中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2011年
4期
200-203
,共4页
张晓静%孟祥艳%黄新莉%戴鸿雁%韦鹏%凌亦凌
張曉靜%孟祥豔%黃新莉%戴鴻雁%韋鵬%凌亦凌
장효정%맹상염%황신리%대홍안%위붕%릉역릉
硫化氢%一氧化碳%肺动脉%脂多糖%肺动脉高压
硫化氫%一氧化碳%肺動脈%脂多糖%肺動脈高壓
류화경%일양화탄%폐동맥%지다당%폐동맥고압
Hydrogen sulfide%Carbon monoxide%Pulmonary artery%Lipopolysaccharide%Pulmonary artery hypertension
目的 观察整体水平应用硫化氢(H2S)后脂多糖(LPS)诱导的离体肺动脉对H2S舒张反应的变化及其与一氧化碳(CO)的关系.方法 将48只大鼠按照随机数字表法分为对照组[给予生理盐水(NS)]、LPS组、H2S供体硫氢化钠(NaHS)+LPS组和NaHS+NS组4组,每组12只.采用经大鼠气管内滴注LPS(0.8 ml/kg)染毒;NaHS±+LPS组和NaHS±NS组滴注LPS或NS之前10 min和之后2 h腹腔注射NaHS各0.5 ml(28 μmol/kg).各组取6只大鼠于染毒后12 h制备肺动脉环(PARs),采用离体血管环张力测定技术检测用血红素氧合酶-1(HO-1)抑制剂锌原卟啉Ⅸ(ZnPPⅨ)孵育前后PARs对累积浓度NaHS的舒张反应变化;各组另取6只大鼠于染毒后12 h检测出肺血(EPB)和入肺血(APB)中碳氧血红蛋白(COHb)含量,以其差值反映肺循环CO生成的水平.结果 与对照组相比,滴注LPS后PARs对NaHS的最大舒张反应百分比明显降低[(75.72±7.22)%比(96.40±4.40)%,P＜0.01＝;用ZnPPⅨ孵育PARs后,LPS诱导的PARs对NaHS舒张反应进一步降低[(62.91±8.22)%比(75.72±7.22)%,P＜0.01＝.腹腔注射NaHS可明显逆转LPS诱导的PARs对NaHS的低反应性,PARs对NaHS的最大舒张反应百分比明显升高[(94.65±8.45)%比(75.72±7.22)%,P＜0.01＝;但用ZnPPⅨ孵育PARs后,PARs对NaHS的舒张反应较孵育前显著下降[(83.75±9.76)%比(94.65±8.45)%,P＜0.01＝.NaHS+NS组中PARs对NaHS的舒张反应与对照组相比无明显差异,且在ZnPPⅨ孵育前后也无明显变化.COHb检测结果显示,与对照组相比,滴注LPS后APB和EPB中COHb水平的差值明显增高[(3.12±0.48)%比(2.12±0.32)%,P＜0.05＝;腹腔注射NaHS后,COHb水平的差值[(4.03±0.56)%]较LPS组进一步升高(P＜0.01＝.结论 腹腔注射H2S可以改善LPS诱导的离体肺动脉对H2S的低反应性,其机制可能与增强肺动脉HO-1/CO体系有关.
目的 觀察整體水平應用硫化氫(H2S)後脂多糖(LPS)誘導的離體肺動脈對H2S舒張反應的變化及其與一氧化碳(CO)的關繫.方法 將48隻大鼠按照隨機數字錶法分為對照組[給予生理鹽水(NS)]、LPS組、H2S供體硫氫化鈉(NaHS)+LPS組和NaHS+NS組4組,每組12隻.採用經大鼠氣管內滴註LPS(0.8 ml/kg)染毒;NaHS±+LPS組和NaHS±NS組滴註LPS或NS之前10 min和之後2 h腹腔註射NaHS各0.5 ml(28 μmol/kg).各組取6隻大鼠于染毒後12 h製備肺動脈環(PARs),採用離體血管環張力測定技術檢測用血紅素氧閤酶-1(HO-1)抑製劑鋅原卟啉Ⅸ(ZnPPⅨ)孵育前後PARs對纍積濃度NaHS的舒張反應變化;各組另取6隻大鼠于染毒後12 h檢測齣肺血(EPB)和入肺血(APB)中碳氧血紅蛋白(COHb)含量,以其差值反映肺循環CO生成的水平.結果 與對照組相比,滴註LPS後PARs對NaHS的最大舒張反應百分比明顯降低[(75.72±7.22)%比(96.40±4.40)%,P＜0.01＝;用ZnPPⅨ孵育PARs後,LPS誘導的PARs對NaHS舒張反應進一步降低[(62.91±8.22)%比(75.72±7.22)%,P＜0.01＝.腹腔註射NaHS可明顯逆轉LPS誘導的PARs對NaHS的低反應性,PARs對NaHS的最大舒張反應百分比明顯升高[(94.65±8.45)%比(75.72±7.22)%,P＜0.01＝;但用ZnPPⅨ孵育PARs後,PARs對NaHS的舒張反應較孵育前顯著下降[(83.75±9.76)%比(94.65±8.45)%,P＜0.01＝.NaHS+NS組中PARs對NaHS的舒張反應與對照組相比無明顯差異,且在ZnPPⅨ孵育前後也無明顯變化.COHb檢測結果顯示,與對照組相比,滴註LPS後APB和EPB中COHb水平的差值明顯增高[(3.12±0.48)%比(2.12±0.32)%,P＜0.05＝;腹腔註射NaHS後,COHb水平的差值[(4.03±0.56)%]較LPS組進一步升高(P＜0.01＝.結論 腹腔註射H2S可以改善LPS誘導的離體肺動脈對H2S的低反應性,其機製可能與增彊肺動脈HO-1/CO體繫有關.
목적 관찰정체수평응용류화경(H2S)후지다당(LPS)유도적리체폐동맥대H2S서장반응적변화급기여일양화탄(CO)적관계.방법 장48지대서안조수궤수자표법분위대조조[급여생리염수(NS)]、LPS조、H2S공체류경화납(NaHS)+LPS조화NaHS+NS조4조,매조12지.채용경대서기관내적주LPS(0.8 ml/kg)염독;NaHS±+LPS조화NaHS±NS조적주LPS혹NS지전10 min화지후2 h복강주사NaHS각0.5 ml(28 μmol/kg).각조취6지대서우염독후12 h제비폐동맥배(PARs),채용리체혈관배장력측정기술검측용혈홍소양합매-1(HO-1)억제제자원계람Ⅸ(ZnPPⅨ)부육전후PARs대루적농도NaHS적서장반응변화;각조령취6지대서우염독후12 h검측출폐혈(EPB)화입폐혈(APB)중탄양혈홍단백(COHb)함량,이기차치반영폐순배CO생성적수평.결과 여대조조상비,적주LPS후PARs대NaHS적최대서장반응백분비명현강저[(75.72±7.22)%비(96.40±4.40)%,P＜0.01＝;용ZnPPⅨ부육PARs후,LPS유도적PARs대NaHS서장반응진일보강저[(62.91±8.22)%비(75.72±7.22)%,P＜0.01＝.복강주사NaHS가명현역전LPS유도적PARs대NaHS적저반응성,PARs대NaHS적최대서장반응백분비명현승고[(94.65±8.45)%비(75.72±7.22)%,P＜0.01＝;단용ZnPPⅨ부육PARs후,PARs대NaHS적서장반응교부육전현저하강[(83.75±9.76)%비(94.65±8.45)%,P＜0.01＝.NaHS+NS조중PARs대NaHS적서장반응여대조조상비무명현차이,차재ZnPPⅨ부육전후야무명현변화.COHb검측결과현시,여대조조상비,적주LPS후APB화EPB중COHb수평적차치명현증고[(3.12±0.48)%비(2.12±0.32)%,P＜0.05＝;복강주사NaHS후,COHb수평적차치[(4.03±0.56)%]교LPS조진일보승고(P＜0.01＝.결론 복강주사H2S가이개선LPS유도적리체폐동맥대H2S적저반응성,기궤제가능여증강폐동맥HO-1/CO체계유관.
Objective To explore the effect of hydrogen sulfide (H2S) on abnormal pulmonary artery reactivity induced by lipopolysaccharide (LPS) and its relationship with carbon monoxide (CO). Methods Forty-eight rats were divided into four groups randomly according to table of random number: control group (normal saline, NS), LPS group, a donor of H2S sodium hydrosulfide (NaHS)+LPS group, and NaHS+NS group (n=12 in each group). Rats were given LPS by intratracheal instillation (0. 8 ml/kg). 0. 5 ml of NaHS (28 μmol/kg) was injected intraperitoneally 10 minutes before LPS or NS instillation and 2 hours after LPS or NS instillation in NaHS+LPS and NaHS+NS groups. Twelve hours after instillation of LPS, 6 rats from each group were sacrificed. The pulmonary artery rings (PARs) were prepared and the changes in cumulative relaxation response of PARs to NaHS were detected before and after incubation with an inhibitor of heme oxygenase-1 (HO-1) zinc protoporphyrin Ⅸ (ZnPP Ⅸ ) using isolated vascular ring tension detecting technique. Twelve hours after LPS instillation, the remaining 6 rats in each group were sacrificed, and the contents of carboxyhemoglobin (COHb) in efferent pulmonary blood (EPB) and afferent pulmonary blood (APB) were measured, and the difference between the contents of COHb in EPB and that of APB was calculated to represent content of CO from pulmonary circulation. Results In the present study, compared with control group, after the instillation of LPS the percentage of relaxation response of PARs to NaHS was significantly declined [(75. 72±7. 22)% vs. (96. 40±4. 40)%, P＜0. 01]. After being incubated with ZnPP Ⅸ, the decreased relaxation response of PARs to NaHS induced by LPS was further depressed [(62. 91 ±8. 22) % vs. ( 75. 72 ± 7. 22) %, P ＜ 0. 01]. Administration of NaHS intraperitoneally reversed the hyporesponsiveness of PARs to NaHS, the percentage of relaxation response of PARs to NaHS was significantly increased [(94.65± 8.45)% vs. (75.72 ± 7.22)%, P＜0.01]. However ZnPP Ⅸ also attenuated the effect [(83. 75 ± 9. 76)% vs. (94. 65 ± 8. 45)%, P ＜ 0. 01]. NO significant changes were observed between NaHS+NS group and control group, also between the results before and after ZnPP Ⅸincubation. Compared with control group, the difference between the contents of COHb in EPB and that of APB increased after instillation of LPS [(3. 12±0. 48)% vs. (2. 12±0. 32)%, P＜0. 05], which further increased after intraperitoneal administration of NaHS [(4.03 ± 0. 56) %, P ＜ 0. 01]. Conclusion The results suggested that intraperitoneal administration of H2S could reverse hyporesponsiveness of PARs to H2S induced by LPS, and the result might be related to an intensification of HO-1/CO system in pulmonary artery tissue.
