Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

Dobutamine (dob) can precondition the heart against ischemia/reperfusion (I/R) injury by an unknown mechanism. During ischemia, mitochondria (M) lose adenine nucleotides (AdN). Abnormally low levels of MAdN (ATP+ADP+AMP) can exacerbate mitochondrial injury due to calcium overload, which occurs during I/R. The purpose of the present study was to determine if dob can attenuate the loss of MAdN during prolonged ischemia. Isolated rat hearts received 30 min perfusion followed by 40 min of global ischemia. The dob group received dob for 5 min followed by 5 min of perfusion without dob immediately prior to ischemia. The control (Cn) group did not receive dob. M were isolated from the hearts at the end of ischemia. M were also isolated from some hearts immediately prior to ischemia. In an additional study, hearts were reperfused for 30 min following 40 min ischemia. Left ventricular developed pressure (LVDP) was monitored with an intraventricular balloon. Pre-ischemic MAdN levels were 7.5+/-0.1 and 7.1+/-0.7 nmol/mg protein for the Cn(n=4) and Dob(n=4) groups, respectively (p=ns). At the end of ischemia, the MAdN levels were 2.5+/-0.2 and 3.4+/-0.3 for the Cn (n=9)and Dob (n=9) groups, respectively (p=0.024). Postischemic LVDP was 40+/-5 and 89+/-9 percent of pre-treatment values for the Cn (n=10) and Dob (n=7) groups, respectively (p < 0.001). We conclude that dob pre-treatment can attenuate the loss of MAdN during ischemia. This protection of the MAdN pool may contribute to the cardioprotective effect of dob preconditioning.

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Presentation Number SAasimakis0395
Keywords: Heart, Ischemia, Dobutamine, Mitochondria, Nucleotides