中华胸心血管外科杂志
中華胸心血管外科雜誌
중화흉심혈관외과잡지
Chinese Journal of Thoracic and Cardiovascular Surgery
2012年
4期
237-240
,共4页
常凤军%魏玮%欧志君%胡晓侠%杨晓霞%王治平%张希%区景松
常鳳軍%魏瑋%歐誌君%鬍曉俠%楊曉霞%王治平%張希%區景鬆
상봉군%위위%구지군%호효협%양효하%왕치평%장희%구경송
高血压,肺性%一氧化氮合酶%弹性蛋白 野百合碱%左旋精氨酸
高血壓,肺性%一氧化氮閤酶%彈性蛋白 野百閤堿%左鏇精氨痠
고혈압,폐성%일양화담합매%탄성단백 야백합감%좌선정안산
Hypertension,pulmonary%Nitric Oxide Synthase%Elastin%Monocrotaline%L-arginine
目的 探讨诱导型一氧化氮合酶(iNOS)在中、晚期肺动脉高压(PH)发病中的作用机制及左旋精氨酸 (L-Arg)对其产生的影响.方法 30只雄性SD大鼠随机均分为5组,对照组(C组)、MCT3组(M3组)、MCT5组(M5组)、L-Arg3/MCT3组(L3组)、L-Arg5/MCT5组(L5组).除C组外其他组大鼠均用野百合碱一次性腹腔注射诱导PH模型.此后L3组和L5组分别连续每天腹腔注射L-Arg 3周和5周,M3组和M5组分别连续每天腹腔注射与L-Arg等量的生理盐水3周和5周,C组连续每天腹腔注射与L-Arg等量的生理盐水共5周.实验周期结束则用右心导管法测定右心室收缩压(RVSP),间接反映肺动脉压力,然后取大鼠肺组织做免疫组化,检测各组iNOS、内皮一氧化氮合酶(eNOS)和弹性蛋白(elastin)的表达变化.结果 M3和M5组中iNOS和elastin的表达明显高于C组,而eNOS表达明显少于C组；L3和L5组iNOS和elastin的表达少于相应M3和M5组,但L5组两种蛋白表达仍高于C组,L3和L5组eNOS的减少明显比相应M3和M5组少,但不及C组.结论 PH形成的中、晚期,肺组织中eNOS表达减少,而此时iNOS的表达增高可能产生大量一氧化氮(NO),但并没有改善PH的病情,而L-Arg能够恢复eNOS和iNOS之间的平衡并有效抑制PH的进展.
目的 探討誘導型一氧化氮閤酶(iNOS)在中、晚期肺動脈高壓(PH)髮病中的作用機製及左鏇精氨痠 (L-Arg)對其產生的影響.方法 30隻雄性SD大鼠隨機均分為5組,對照組(C組)、MCT3組(M3組)、MCT5組(M5組)、L-Arg3/MCT3組(L3組)、L-Arg5/MCT5組(L5組).除C組外其他組大鼠均用野百閤堿一次性腹腔註射誘導PH模型.此後L3組和L5組分彆連續每天腹腔註射L-Arg 3週和5週,M3組和M5組分彆連續每天腹腔註射與L-Arg等量的生理鹽水3週和5週,C組連續每天腹腔註射與L-Arg等量的生理鹽水共5週.實驗週期結束則用右心導管法測定右心室收縮壓(RVSP),間接反映肺動脈壓力,然後取大鼠肺組織做免疫組化,檢測各組iNOS、內皮一氧化氮閤酶(eNOS)和彈性蛋白(elastin)的錶達變化.結果 M3和M5組中iNOS和elastin的錶達明顯高于C組,而eNOS錶達明顯少于C組；L3和L5組iNOS和elastin的錶達少于相應M3和M5組,但L5組兩種蛋白錶達仍高于C組,L3和L5組eNOS的減少明顯比相應M3和M5組少,但不及C組.結論 PH形成的中、晚期,肺組織中eNOS錶達減少,而此時iNOS的錶達增高可能產生大量一氧化氮(NO),但併沒有改善PH的病情,而L-Arg能夠恢複eNOS和iNOS之間的平衡併有效抑製PH的進展.
목적 탐토유도형일양화담합매(iNOS)재중、만기폐동맥고압(PH)발병중적작용궤제급좌선정안산 (L-Arg)대기산생적영향.방법 30지웅성SD대서수궤균분위5조,대조조(C조)、MCT3조(M3조)、MCT5조(M5조)、L-Arg3/MCT3조(L3조)、L-Arg5/MCT5조(L5조).제C조외기타조대서균용야백합감일차성복강주사유도PH모형.차후L3조화L5조분별련속매천복강주사L-Arg 3주화5주,M3조화M5조분별련속매천복강주사여L-Arg등량적생리염수3주화5주,C조련속매천복강주사여L-Arg등량적생리염수공5주.실험주기결속칙용우심도관법측정우심실수축압(RVSP),간접반영폐동맥압력,연후취대서폐조직주면역조화,검측각조iNOS、내피일양화담합매(eNOS)화탄성단백(elastin)적표체변화.결과 M3화M5조중iNOS화elastin적표체명현고우C조,이eNOS표체명현소우C조；L3화L5조iNOS화elastin적표체소우상응M3화M5조,단L5조량충단백표체잉고우C조,L3화L5조eNOS적감소명현비상응M3화M5조소,단불급C조.결론 PH형성적중、만기,폐조직중eNOS표체감소,이차시iNOS적표체증고가능산생대량일양화담(NO),단병몰유개선PH적병정,이L-Arg능구회복eNOS화iNOS지간적평형병유효억제PH적진전.
Objective To investigate the role of iNOS in the middle and late stage of pulmonary hypertension (PH) and the effect of L-Arginine(L-Arg) on these stage.Methods Thirty healthy male SD rats were randomly divided into five groups.All rats except those in control group were injected intraperitoneally (ip) with a single dose (50 mg/kg) of MCT to induce PH.Then the L3 and L5 groups were injected ip with 500 mg/kg L-Arg daily for 3 weeks and 5weeks respectively,the M3 and M5groups received a daily ip injection of the same amount of saline as L-Arg for 3 weeks and 5 weeks respectively; the same amount of saline was injected ip daily in control group for 5 weeks.Right ventricular systolic pressure(RVSP) was measured before lungs were excised for immunohistochemistry at the end of experiments. Results The expressions of iNOS and elastin in M3 and M5 were higher compared to the control group,but L-Arg partly reduced the expressions of iNOS and elastin both at 3weeks and 5 weeks post-MCT.The reduction of eNOS expression in L3 and L5 groups were lower compared to M3 and M5 groups,but the eNOS expression in L3 and L5 groups were still lower than control group.Conclusion During the middle and late stage of PH,the expression of eNOS was decreased.The expression of iNOS was induced,which would produce numerous NO.However,these NO had no benefit on the development of PH.L-Arg could restore the balance of eNOS and iNOS,and could inhibit the development of PH,which may provide a new clues to explore the pathogenesis and treatment of PH.
