Protective effect of warmblood cardioplegia on ischemic rabbit myocardium

Abstract

Abstract: AIM: To investigate the effect of warm blood cardioplegic solution on myocardial protection.METHODS: Twenty-four rabbits were randomly dividedinto three groups.Immediately after aortic clamping and just before aortic unclamping, the rabbithearts received warm (37 ℃) blood cardioplegic solution in group Ⅰ(n = 8), cold crystalloid crdioplegic solution in group Ⅱ (n = 8), and warm (37 ℃) crystalloid cardioplegic solution in group Ⅲ (n =8) respectively.During 120 min of ischemia, all hearts were reinfused with cold crystalloid cardioplegic solution every 20min.Samples were taken 1min after cross-clamp removal to assess lactate dehydrogease1 (LDH1) and creatine phosphonate kinase (CK) in coronary sinus blood, and glutamate dehydrogenase (GLDH) within mitochondrion and myocardium water content.Myocardial biopsies were obtained for electron microscopical study and stereological quantitative analysis of mitochondria.RESULTS: 1 min following aortic unclamping, there were no significant differences among the three groups in LDH1 (P >0.05).GLDH was significantly higher (P<0.05) in group Ⅰ than that in group Ⅱand Ⅲ, while there was no statistical difference between group Ⅱand Ⅲ (P > 0.05).The value of CK-MB was significantly lower (P<0.05) in group Ⅰthan that in group Ⅱand Ⅲ, and the difference was not significant between group Ⅱ and Ⅲ (P > 0.05).Myocardium water content in group Ⅰwas the lowest among the three groups (P<0.05), and no significant difference existed between the latter two groups (P > 0.05).Myocardial ultrastructure study showed that group Ⅰ was better protected than the other two groups, and group Ⅱbetter than group Ⅲ.Stereological quantitative analysis determined by calculation of mitochondria area density revealed significant differences between the three groups, in which group Ⅰwas lower than group Ⅱ (P<0.05) and group Ⅲ (P<0.01), and group Ⅱ lower than group Ⅲ (P<0.05).CONCLUSION: Warm blood cardioplegic solution, applied at the start and the end of aortic clamping, results in better myocardial protection than does the crystalloid solution used alone.

Key words: warm blood cardioplegic solution, myocardial protection, extracorporeal circulation

CLC Number:

R965.3

YANG Li, ZHANG Shi-Jiang, GAO Sheng-Fu. Protective effect of warmblood cardioplegia on ischemic rabbit myocardium[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2002, 7(3): 213-216.

References

1 Follette DM, Maloney JV, Buckberg GD, et al.Advantages of blood cardioplegia over continuous coronary perfusion or intermittent ischemia[J].J Thorac Cardiovasc Surg, 1987;76:604-12
2 Biong OHL, La Raia PJ, Gaasch WHJ, et al.Independent protection provided by red blood cells during cardioplegia[J].Circulation, 1982;66:I1-81
3 Heitmiller RF, DoBoer LWV, Geffin GA, et al.Myocardial recovery after hypothermic arrest:A comparison of oxygenated crystalloid to blood cardioplegia:the role of calcium[J].Circulation, 1985;72(Pt2):241-53
4 Bodenhamer RM, DoBoer LWV, Geffin GA, et al.Enhanced myocardial protection during ischemic arrest:oxygenation of a crystalloid cardioplegic solution[J].J Thorac Cardiovasc Surg, 1983;85:769-79
5 Guyton RA, Dorsey LMA, Craver JM, et al.Improved myocardial recovery after cardioplegic arrest with an oxygenated crystalloid solution[J].J Thorac Cardiovasc Surg, 1985;89:877-83
6 Coetzee A, Kotze J, Louw J, et al.Effect of oxygenated crystalloid cardioplegia on the functional and metabolic recovery of the isolated perfused ratheart[J].J Thorac Cardiovasc Surg, 1986; 91:259-66
7 Buckberg GD.Benefits of normothermic induction of blood cardioplegia in energy-depleted hearts, with maintenance of arrest by multidose cold blood cardioplegic infusions[J].J Thorac Cardiovasc Surg, 1985;84:677-85
8 Teoh KH, George TC, Richard DW, et al.Accelerated myocardial metabolic recovery with terminal warm blood cardioplegia[J]. J Thorac Cardiovasc Surg, 1986;91:888-95
9 Oguma F:Role played by oxygen in myocardial protection with crystalloid cardioplegic solution[J].Ann Thorac Surg, 1986;42: 172-82
10 Severinghous JW.Oxyhemoglobin dissociation curve correction for temperature and pH variation in human blood[J].J Appl Physiol, 1958;12:485-6
11 Magovern GJ, Flaherty JT, Gott VL, et al.Failure of blood cardioplegia to protect myocardium at lower temperatures[J].Circulation, 1982;66:60-7
12 Lucas SK, Kanter KR, Schaff HV, et al.Reduced oxygen extraction during reperfusion:a consequence of global ischemia arrest[J].J Surg Res, 1980;28:434-41

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