| Background: The tissue dysfunction is still a popular clinic question after cardiopulmonary bypass(CPB).Thus, how to relieve the tissue damage during or after CPB, as well as the mechanism of this damage is the focus point in the laboratory and clinic research.CPB-associated systemic inflammatory response induce the tissue damage after CPB, and the activated leukocyte play an important role during this period. The immature tissue ,meanwhile, is different from the mature tissue in the structure, function and metabolism. Thus, we pay more attention to the immature tissue protection during CPB.Methods: In accordance with the theory aboved, we have consideration for instituting a CPB model in neonatal canine, using a leukocyte filtration, and we want to find whether the leukocyte-depletion is benefit to the protection of the tissue during the CPB.After the institution of CPB, the 12 neonatal canines were divided into two groups randomly. In the LD-CPB group(n=6), a Pall LG6 arterial line LD filter was inserted in the CPB circuit. In the NO-LD group(n=6), no LD filter was inserted in the CPB circuit. The time of the aorta cross-clamping(ACC) is 60min, and the time of CPB is 180min.During the CPB, a catheter was inserted into the left ventricle to measure left ventricular end-diastolic pressure, and electrocardiographic leads were placed to measure heart rate and to monitor electrical activity. The blood of CPB was sampled from boththe inlet and outlet of LD filter. Leukocytes was counted, and the depletion ratio was calculated to evaluate the efficiency of leukocyte depletion.Myocardial and pulmonary tissue were obtained at the beginning of CPB and of ACC and the end of CPB, and we measured the concentration of malondialdehyde(MDA) and myeloperoxidase(MPO). We quantified the gene expression of the isozymes of NOS by using reverse transcription-polymerase chain reaction(RT-PCR), analyzed the myocardial NOS, pulmonary and myocardial water content, and measure pulmonary capillary permeability. Coronary sinus effluent blood were obtained 120 min after reperfusion, we measure the plasma cTnl concentrations. Finally, we observe the ultrastructure of the myocardial and pulmonary tissue using electron microscope.Result: Leukocyte-depletion filter can removed most of blood leukocyte and platelet (the depletion ratio was 0.90+0.01and 0.59+0.01), and has no effect on the blood erythrocyte(the depletion ratio was 0.03+0.02). The recovery ratio of left ventricular end-diastolic pressure was significantly higher in the LD-CPB group than that in the NO-LD group(p<0.01), but heart rate was no significant difference between two groups.The coronary sinus effluent blood and pulmonary tissue MDA concentrations were significantly higher in the NO-LD group than that in the LD-CPB group at 120min after reperfusion(p <0.01,p<0.01), so did before ACC (P<0.01, p<0.01). The myocardial and pulmonary tissue MPO competence were significant higher in the NO-LD group that in the LD-CPB group (p<0.01,p<0.01;p<0.01, p<0.01)before aorta clamped and at 120min after reperfusion.The coronary sinus effluent plasma cTnl concentrations in the two groups were higher than the normal value(0.6ug/l), but that in theNO-LD group was significantly higher than that in the LD-CPB group(p<0.05). Evan's Blue value(EB),which stand for the pulmonary capillary permeability, was significantly lower in the LD-CPB group than that in the NO-LD group( 0.0861+0.0094 versus 0.203 1+0.0267, P =0.008), so did in the myocardial and pulmonary water content ( PThe coronary sinus effluent plasma NO concentration was significantly higher in the LD-CPB group than that in the NO-LD group(P =0.0001). In the NO-LD group, compared with the LD-CPB group , the expression of cNOSmRNA was downregulated, concentration of cNOS was reduced, but that of iNOS was still not changed.Conclusion: The LD filter in the CPB circuit can relieve the immature tissue damage resulted from the inflammatory response induced by CPB, and reduced the mount of activated neutrop...
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