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[The effects of cardioplegia and reperfusional blood containing captopril on myocardial ultrastructure alterations after cardiac arrest].

OBJECTIVE
To investigate the myocardial protective effect of captopril on the ischemia and reperfusion injury in the canine heart.


METHODS
Twelve mongrel dogs were randomly divided into control and captopril groups. In the former, only modified St. Thomas cardioplegia was used, and in the latter, modified St. Thomas cardioplegia and reperfusional blood containing 4.6mumol/L captopril were used. Sixty minutes after reperfusion, myocardial renin activity (MRA), angiotensin II (AII) and melondyldialdehyde (MDA) content in myocardium were measured, and the subendocardial myocardium of the left ventricle was taken for electromicroscopy.


RESULTS
The MRA in the Cp1 group was significantly higher than that in the control group (P < 0.01), while the AII and MDA content in the myocardium in the Cp1 group were significantly lower than those in the control group (P < 0.01). Electronmicroscopically, the damage of the myocardium including sarcomeres, mitochondria and microvascular endothelial cells were less obvious in the Cp1 group than that in the control. The mitochondrial average cross-section area and average volume (0.59 +/- 0.15 micron2 and 0.74 +/- 0.23 micron3) in the Cp1 group were significantly lower than those in the control (0.83 +/- 0.34 micron2, P < 0.01 and 1.1 +/- 0.4 micron3, P < 0.01). The numerical density (0.46 +/- 0.16 micron-3), specific surface of mitochondria (6.4 +/- 1.1 microns-1) and memberance density of mitochondrial cristae (21 +/- 10 microns-1) in the Cp1 group were significantly higher than those in the control (0.29 +/- 0.06 micron-3, P < 0.05, 4.8 +/- 0.8 micron-1, P < 0.01 and 15.3 +/- 2.0 microns-1, P < 0.01):


CONCLUSION
Cardioplegia and reperfusional blood containing 4.6 mumol/L captopril could effectively protect the myocardial mitochondria and microvascular endothelial cells against ischemia and reperfusion injury.