中华器官移植杂志
中華器官移植雜誌
중화기관이식잡지
CHINESE JOURNAL OF ORGAN TRANSPLANTATION
2008年
5期
283-285
,共3页
翟伟%W.Weder%S.Korom
翟偉%W.Weder%S.Korom
적위%W.Weder%S.Korom
肺移植%二肽基肽酶类%移植物%再灌注损伤
肺移植%二肽基肽酶類%移植物%再灌註損傷
폐이식%이태기태매류%이식물%재관주손상
Lung transplantation%Dipeptidyl peptidase%Transplants%Reperfusion injury
目的 探讨抑制CD26/二肽酰肽酶Ⅳ(DPP Ⅳ)的活性对移植肺缺血再灌注损伤的影响.方法 实验分两组进行,采用简化套管技术进行Lewis大鼠左肺原位移植,实验组的供肺以含特异性不可逆的DPP Ⅳ抑制剂AB192(终浓度为25 μmol/L)的4 ℃低钾右旋糖苷液灌洗及保存,对照组的供肺以4 ℃低钾右旋糖苷液灌洗及保存.供肺保存18 h后进行移植.分别于气管插管后、进入左胸腔、再灌注前以及再灌注后1、5、10、15 min记录受者气道的峰值压力(PawP),其后每15 min记录1次.再灌注2 h末,抽取移植肺静脉血,测定血氧分压(PO2),切取移植肺,测定移植肺组织湿重/干重比值和硫代巴比妥酸反应物(TBARS)的含量.结果 再灌注2 h后,实验组的PO2为(298.4±87.6)mm Hg,明显高于对照组的(120.9±48.0)mm Hg(P＜0.01);实验组移植肺组织湿重/干重比值为6.5±0.8,明显低于对照组的8.6±0.6(P＜0.01);实验组移植肺组织中TBARS的含量为(9.3±2.0)μmol/g,明显低于对照组的(13.8±1.8)μmol/g(P＜0.01).整个再灌注期间(2 h共14个时点),两组间PawP的差异有统计学意义(P＜0.01);再灌注2 h末,实验组的PawP为(11.8±0.9)mm Hg,显著低于对照组的(16.0±1.4)mm Hg(P＜0.01).结论 通过抑制肺组织内CD26/DPP Ⅳ的活性,可以明显减轻移植肺的缺血再灌注损伤.
目的 探討抑製CD26/二肽酰肽酶Ⅳ(DPP Ⅳ)的活性對移植肺缺血再灌註損傷的影響.方法 實驗分兩組進行,採用簡化套管技術進行Lewis大鼠左肺原位移植,實驗組的供肺以含特異性不可逆的DPP Ⅳ抑製劑AB192(終濃度為25 μmol/L)的4 ℃低鉀右鏇糖苷液灌洗及保存,對照組的供肺以4 ℃低鉀右鏇糖苷液灌洗及保存.供肺保存18 h後進行移植.分彆于氣管插管後、進入左胸腔、再灌註前以及再灌註後1、5、10、15 min記錄受者氣道的峰值壓力(PawP),其後每15 min記錄1次.再灌註2 h末,抽取移植肺靜脈血,測定血氧分壓(PO2),切取移植肺,測定移植肺組織濕重/榦重比值和硫代巴比妥痠反應物(TBARS)的含量.結果 再灌註2 h後,實驗組的PO2為(298.4±87.6)mm Hg,明顯高于對照組的(120.9±48.0)mm Hg(P＜0.01);實驗組移植肺組織濕重/榦重比值為6.5±0.8,明顯低于對照組的8.6±0.6(P＜0.01);實驗組移植肺組織中TBARS的含量為(9.3±2.0)μmol/g,明顯低于對照組的(13.8±1.8)μmol/g(P＜0.01).整箇再灌註期間(2 h共14箇時點),兩組間PawP的差異有統計學意義(P＜0.01);再灌註2 h末,實驗組的PawP為(11.8±0.9)mm Hg,顯著低于對照組的(16.0±1.4)mm Hg(P＜0.01).結論 通過抑製肺組織內CD26/DPP Ⅳ的活性,可以明顯減輕移植肺的缺血再灌註損傷.
목적 탐토억제CD26/이태선태매Ⅳ(DPP Ⅳ)적활성대이식폐결혈재관주손상적영향.방법 실험분량조진행,채용간화투관기술진행Lewis대서좌폐원위이식,실험조적공폐이함특이성불가역적DPP Ⅳ억제제AB192(종농도위25 μmol/L)적4 ℃저갑우선당감액관세급보존,대조조적공폐이4 ℃저갑우선당감액관세급보존.공폐보존18 h후진행이식.분별우기관삽관후、진입좌흉강、재관주전이급재관주후1、5、10、15 min기록수자기도적봉치압력(PawP),기후매15 min기록1차.재관주2 h말,추취이식폐정맥혈,측정혈양분압(PO2),절취이식폐,측정이식폐조직습중/간중비치화류대파비타산반응물(TBARS)적함량.결과 재관주2 h후,실험조적PO2위(298.4±87.6)mm Hg,명현고우대조조적(120.9±48.0)mm Hg(P＜0.01);실험조이식폐조직습중/간중비치위6.5±0.8,명현저우대조조적8.6±0.6(P＜0.01);실험조이식폐조직중TBARS적함량위(9.3±2.0)μmol/g,명현저우대조조적(13.8±1.8)μmol/g(P＜0.01).정개재관주기간(2 h공14개시점),량조간PawP적차이유통계학의의(P＜0.01);재관주2 h말,실험조적PawP위(11.8±0.9)mm Hg,현저저우대조조적(16.0±1.4)mm Hg(P＜0.01).결론 통과억제폐조직내CD26/DPP Ⅳ적활성,가이명현감경이식폐적결혈재관주손상.
Objective To investigate the effect of enzymatic DPP Ⅳ inhibition on ischemiareperfnsion (I/R) injury after extended ischemia prior to transplantation. Methods A simplified syngeneic rat (Lewis) orthotopic left lung transplantation model was used in two groups. In the control group (group Ⅰ) ,donor lungs were flushed and preserved in Perfadex (R) for 18 h at 4 ℃ ,then transplanted and reperfused for 2 h. In the treated group (group Ⅱ ) donor lungs were perfused with and stored in Perfadex (R) + 25 mol/L AB192 [bis(4-acetamidophenyi) 1-(S)-prolylpyrrolidine-2(R,S)-phosphonate],a small molecular weight DPP Ⅳ inhibitor. Peak airway pressure (PawP) was recorded after intubation, upon entering the chest, before reperfusion, at 1,5,10 and 15 min after reperfusion,and then every 15 min thereafter. At the end of a 2 h-reperfusion, blood gas analysis,PawP,wet to dry weight ratio (W/D) and thiobarbiturie acid reactive substances (TBARS) were measured. Results In grafts of group Ⅱ as compared with group Ⅰ ,oxygenation capacity was significantly greater (298.4 ±87. 6 mm Hg vs. 120. 9 ± 48.0 mm Hg, P＜0.01), PawP lower (11.8 ± 0. 9 mm Hg vs. 16.0 ±1.4 mm Hg,P＜0. 01 ) ,W/D ratio lower (6. 5 ± 0. 8 vs. 8. 6 ± 0. 6,P＜0. 01 ) and TBARS less (9. 3 ±2. 0 μmol/g vs. 13. 8 ± 1.8 μmol/g, P＜0. 01 ). Conclusion Inhibiting intragraft DPP Ⅳ enzymatic activity significantly reduces I/R-associated pulmonary injury, allowing for successful transplantation after 18 h of ischemia.
