• Top
• Introduction
• Method
• Results
• Conclusion

Introduction

We investigated the capacity of heat stress to improve myocardial tolerance and cardiac energy metabolism in the isolated perfused neonatal rabbit heart subjected to prolonged cold cardioplegic ischemia.

Method

Hearts from anaesthetized male neonatal New Zealand White rabbits (aged 8-10 days) were excised, isolated, perfused with modified Krebs-Henseleit buffer, and arrested for 2 h of cold cardioplegic ischaemia. In order to induce the expression of heat shock proteins (HSPs; HSP72⁺/73⁺) the rectal temperature of five neonatal rabbits was raised to 42.0-42.5°C (in a whole-body water bath) for 15 min before the onset of global, hypothermic cardioplegic arrest. Another set of five hearts without hyperthermia pretreatment served as controls. The recovery of left ventricular (LV) function was assessed by LV developed pressure, max +dP/dt and LV pressure. The status of phosphorylated energy metabolites (β-adenosine triphosphate [β-ATP], phosphocreatine [PCr] and inorganic phosphate) was measured by ³¹phosphorus nuclear magnetic resonance spectroscopy. HSPs were also detected by immunoblot analysis.

Results

Heat stress pretreatment resulted in significantly better recovery of LV function, as indicated by LV developed pressure (74.6 ± 10 versus 52.1 ± 8.5%: P < 0.05), max dP/dt (910 ± 170 versus 530 ± 58 mmHg/s; P < 0.01), LV end-diastolic pressure (8 ± 2 versus 18.4 ± 5 mmHg; P < 0.05) and coronary blood flow (P < 0.05), than occurred in the control group 60 min after reperfusion. During reperfusion, myocardial energy metabolism was also better preserved in the HSP-group hearts as a result of significantly (P < 0.05) increased β-ATP and PCr values as compared with control animals. Immunoblot analysis showed that the brief period of systemic hyperthermia induced HSP (HSP 72⁺/73⁺) expression.

Conclusion

These data contribute to the evidence that heat stress mediates a beneficial effect on recovery of the neonatal left ventricle and cardiac energy metabolism after prolonged cold cardioplegic ischaemia in rabbits.

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