中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2003年
1期
87-91
,共5页
丁学琴%刘贵明%王俊科%盛卓人
丁學琴%劉貴明%王俊科%盛卓人
정학금%류귀명%왕준과%성탁인
低氧%一氧化碳%血红素氧化酶%高血压,肺性%大鼠
低氧%一氧化碳%血紅素氧化酶%高血壓,肺性%大鼠
저양%일양화탄%혈홍소양화매%고혈압,폐성%대서
Anoxia%Carbon monoxide%Heme oxygenase%Hypertension,pulmonary%Rats
目的:观察急性缺氧时血浆、组织内源性一氧化碳的变化及外源性一氧化碳对急性肺动脉高压的影响.方法:实验分为两部分:实验1:30只雄性Wistar大鼠随机分为3组:组I (对照组):大鼠吸入21%O2 30 min;组II(缺氧组):大鼠吸入10%O2 30 min;组III (ZnPPIX组):腹腔注入血红素氧化酶抑制剂ZnPPIX 10 μmol/kg后,大鼠吸入10%O2 30 min.实验结束时取血样进行一氧化碳及环磷酸鸟苷分析,取组织样品进行匀浆、离心测组织一氧化碳含量;实验2:10只大鼠吸入10%O2 20 min,待肺动脉压力曲线恢复基线后,给大鼠吸入50×10-6的一氧化碳与缺氧气体的混合气30 min,观察血流动力学和血气的变化.结果:急性缺氧增加了血浆、组织一氧化碳含量及血浆环磷酸鸟苷含量,ZnPPIX降低了缺氧大鼠的血浆、组织一氧化碳含量及血浆环磷酸鸟苷含量,缺氧明显升高了平均肺动脉压,而吸入50×10-6的一氧化碳可明显降低肺动脉压,而且吸入一氧化碳可明显增加缺氧大鼠的动脉氧分压.结论:急性缺氧明显增加了血浆、组织一氧化碳含量及血浆环磷酸鸟苷含量.外源性一氧化碳可明显降低缺氧时肺动脉高压.
目的:觀察急性缺氧時血漿、組織內源性一氧化碳的變化及外源性一氧化碳對急性肺動脈高壓的影響.方法:實驗分為兩部分:實驗1:30隻雄性Wistar大鼠隨機分為3組:組I (對照組):大鼠吸入21%O2 30 min;組II(缺氧組):大鼠吸入10%O2 30 min;組III (ZnPPIX組):腹腔註入血紅素氧化酶抑製劑ZnPPIX 10 μmol/kg後,大鼠吸入10%O2 30 min.實驗結束時取血樣進行一氧化碳及環燐痠鳥苷分析,取組織樣品進行勻漿、離心測組織一氧化碳含量;實驗2:10隻大鼠吸入10%O2 20 min,待肺動脈壓力麯線恢複基線後,給大鼠吸入50×10-6的一氧化碳與缺氧氣體的混閤氣30 min,觀察血流動力學和血氣的變化.結果:急性缺氧增加瞭血漿、組織一氧化碳含量及血漿環燐痠鳥苷含量,ZnPPIX降低瞭缺氧大鼠的血漿、組織一氧化碳含量及血漿環燐痠鳥苷含量,缺氧明顯升高瞭平均肺動脈壓,而吸入50×10-6的一氧化碳可明顯降低肺動脈壓,而且吸入一氧化碳可明顯增加缺氧大鼠的動脈氧分壓.結論:急性缺氧明顯增加瞭血漿、組織一氧化碳含量及血漿環燐痠鳥苷含量.外源性一氧化碳可明顯降低缺氧時肺動脈高壓.
목적:관찰급성결양시혈장、조직내원성일양화탄적변화급외원성일양화탄대급성폐동맥고압적영향.방법:실험분위량부분:실험1:30지웅성Wistar대서수궤분위3조:조I (대조조):대서흡입21%O2 30 min;조II(결양조):대서흡입10%O2 30 min;조III (ZnPPIX조):복강주입혈홍소양화매억제제ZnPPIX 10 μmol/kg후,대서흡입10%O2 30 min.실험결속시취혈양진행일양화탄급배린산조감분석,취조직양품진행균장、리심측조직일양화탄함량;실험2:10지대서흡입10%O2 20 min,대폐동맥압력곡선회복기선후,급대서흡입50×10-6적일양화탄여결양기체적혼합기30 min,관찰혈류동역학화혈기적변화.결과:급성결양증가료혈장、조직일양화탄함량급혈장배린산조감함량,ZnPPIX강저료결양대서적혈장、조직일양화탄함량급혈장배린산조감함량,결양명현승고료평균폐동맥압,이흡입50×10-6적일양화탄가명현강저폐동맥압,이차흡입일양화탄가명현증가결양대서적동맥양분압.결론:급성결양명현증가료혈장、조직일양화탄함량급혈장배린산조감함량.외원성일양화탄가명현강저결양시폐동맥고압.
AIM: To investigate changes of carbon monoxide (CO) in plasma and tissue during acute hypoxia and effect of exogenous CO on acute hypoxic pulmonary arterial hypertension. METHODS: Experiment was divided into two protocols : Protocol 1: 30 Male Wistar rats (180-250 g) were randomly assigned into three groups: Group I (control) : rats were inhaled with 21%O2 for 30 min. Group II (hypoxia) : rats were inhaled with 10%O2 for 30 min. Group III (ZnPPIX): after heme oxygenase (HO) inhibitor ZnPPIX was administered, rats were inhaled with 10%O2 for 30 min. At the end of experiment, blood samples were collected for carbon monoxide and cGMP assay. Tissue samples were homogenized and centrifuged for CO assay. Protocol 2: 10 male Wistar rats (180-250g) were inhaled with 10%O2 for 20min. When the pressure curve of mean pulmonary arterial pressure returned to baseline, the mixture of 50×10-6 CO and hypoxic gases was administered to rats and the change of mean pulmonary arterial pressure (MPAP) was also observed. RESULTS: Hypoxia increased CO levels in plasma and tissue as well as cGMP level in plasma. ZnPPIX reduced CO levels of plasma and tissue as well as cGMP level of plasma in hypoxic rats. Hypoxia elevated MPAP significantly while inhalation of 50×10-6 CO reduced MPAP markedly. Moreover, CO increased PaO2 significantly in hypoxic rats. CONCLUSION: Acute hypoxia increased CO levels in plasma and tissue as well as cGMP levels in plasma. Exogenous CO reduced MPAP significantly.