生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2005年
6期
725-730
,共6页
王向红%刘声远%陈宝生%余上斌%叶仕乔%陈琪玲
王嚮紅%劉聲遠%陳寶生%餘上斌%葉仕喬%陳琪玲
왕향홍%류성원%진보생%여상빈%협사교%진기령
组胺%哮喘%气道重塑
組胺%哮喘%氣道重塑
조알%효천%기도중소
histamine%asthma%airway remodeling
本研究旨在探讨组胺在哮喘豚鼠气道重塑中的作用.将50只健康雄性豚鼠随机分为5组.正常对照组:雾化吸入蒸馏水8周;哮喘模型组:致敏后雾化吸入卵白蛋白(ovalbumin,OVA)8周;哮喘模型延续组:致敏后雾化吸入OVA 14周;组胺组:致敏后雾化吸入OVA 14周,最后6周同时加用组胺;组胺受体拮抗剂组:致敏后雾化吸入OVA 14周,最后6周同时加用组胺受体拈抗剂.检测血清组胺、Na+、Cl-浓度、动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)、pH、实际碳酸氢盐(actual bicarbonate,AB)、标准碳酸氢盐(standard bicarbonate,SB)以及气道壁粘膜层、基底膜层和平滑肌层厚度.所得结果如下:(1)哮喘模型组血清组胺浓度、气道壁厚度明显高于正常对照组(P<0.01);哮喘模型延续组明显高于哮喘模型组(P<0.01);组胺组明显高于哮喘模型延续组(P<0.01);组胺受体拮抗剂组低于哮喘模型延续组(P<0.05,0.01).(2)哮喘模型组PaO2小于正常对照组(P<0.01);哮喘模型延续组PaO2、pH、AB、SB小于哮喘模型组(P<0.01),而PaCO2大于哮喘模型组(P<0.01);组胺组PaO2、pH、AB、SB小于哮喘模型延续组(P<0.01),而PaCO2大于哮喘模型延续组(P<0.01);组胺受体拮抗剂组PaO2、pH、AB、SB高于哮喘模型延续组(P<0.01),而PaCO2低于哮喘模型延续组(P<0.01);血清Na+、Cl-浓度各组间差异不明显.以上结果提示:(1)组胺在哮喘气道重塑中起介导作用.(2)应用组胺受体拮抗剂对防治哮喘气道重塑有一定作用.(3)PaO2、pH与气管、肺门支气管、肺外周小气道气道壁厚度呈负相关(P<0.01),而PaCO2、阴离子间隙(anion gap,AG)值与上述气道壁厚度呈正相关(P<0.01).
本研究旨在探討組胺在哮喘豚鼠氣道重塑中的作用.將50隻健康雄性豚鼠隨機分為5組.正常對照組:霧化吸入蒸餾水8週;哮喘模型組:緻敏後霧化吸入卵白蛋白(ovalbumin,OVA)8週;哮喘模型延續組:緻敏後霧化吸入OVA 14週;組胺組:緻敏後霧化吸入OVA 14週,最後6週同時加用組胺;組胺受體拮抗劑組:緻敏後霧化吸入OVA 14週,最後6週同時加用組胺受體拈抗劑.檢測血清組胺、Na+、Cl-濃度、動脈血氧分壓(PaO2)、動脈血二氧化碳分壓(PaCO2)、pH、實際碳痠氫鹽(actual bicarbonate,AB)、標準碳痠氫鹽(standard bicarbonate,SB)以及氣道壁粘膜層、基底膜層和平滑肌層厚度.所得結果如下:(1)哮喘模型組血清組胺濃度、氣道壁厚度明顯高于正常對照組(P<0.01);哮喘模型延續組明顯高于哮喘模型組(P<0.01);組胺組明顯高于哮喘模型延續組(P<0.01);組胺受體拮抗劑組低于哮喘模型延續組(P<0.05,0.01).(2)哮喘模型組PaO2小于正常對照組(P<0.01);哮喘模型延續組PaO2、pH、AB、SB小于哮喘模型組(P<0.01),而PaCO2大于哮喘模型組(P<0.01);組胺組PaO2、pH、AB、SB小于哮喘模型延續組(P<0.01),而PaCO2大于哮喘模型延續組(P<0.01);組胺受體拮抗劑組PaO2、pH、AB、SB高于哮喘模型延續組(P<0.01),而PaCO2低于哮喘模型延續組(P<0.01);血清Na+、Cl-濃度各組間差異不明顯.以上結果提示:(1)組胺在哮喘氣道重塑中起介導作用.(2)應用組胺受體拮抗劑對防治哮喘氣道重塑有一定作用.(3)PaO2、pH與氣管、肺門支氣管、肺外週小氣道氣道壁厚度呈負相關(P<0.01),而PaCO2、陰離子間隙(anion gap,AG)值與上述氣道壁厚度呈正相關(P<0.01).
본연구지재탐토조알재효천돈서기도중소중적작용.장50지건강웅성돈서수궤분위5조.정상대조조:무화흡입증류수8주;효천모형조:치민후무화흡입란백단백(ovalbumin,OVA)8주;효천모형연속조:치민후무화흡입OVA 14주;조알조:치민후무화흡입OVA 14주,최후6주동시가용조알;조알수체길항제조:치민후무화흡입OVA 14주,최후6주동시가용조알수체념항제.검측혈청조알、Na+、Cl-농도、동맥혈양분압(PaO2)、동맥혈이양화탄분압(PaCO2)、pH、실제탄산경염(actual bicarbonate,AB)、표준탄산경염(standard bicarbonate,SB)이급기도벽점막층、기저막층화평활기층후도.소득결과여하:(1)효천모형조혈청조알농도、기도벽후도명현고우정상대조조(P<0.01);효천모형연속조명현고우효천모형조(P<0.01);조알조명현고우효천모형연속조(P<0.01);조알수체길항제조저우효천모형연속조(P<0.05,0.01).(2)효천모형조PaO2소우정상대조조(P<0.01);효천모형연속조PaO2、pH、AB、SB소우효천모형조(P<0.01),이PaCO2대우효천모형조(P<0.01);조알조PaO2、pH、AB、SB소우효천모형연속조(P<0.01),이PaCO2대우효천모형연속조(P<0.01);조알수체길항제조PaO2、pH、AB、SB고우효천모형연속조(P<0.01),이PaCO2저우효천모형연속조(P<0.01);혈청Na+、Cl-농도각조간차이불명현.이상결과제시:(1)조알재효천기도중소중기개도작용.(2)응용조알수체길항제대방치효천기도중소유일정작용.(3)PaO2、pH여기관、폐문지기관、폐외주소기도기도벽후도정부상관(P<0.01),이PaCO2、음리자간극(anion gap,AG)치여상술기도벽후도정정상관(P<0.01).
To investigate the role of histamine in airway remodeling, 50 healthy guinea pigs were divided into 5 groups: control group:nebulized inhalation of distilled water for 8 weeks; asthma model group: nebulized inhalation of ovalbumin (OVA) for 8 weeks after sensitization; continued asthma model group: nebulized inhalation of OVA for 14 weeks after sensitization; histamine group: nebulized inhalation of OVA for 14 weeks after sensitization and histamine was added in the last 6 weeks; antagonist group: nebulized inhalation of OVA for 14 weeks after sensitization and histamine receptor antagonists were added in the last 6 weeks. For each group, the concentration of histamine, sodium ion (Na+), chlorine ion (Cl-), arterial partial pressure of oxygen (PaO2), arterial partial pressure of carbon dioxide (PaCO2), pH, actual bicarbonate (AB), standard bicarbonate (SB) in serum, and thickness of airway mucosa, base membrane and smooth muscle were measured and compared with each other. The results showed that: (1) the concentration of histamine in serum and the thickness of airway increased, the following order was, the control group, the asthma model group, the continued asthma model group and histamine group (P<0.01); and the concentration of histamine in serum and the thickness of airway of antagonist group was lower than that of the continued asthma model group (P<0.05, 0.01). (2) PaO2 of the asthma model group was lower than that of the normal control group (P<0.01); PaO2, pH, AB, SB decreased, the following order was, the asthma model group,the continued asthma model group and the histamine group (P<0.01); and PaO2, pH, AB, SB of the antagonist group was higher than that of the continued asthma model group (P<0.01); but for PaCO2, the order was converse (P<0.01); For the concentration of Na+ and Cl- in serum, there was no difference among these groups. It is concluded that: (1) Histamine is one of the mediators in the airway remodeling of asthma. (2) Histamine receptor antagonists may play a role in preventing and treating airway remodeling. (3) There is a negative correlation between the PaO2, pH and the wall thickness of the airway (P<0.01), while a positive correlation between the PaCO2, anion gap (AG) and the wall thickness of the airway (P<0.01).