine groups (n >/= 5) were involved in this study with the Brown-Norway to Lewis rat combination treated with aprikalim, glibenclamide, gliclazide, and/or cyclosporine. The results indicate that modulators of K(+) ATP-dependent channels can improve the survival of rat heart allograft without interfering with the immunosuppressive properties of cyclosporine.

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Section: Discussionsupporting

confidence: 90%

Prolongation of rat heart allograft survival with K+ATP-dependent channel modulators

et al. 1999

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“…High-risk patients with poor preoperative left ventricular function, extensive coronary artery disease, or severe left ventricular hypertrophy could certainly benefit if the degree of protection were improved by invoking endogenous cellular adaptive mechanisms. The possibility that organ preservation before transplantation might be amenable to the same improved protection, as suggested by some experimental evidence, 81,82 is also of significant interest. This might allow an extension of the "cold ischemic time" between harvesting and implantation, facilitating optimal matching of recipient to donor, as well as affording a potential improvement in early myocardial function.…”

Section: Which Patients May Benefit?mentioning

confidence: 99%

The Preconditioning Phenomenon

Yellon

Dana

2000

Circulation Research

118

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Abstract-The possibility that an innate mechanism of myocardial protection might be inducible in the human heart has generated considerable excitement and enthusiastic research. The potential to enhance myocardial resistance to ischemic injury in patients suffering the consequences of coronary artery disease has led to studies with more direct clinical relevance. However, in common with many other areas of clinical interest based on advances in basic scientific understanding, early enthusiasm may be disproportionate to ultimate therapeutic significance. There can be little doubt that our understanding of the mechanisms underlying the pathogenesis of ischemia-reperfusion injury has been enhanced significantly by the plethora of research stimulated by interest in endogenous myocardial protection. Direct extrapolation of observations in the laboratory to the cardiology clinic or operating theater is tempting but should be avoided. The results of recent clinical experiments that suggest that preconditioning can protect against ischemia, although encouraging, should be interpreted cautiously, with particular attention to the limitations of the end points available. A reasoned evaluation of recent research should prevent unrealistic expectations and allow improved design of future trials so that this potent adaptive phenomenon can be exploited to its maximum potential. (Circ Res. 2000;87:543-550.)

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“…So far HSP72 has been implicated with protection of graft survival in several studies [13, 24, 25, 26, 27, 28]. For instance, Amrani et al [28]showed that hearts from animals subjected to heat shock before hypothermic storage demonstrated superior recovery of graft function and protection was correlated with increased inducible HSP70 protein expression.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, in addition to characterizing the pattern of HSP induction, we also wanted to investigate the effects of HP on kidney graft function in order to determine possible mechanisms of protection. Since recipient kidneys were not removed upon transplantation in most other studies [25], these studies allow no analysis of the effects of HP on renal functional parameters [14]. Therefore, we removed both native kidneys at transplantation so that functional parameters truly assessed solely graft function.…”

Section: Discussionmentioning

confidence: 99%

Hyperthermia Preconditioning Induces Renal Heat Shock Protein Expression, Improves Cold Ischemia Tolerance, Kidney Graft Function and Survival in Rats

Redaelli¹,

Tien²,

Kubulus

et al. 2002

Nephron

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Background: Evidence indicates that hyperthermia preconditioning (HP) can be protective in kidney transplantation, possibly through increased heat shock protein (HSP) expression. A detailed study about individual HSPs and functional preservation is lacking, however. Therefore, we studied the effects of HP on kidney graft survival, function and HSP expression. Methods: Male Lewis rats were or were not subjected to whole-body hyperthermia 24 h prior to kidney procurement. Kidneys were stored in UW solution at 4°C for 32, 40 or 45 h. Recipient kidneys were both removed and single isografts transplanted orthotopically. Results: HP strongly induced HSP72 and HSP32 expression. Following 32-hour cold ischemia, most animals survived even without prior HP. However, HP strongly reduced functional impairment induced by cold ischemia. Following 40-hour cold ischemia, kidneys from donors without HP did not recover function and all animals died within 3 days. In contrast, HP-exposed kidneys tolerated 40-hour storage significantly better, with 44% of rats surviving until sacrifice on day 7. In these animals, renal function was still better compared to animals with 32-hour-stored kidneys without HP. Histological alterations were also diminished following HP. Conclusion: Our data show that HP induces renal HSP72 and, for the first time, HSP32. HP increases survival following transplantation and acts by improving several parameters of kidney function including proteinuria, volume output and creatinine clearance.

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Preconditioning with cromakalim improves long-term myocardial preservation for heart transplantation

Cited by 17 publications

References 27 publications

Prolongation of rat heart allograft survival with K+ATP-dependent channel modulators

Prolongation of rat heart allograft survival with K+ATP-dependent channel modulators

The Preconditioning Phenomenon

Hyperthermia Preconditioning Induces Renal Heat Shock Protein Expression, Improves Cold Ischemia Tolerance, Kidney Graft Function and Survival in Rats

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