中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
6期
967-969
,共3页
宋帅%姜格宁%何文新%刘明%王海峰%韩炳强
宋帥%薑格寧%何文新%劉明%王海峰%韓炳彊
송수%강격저%하문신%류명%왕해봉%한병강
肺移植%再灌注损伤%一氧化氮合酶%精氨酸%氨基胍
肺移植%再灌註損傷%一氧化氮閤酶%精氨痠%氨基胍
폐이식%재관주손상%일양화담합매%정안산%안기고
Lung transplantation%Reperfusion injury%Nitric oxide synthase%Arginine%Aminoguanidine
目的 观察L-精氨酸(L-Arg)和氨基胍对大鼠肺移植后缺血再灌注的保护作用.方法 建立大鼠左单肺移植模型,术后随机分为A组(对照组,腹腔注射生理盐水),B组(腹腔注射L-Arg)、C组(腹腔注射氨基胍)和D组(腹腔注射L-Arg和氨基胍),每组6只.移植肺再灌注2 h后,检测肺组织髓过氧化物酶(MPO)、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力、内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)活性并测定移植肺干湿重比(W/D)及静脉血中一氧化氮(NO)含量,观察移植肺的病理学形态.结果 再灌注2 h后,B组移植肺的W/D(5.10±0.21)、MPO(1.74±0.26)U/g和MDA(20.87±2.90)μmol/g均低于A组W/D(5.74 ±0.14)、MPO(2.36±0.32)U/g和MDA(31.33 ±3.46)μmol/g;SOD活性(424.29±27.86)U/mgprot、NO含量(175.12 ±17.40)μmol/L、iNOS活性(3.62 ±0.26)U/mgprot和eNOS活性(5.36±0.28)U/mgprot均较A组SOD活性(268.01±26.06)U/mgpro、NO含量(98.29±6.95)μmol/L、iNOS活性(2.53 ±0.22)U/mgprot和eNOS活性(3.57 ±0.40)U/mgprot高(P＜0.05).C组的NO含量(84.13±5.18)μmol/L、iNOS活性(1.81 ±0.09)U/mgprot均较A组低(P＜0.05).D组的W/D(4.79 ±0.19)、MPO(1.24±0.13)U/g、MDA(14.60±4.14)μmol/g、iNOS活性(1.99±0.17)U/mgprot低于A组,SOD活性(493.75±24.95)、NO含量(149.61±10.70)μmol/L、eNOS活性(5.50±0.27)U/mgprot高于A组(P＜0.05).与B组比较,D组的W/D、MPO、MDA、NO含量、iNOS活性降低,SOD升高(P＜0.05).病理形态学检查显示D组炎细胞浸润及渗出最轻,B组次之,A组和C组最差.结论 移植后再灌注早期应用L-Arg可减轻缺血再灌注损伤,应用氨基胍并不能减轻移植肺的损伤,但联合应用L-Arg和氨基胍优于单纯应用L-Arg.
目的 觀察L-精氨痠(L-Arg)和氨基胍對大鼠肺移植後缺血再灌註的保護作用.方法 建立大鼠左單肺移植模型,術後隨機分為A組(對照組,腹腔註射生理鹽水),B組(腹腔註射L-Arg)、C組(腹腔註射氨基胍)和D組(腹腔註射L-Arg和氨基胍),每組6隻.移植肺再灌註2 h後,檢測肺組織髓過氧化物酶(MPO)、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力、內皮型一氧化氮閤酶(eNOS)和誘導型一氧化氮閤酶(iNOS)活性併測定移植肺榦濕重比(W/D)及靜脈血中一氧化氮(NO)含量,觀察移植肺的病理學形態.結果 再灌註2 h後,B組移植肺的W/D(5.10±0.21)、MPO(1.74±0.26)U/g和MDA(20.87±2.90)μmol/g均低于A組W/D(5.74 ±0.14)、MPO(2.36±0.32)U/g和MDA(31.33 ±3.46)μmol/g;SOD活性(424.29±27.86)U/mgprot、NO含量(175.12 ±17.40)μmol/L、iNOS活性(3.62 ±0.26)U/mgprot和eNOS活性(5.36±0.28)U/mgprot均較A組SOD活性(268.01±26.06)U/mgpro、NO含量(98.29±6.95)μmol/L、iNOS活性(2.53 ±0.22)U/mgprot和eNOS活性(3.57 ±0.40)U/mgprot高(P＜0.05).C組的NO含量(84.13±5.18)μmol/L、iNOS活性(1.81 ±0.09)U/mgprot均較A組低(P＜0.05).D組的W/D(4.79 ±0.19)、MPO(1.24±0.13)U/g、MDA(14.60±4.14)μmol/g、iNOS活性(1.99±0.17)U/mgprot低于A組,SOD活性(493.75±24.95)、NO含量(149.61±10.70)μmol/L、eNOS活性(5.50±0.27)U/mgprot高于A組(P＜0.05).與B組比較,D組的W/D、MPO、MDA、NO含量、iNOS活性降低,SOD升高(P＜0.05).病理形態學檢查顯示D組炎細胞浸潤及滲齣最輕,B組次之,A組和C組最差.結論 移植後再灌註早期應用L-Arg可減輕缺血再灌註損傷,應用氨基胍併不能減輕移植肺的損傷,但聯閤應用L-Arg和氨基胍優于單純應用L-Arg.
목적 관찰L-정안산(L-Arg)화안기고대대서폐이식후결혈재관주적보호작용.방법 건립대서좌단폐이식모형,술후수궤분위A조(대조조,복강주사생리염수),B조(복강주사L-Arg)、C조(복강주사안기고)화D조(복강주사L-Arg화안기고),매조6지.이식폐재관주2 h후,검측폐조직수과양화물매(MPO)、병이철(MDA)함량、초양화물기화매(SOD)활력、내피형일양화담합매(eNOS)화유도형일양화담합매(iNOS)활성병측정이식폐간습중비(W/D)급정맥혈중일양화담(NO)함량,관찰이식폐적병이학형태.결과 재관주2 h후,B조이식폐적W/D(5.10±0.21)、MPO(1.74±0.26)U/g화MDA(20.87±2.90)μmol/g균저우A조W/D(5.74 ±0.14)、MPO(2.36±0.32)U/g화MDA(31.33 ±3.46)μmol/g;SOD활성(424.29±27.86)U/mgprot、NO함량(175.12 ±17.40)μmol/L、iNOS활성(3.62 ±0.26)U/mgprot화eNOS활성(5.36±0.28)U/mgprot균교A조SOD활성(268.01±26.06)U/mgpro、NO함량(98.29±6.95)μmol/L、iNOS활성(2.53 ±0.22)U/mgprot화eNOS활성(3.57 ±0.40)U/mgprot고(P＜0.05).C조적NO함량(84.13±5.18)μmol/L、iNOS활성(1.81 ±0.09)U/mgprot균교A조저(P＜0.05).D조적W/D(4.79 ±0.19)、MPO(1.24±0.13)U/g、MDA(14.60±4.14)μmol/g、iNOS활성(1.99±0.17)U/mgprot저우A조,SOD활성(493.75±24.95)、NO함량(149.61±10.70)μmol/L、eNOS활성(5.50±0.27)U/mgprot고우A조(P＜0.05).여B조비교,D조적W/D、MPO、MDA、NO함량、iNOS활성강저,SOD승고(P＜0.05).병리형태학검사현시D조염세포침윤급삼출최경,B조차지,A조화C조최차.결론 이식후재관주조기응용L-Arg가감경결혈재관주손상,응용안기고병불능감경이식폐적손상,단연합응용L-Arg화안기고우우단순응용L-Arg.
Objective To investigate the effects of L-arginine (L-Arg) and aminoguanidine on ischemia-reperfusion injury following rat lung transplantation. Methods The models of rats lung transplantation were established and 4 groups ( n = 6 each) were randomly set up: group A ( normal control group)and treated groups B, C and D. In these groups, different medicines (NS, group A; L-Arg, group B;aminoguanidine, group C; L-Arg and aminoguanidine, group D) were intraperitoneally administered to the recipient rats before reperfusion. After reperfusion for 2 h, the lung graft was harvested for measurements of lung wet/dry ratio ( W/D ) , myeloperoxidase ( MPO ) , malondialdehyde ( MDA ) , superoxide dismutase (SOD) , endothelial nitric oxide synthase (eNOS) , inducible nitric oxide synthase (iNOS). The contents of plasma nitric oxide (NO) were determined. The pathological changes in the lung grafts were observed.Results After reperfusion for 2 h, W/D (5. 10 ±0.21), MPO (1.74 ±0.26) U/g, MDA (20.87 ±2. 90) μmol/g in group B were significantly lower [W/D (5. 74 ± 0. 14), MPO (2. 36 ± 0. 32) U/g,MDA (31. 33 ±3.46) μmol/g] (P ＜ 0. 05), and the levels of SOD (424. 29 ± 27. 86) U/mg protein,NO (175. 12 ± 17. 40) μmol/L, iNOS (3. 62 ±0. 26) U/mg protein and eNOS (5. 36 ±0. 28) U/mg protein were significantly higher than in group A [SOD (268.01 ±26.06) U/mg protein, NO (98.29 ±6.95) μmol/L, iNOS (2.53 ±0.22) U/mg protein and eNOS (3. 57 ±0.40) U/mg protein] (P＜0. 05). The contents of NO (84. 13 ±5. 18) μmol/L and iNOS (1. 81 ±0. 09) U/mg protein in group C were significantly lower than in group A (P ＜ 0. 05). W/D (4. 79 ± 0. 19) , MPO (1. 24 ± 0. 13 ) U/g,MDA (14. 60 ±4. 14) μmol/g, iNOS (1. 99 ±0. 17) U/mg protein were significantly lower than in group A (P ＜0. 05) , and SOD (493. 75 ±24. 95) , NO (149. 61 ± 10. 70) μmol/L and eNOS (5. 50 ±0. 27)U/mg protein in group D were significantly higher than in group A (P＜0. 05). W/D, MPO, MDA, NO and iNOS in group D were significantly reduced as compared with group B (P ＜ 0. 05 ) , and SOD was significantly increased in group B ( P ＜ 0. 05 ) . The pathological examination revealed that the inflammatory cell infiltration in group D was the mildest, followed by groups B, A and C. Conclusion The L-Arg could alleviate the lung ischemia-reperfusion injury after transplantation, the combined used of L-Arg and aminoguanidine could obtain better effects than L-Arg used alone. The aminoguanidine used alone could not alleviate ischemia-reperfusion injury after transplantation.
