摘要
目的 探讨新生儿坏死性小肠结肠炎 (NEC)发病机理 ,为寻找其内源性保护物质提供实验室依据。 方法 以健康 7日龄 Wistar新生鼠分组并制备缺血再灌注 (I/ R)及缺血预处理 (IPC)实验模型 ,分别测定血浆降钙素基因相关肽 (CGRP)浓度、乳酸脱氢酸 (L DH )活性、小肠组织丙二醛(MDA)含量及湿重 /干重 (WW/ DW)比值 ,并制备病理切片光镜下观察形态学变化。 结果 实验各组血浆 CGRP浓度除 IPC组与 IPC+I/ R组差异无显著性外 [(2 92± 17与 2 82± 19) pg/ L(q=1.82 ,P>0 .0 5 ) ],其余各组间差异均有显著性 [(12 4± 10与 16 2± 2 4 ) pg/ L(q=7.16 ) ;(12 4± 10与 2 92± 17)pg/ L(q=4 2 .0 1) ;(16 2± 2 4与 2 92± 17) pg/ L(q=2 1.73,P值均 <0 .0 1) ],IPC组 CGRP较对照组及I/ R组均明显升高。血浆 L DH在 I/ R时较对照组明显升高 [(190± 2 4与 4 6± 9) U / L (q=2 6 .70 ,P<0 .0 1) ],而在 IPC组及 IPC+I/ R组较 I/ R组又有明显下降 [(12 2± 15与 190± 2 4 ) U / L (q=11.77) ;(138± 15与 190± 2 4 ) U/ L(q=6 .39;P值均 <0 .0 1) ]。 I/ R时小肠 MDA含量较对照组明显增加[(1.5 1± 0 .10与 0 .6 1± 0 .0 7) nm ol/ mg(q=36 .12 ,P<0 .0 1) ],而在 IPC及 IPC+I/ R时较 I/
Objective To investigate the pathogenesis of neonatal necrotizing enterocolitis (NEC), to explore the laboratory basis for endogenous protective substance. Method Experimental models of both ischemia/reperfusion (I/R) group and ischemic preconditioning (IPC) group were set up using healthy male Wistar neonatal rats. Serum CGRP concentration, activity of LDH, the contents of MDA and the ratio of wet weight/dry weight (WW/DW) were measured respectively. Pathological sections of small intestines were prepared and observed under microscope. Results The serum CGRP concentration were statistically different between one group to another [control vs IPC: (124±10)pg/L vs (292±17)pg/L( q =42.01); control vs I/R: (124±10)pg/L vs (162±24)pg/L( q=7.16 ); control vs IPC+I/R:(124±10)pg/L vs (282±19)pg/L( q=35.76 ); IPC vs I/R: (292±17)pg/L vs (162±24)pg/L,( q=21.73 );I/R vs IPC+I/R:(162±24)pg/L vs (282±19)pg/L,( q=19.19 ; all P <0.01)] except that between IPC group and IPC+I/R group[(292±17)pg/L vs (282±19)pg/L ( q=1.82,P >0.05)]. CGRP concentration in IPC group was higher than that in control and I/R group. Serum LDH concentration was higher in I/R group than that in control group[(190±24)u/L vs (46±9)U/L( q=26.70,P<0.01) ]. While both in IPC and IPC+I/R groups, serum LDH concentrations lowered overtly than that in I/R group[(122±15)U/L vs (190±24)U/L( q=11.77 ); (138±15)U/L vs (190±24)u/L( q=6.39 , both P <0.01)]. MDA content of small intestine in I/R group was higher than that in control group [(1.51±0.10)nmol/mg vs ( 0.61±0.07 )( q=36.12,P <0.01)]. It lowered down significantly in both IPC and IPC+I/R groups [(0.68±0.08)nmol/mg vs (1.51± 0.10 )nmol/mg( q=31.75 ); (0.88±0.11)nmol/mg vs (1.51±0.10)nmol/mg( q=20.76 ; both P<0.01 )]. There was remarkable edema of small intestinal tissues in I/R group. The value of WW/DW was bigger than that of control group [(4.86±0.37)pro wt vs (3.96±0.28)pro wt( q=9.50,P<0.01 )]. In IPC group, the edema of small intestinal tissues lessened obviously. In terms of morphological changes, it had little injuries of small intestinal mucosae in IPC group. Whereas in I/R group, it presented with large quantities of deciduous villi, swelling of epithelial cells, and disappearing or dissolution of the structure of normal cells. And there were large amounts of intervillous inflammatory or hemorrhagic exudation. Conclusion There is ischemic preconditioning phenomenon in small intestine of neonatal rats. IPC of small intestines has obvious protection on I/R of small intestine in neonatal rats. CGRP may be an important endogenous active substance that mediated the protection of IPC of small intestines in neonatal rats.
出处
《中华围产医学杂志》
CAS
2003年第3期168-171,共4页
Chinese Journal of Perinatal Medicine
基金
山西省教委基金资助项目 (2 0 0 3 )
