中国医药
中國醫藥
중국의약
CHINA MEDICINE
2013年
9期
1264-1266
,共3页
叶光耀%霍砚淼%陈炜%纪均
葉光耀%霍硯淼%陳煒%紀均
협광요%곽연묘%진위%기균
肝肺综合征%一氧化氮%内皮素1%肿瘤坏死因子α%慢性肝病
肝肺綜閤徵%一氧化氮%內皮素1%腫瘤壞死因子α%慢性肝病
간폐종합정%일양화담%내피소1%종류배사인자α%만성간병
Hepatopulmonary syndrome%Nitrogen oxide%Endothelin 1%Tumor necrosis factor α%Chronic liver disease
目的 分析肝肺综合征(HPS)患者体循环和肺循环中血管活性物质的含量及意义.方法 将上海交通大学医学院附属仁济医院2009年8月至2011年6月接受门静脉高压症手术和肝移植手术治疗的患者分为HPS组(18例),慢性肝病组(18例,无原发心肺疾病、非HPS的慢性肝病患者)和对照组(18例,同期因胃肠道肿瘤接受手术的患者),经桡动脉置管和右心导管法抽取桡动脉和肺动脉血,以酶联免疫吸附法检测NO、内皮素1、肿瘤坏死因子α(TNF-α)、前列环素代谢物(6-keto-PGF1α)、血管活性肠肽(VIP)和雌激素等血管活性物质含量.结果 HPS组、慢性肝病组和对照组肺动脉和桡动脉中NO、内皮素1和TNF-α分别为(122±16)、(111±10)、(102±12)μmol/L(肺动脉NO)；(141±21)、(123±21)、(107±13) μmol/L(桡动脉NO)；(149±16)、(116±24)、(92±22) ng/L(肺动脉内皮素1)；(123±26)、(103±14)、(89±16)ng/L(桡动脉内皮素1)；(360±43)、(317±68)、(278±38) ng/L(肺动脉TNF-α)；(404±39)、(363±49)、(257±49) ng/L(桡动脉TNF-α),组间两两比较差异均有统计学意义(均P＜0.05).HPS组和慢性肝病组肺动脉和桡动脉中,VIP、6-keto-PGF1α和雌激素均高于对照组[(184±34),(169±24) ng/L比(139±13) ng/L(肺动脉VIP)；(204±26),(181±24) ng/L比(141±14) ng/L(桡动脉VIP)；(120±15),(119±11) ng/L比(100±11)ng/L(肺动脉6-keto-PGF1α)；(124±22),(124±24) ng/L比(105±23) ng/L(桡动脉6-keto-PGF1α),(45±8),(45±10) pmol/L比(39±8)pmol/L(肺动脉雌激素)；(43±8),(41±11) pmol/L比(33±4)pmol/L(桡动脉雌激素),差异均有统计学意义(均P＜0.05),但HPS组和慢性肝病组组间差异无统计学意义.结论 HPS患者肺循环中NO水平异常升高,可能直接导致肺血管扩张,其肺循环中内皮素1和TNF-α含量明显增加,可能通过不同方式诱导NO的合成,在HPS发生中起到重要作用.
目的 分析肝肺綜閤徵(HPS)患者體循環和肺循環中血管活性物質的含量及意義.方法 將上海交通大學醫學院附屬仁濟醫院2009年8月至2011年6月接受門靜脈高壓癥手術和肝移植手術治療的患者分為HPS組(18例),慢性肝病組(18例,無原髮心肺疾病、非HPS的慢性肝病患者)和對照組(18例,同期因胃腸道腫瘤接受手術的患者),經橈動脈置管和右心導管法抽取橈動脈和肺動脈血,以酶聯免疫吸附法檢測NO、內皮素1、腫瘤壞死因子α(TNF-α)、前列環素代謝物(6-keto-PGF1α)、血管活性腸肽(VIP)和雌激素等血管活性物質含量.結果 HPS組、慢性肝病組和對照組肺動脈和橈動脈中NO、內皮素1和TNF-α分彆為(122±16)、(111±10)、(102±12)μmol/L(肺動脈NO)；(141±21)、(123±21)、(107±13) μmol/L(橈動脈NO)；(149±16)、(116±24)、(92±22) ng/L(肺動脈內皮素1)；(123±26)、(103±14)、(89±16)ng/L(橈動脈內皮素1)；(360±43)、(317±68)、(278±38) ng/L(肺動脈TNF-α)；(404±39)、(363±49)、(257±49) ng/L(橈動脈TNF-α),組間兩兩比較差異均有統計學意義(均P＜0.05).HPS組和慢性肝病組肺動脈和橈動脈中,VIP、6-keto-PGF1α和雌激素均高于對照組[(184±34),(169±24) ng/L比(139±13) ng/L(肺動脈VIP)；(204±26),(181±24) ng/L比(141±14) ng/L(橈動脈VIP)；(120±15),(119±11) ng/L比(100±11)ng/L(肺動脈6-keto-PGF1α)；(124±22),(124±24) ng/L比(105±23) ng/L(橈動脈6-keto-PGF1α),(45±8),(45±10) pmol/L比(39±8)pmol/L(肺動脈雌激素)；(43±8),(41±11) pmol/L比(33±4)pmol/L(橈動脈雌激素),差異均有統計學意義(均P＜0.05),但HPS組和慢性肝病組組間差異無統計學意義.結論 HPS患者肺循環中NO水平異常升高,可能直接導緻肺血管擴張,其肺循環中內皮素1和TNF-α含量明顯增加,可能通過不同方式誘導NO的閤成,在HPS髮生中起到重要作用.
목적 분석간폐종합정(HPS)환자체순배화폐순배중혈관활성물질적함량급의의.방법 장상해교통대학의학원부속인제의원2009년8월지2011년6월접수문정맥고압증수술화간이식수술치료적환자분위HPS조(18례),만성간병조(18례,무원발심폐질병、비HPS적만성간병환자)화대조조(18례,동기인위장도종류접수수술적환자),경뇨동맥치관화우심도관법추취뇨동맥화폐동맥혈,이매련면역흡부법검측NO、내피소1、종류배사인자α(TNF-α)、전렬배소대사물(6-keto-PGF1α)、혈관활성장태(VIP)화자격소등혈관활성물질함량.결과 HPS조、만성간병조화대조조폐동맥화뇨동맥중NO、내피소1화TNF-α분별위(122±16)、(111±10)、(102±12)μmol/L(폐동맥NO)；(141±21)、(123±21)、(107±13) μmol/L(뇨동맥NO)；(149±16)、(116±24)、(92±22) ng/L(폐동맥내피소1)；(123±26)、(103±14)、(89±16)ng/L(뇨동맥내피소1)；(360±43)、(317±68)、(278±38) ng/L(폐동맥TNF-α)；(404±39)、(363±49)、(257±49) ng/L(뇨동맥TNF-α),조간량량비교차이균유통계학의의(균P＜0.05).HPS조화만성간병조폐동맥화뇨동맥중,VIP、6-keto-PGF1α화자격소균고우대조조[(184±34),(169±24) ng/L비(139±13) ng/L(폐동맥VIP)；(204±26),(181±24) ng/L비(141±14) ng/L(뇨동맥VIP)；(120±15),(119±11) ng/L비(100±11)ng/L(폐동맥6-keto-PGF1α)；(124±22),(124±24) ng/L비(105±23) ng/L(뇨동맥6-keto-PGF1α),(45±8),(45±10) pmol/L비(39±8)pmol/L(폐동맥자격소)；(43±8),(41±11) pmol/L비(33±4)pmol/L(뇨동맥자격소),차이균유통계학의의(균P＜0.05),단HPS조화만성간병조조간차이무통계학의의.결론 HPS환자폐순배중NO수평이상승고,가능직접도치폐혈관확장,기폐순배중내피소1화TNF-α함량명현증가,가능통과불동방식유도NO적합성,재HPS발생중기도중요작용.
Objective To investigate the abnormality of vasoactive substances in systemic and pulmonary circulations in hepatopulmonary syndrome.Methods From August 2009 to June 2011,18 patients with hepatopulmonary syndrome (group H) in general surgery department and transplantation center of renji hospital were enrolled in the study,18 patients with chronic liver disease (group C) and 18 with gastrointestinal cancer (group N) were studied as control groups.Blood samples in radial artery and pulmonary artery of all patients were collected and 6 vasoactive substances [nitrogen oxide (NO),endothelin 1 (ET-1),tumor necrosis factor α (TNF-α),6-ketoPGF1 α,vasoactive intestinal peptide(VIP) and estrogen(E)] were tested.Results The concentration of NO-,ET1 and TNF-α in radial artery and pulmonary artery differed significantly among group H,group C and group N seperately [pulmonary artery NO:(122 ± 16),(111 ± 10) μmol/L vs (102 ± 12) μmol/L; radial artery NO:(141 ± 21),(123 ± 21) μmol/L vs (107 ± 13) μmol/L; pulmonary artery ET-1:(149 ± 16),(116 ± 24) ng/L vs (92 ± 22) ng/L;radial artery ET-1:(123 ± 26),(103 ± 14) ng/L vs (89 ± 16) ng/L; pulmonary artery TNF-α:(360 ± 43),(317 ± 68) ng/L vs (278 ± 38) ng/L; radial artery TNF-α:(404 ± 39),(363 ± 49) ng/L vs (257 ± 49) ng/L,P ＜0.05].The VIP,6-keto-PGF1 α and E in radial artery and pulmonary artery in group H and group C were higher than those in group N with statistic differences [pulmonary artery VIP:(184 ± 34),(169 ± 24) ng/L vs (139 ±13)ng/L;radial artery VIP:(204 ± 26),(181 ± 24) ng/L vs (141 ± 14) ng/L; pulmonary artery 6-keto-PGF1o:(120 ±15),(119 ± 11) ng/L vs (100 ± 11) ng/L;radial artery 6-keto-PGF1α:(124 ±22),(124 ± 24) ng/L vs (105 ± 23) ng/L,pulmonary artery E:(45 ± 8),(45 ± 10) pmol/L vs (39 ± 8) pmol/L; radial artery E:(43 ± 8),(41 ± 11)pmol/L vs (33 ± 4)pmol/L,P ＜ 0.05],but there was no significant difference between group H and group C.Conclusion The level of NO in pulmonary circulation in HPS patients is high and may be the cause of dilation of pulmonary vascular bed in HPS patients.ET-1 and TNF-α,which can induce the synthesis of NO and increase in HPS patients may play an important role in the pathogenesis of HPS.
