目的 创新建立肺气肿合并睡眠诱导低氧大鼠模型并探讨凝血功能的变化.方法 纳入30只Wistar大鼠,按暴露条件分3组.每组10只.A组(单纯睡眠诱导低氧组).正常饲养28 d,第29天起在睡眠时段暴露于含12.5%氧的混合气中共3 h(分4次给予,每次45 min);B组(单纯肺气肿组),每天分两次暴露于纸烟烟雾共约1 h(每次约30 min);C组(肺气肿合并睡眠诱导低氧组),前28 d同B组暴露,第29天起继续予熏烟暴露,同时在睡眠时段暴露于含12.5%氧的混合气中共3 h(分4次给予,每次45 min).各组大鼠连续暴露至56 d后处死,采集肺组织和全血.肺组织切片染色后经半定量图像分析,计算肺病理评分、肺平均内衬间隔(MLI)和平均肺泡数(MAN)来评价肺组织病理学改变.而后测定全血中抗凝血酶Ⅲ(AT Ⅲ)、纤维蛋白原(FIB)、血管性血友病因子(vWF)、凝血因子VⅢ(FⅧ)的活性.以SPSS 11.5进行统计学处理.采用单因素方差分析行组间比较,组内比较采用SNK-q检验.结果 B、C组大鼠肺组织切片均呈现明显肺气肿样改变.各组肺病理评分和MLI差异明显(F=520.751、F＝1 037.787,P值均<0.05).B组[(52.00±5.16)%、(91.30+2.26)μm]和C组[(73.30±3.86)%、(99.32±2.81)μm]均高于A组[(16.20±2.53)%、(46.79±3.18)μm,q=28.312、q＝45.157、q＝50.666、q=59.800,P值均<0.053,且C组高于B组(q=16.845、q=9.135,P值均<0.05);各组MAN差异明显(F＝313.304,P<0.05),B组[(103.55±4.45)/mm2]和C组[(83.70±4.72)/mm2]均低于A组[(151.59±8.64)/mm2,q=24.358、q=34.426,P值均<0.053],且C组低于B组(q=10.068.P<0.05).各组大鼠全血ATⅢ活性差异明显(F＝25.386.P<0.05).B组[(107.39±8.05)%]和C组[(99.04±3.99)%]ATⅢ活性均低于A组[(116.20±2.53)%.q＝5.173、q=10.076,P值均<0.05].且C组低于B组(q=4.903,P<0.05);各组大鼠全血FIB、vWF和FⅧ活性差异明显(F=112.969、F=223.666,F＝70.040.P值均<0.05),B组[(1774.60±72.49)mg/L、(64.45±1.72)%、(227.78±10.38)%]和C组[(1984.00c73.69)mg/L、(71.96±1.85)%、(303.25±32.93)%]FIB均高于A组[(1515.50±62.79)mg/L、(56.02±1.47)%、(200.36±4.88)%,q=11.734、q=21.218、q=15.810、q=29.895,q=4.307、q=16.16l,P值均<0.05],且C组高于B组(q=9.483,q＝14.085、q=11.854.P值均<0.05).结论 本研究成功建立了肺气肿合并睡眠诱导低氧大鼠模型.肺组织切片病理提示肺气肿大鼠合并睡眠诱导低氧后肺气肿程度加重;大鼠患肺气肿后血液凝固性增强,而合并睡眠诱导低氧后,该血液高凝状态进一步加重.
目的 創新建立肺氣腫閤併睡眠誘導低氧大鼠模型併探討凝血功能的變化.方法 納入30隻Wistar大鼠,按暴露條件分3組.每組10隻.A組(單純睡眠誘導低氧組).正常飼養28 d,第29天起在睡眠時段暴露于含12.5%氧的混閤氣中共3 h(分4次給予,每次45 min);B組(單純肺氣腫組),每天分兩次暴露于紙煙煙霧共約1 h(每次約30 min);C組(肺氣腫閤併睡眠誘導低氧組),前28 d同B組暴露,第29天起繼續予熏煙暴露,同時在睡眠時段暴露于含12.5%氧的混閤氣中共3 h(分4次給予,每次45 min).各組大鼠連續暴露至56 d後處死,採集肺組織和全血.肺組織切片染色後經半定量圖像分析,計算肺病理評分、肺平均內襯間隔(MLI)和平均肺泡數(MAN)來評價肺組織病理學改變.而後測定全血中抗凝血酶Ⅲ(AT Ⅲ)、纖維蛋白原(FIB)、血管性血友病因子(vWF)、凝血因子VⅢ(FⅧ)的活性.以SPSS 11.5進行統計學處理.採用單因素方差分析行組間比較,組內比較採用SNK-q檢驗.結果 B、C組大鼠肺組織切片均呈現明顯肺氣腫樣改變.各組肺病理評分和MLI差異明顯(F=520.751、F＝1 037.787,P值均<0.05).B組[(52.00±5.16)%、(91.30+2.26)μm]和C組[(73.30±3.86)%、(99.32±2.81)μm]均高于A組[(16.20±2.53)%、(46.79±3.18)μm,q=28.312、q＝45.157、q＝50.666、q=59.800,P值均<0.053,且C組高于B組(q=16.845、q=9.135,P值均<0.05);各組MAN差異明顯(F＝313.304,P<0.05),B組[(103.55±4.45)/mm2]和C組[(83.70±4.72)/mm2]均低于A組[(151.59±8.64)/mm2,q=24.358、q=34.426,P值均<0.053],且C組低于B組(q=10.068.P<0.05).各組大鼠全血ATⅢ活性差異明顯(F＝25.386.P<0.05).B組[(107.39±8.05)%]和C組[(99.04±3.99)%]ATⅢ活性均低于A組[(116.20±2.53)%.q＝5.173、q=10.076,P值均<0.05].且C組低于B組(q=4.903,P<0.05);各組大鼠全血FIB、vWF和FⅧ活性差異明顯(F=112.969、F=223.666,F＝70.040.P值均<0.05),B組[(1774.60±72.49)mg/L、(64.45±1.72)%、(227.78±10.38)%]和C組[(1984.00c73.69)mg/L、(71.96±1.85)%、(303.25±32.93)%]FIB均高于A組[(1515.50±62.79)mg/L、(56.02±1.47)%、(200.36±4.88)%,q=11.734、q=21.218、q=15.810、q=29.895,q=4.307、q=16.16l,P值均<0.05],且C組高于B組(q=9.483,q＝14.085、q=11.854.P值均<0.05).結論 本研究成功建立瞭肺氣腫閤併睡眠誘導低氧大鼠模型.肺組織切片病理提示肺氣腫大鼠閤併睡眠誘導低氧後肺氣腫程度加重;大鼠患肺氣腫後血液凝固性增彊,而閤併睡眠誘導低氧後,該血液高凝狀態進一步加重.
목적 창신건립폐기종합병수면유도저양대서모형병탐토응혈공능적변화.방법 납입30지Wistar대서,안폭로조건분3조.매조10지.A조(단순수면유도저양조).정상사양28 d,제29천기재수면시단폭로우함12.5%양적혼합기중공3 h(분4차급여,매차45 min);B조(단순폐기종조),매천분량차폭로우지연연무공약1 h(매차약30 min);C조(폐기종합병수면유도저양조),전28 d동B조폭로,제29천기계속여훈연폭로,동시재수면시단폭로우함12.5%양적혼합기중공3 h(분4차급여,매차45 min).각조대서련속폭로지56 d후처사,채집폐조직화전혈.폐조직절편염색후경반정량도상분석,계산폐병리평분、폐평균내츤간격(MLI)화평균폐포수(MAN)래평개폐조직병이학개변.이후측정전혈중항응혈매Ⅲ(AT Ⅲ)、섬유단백원(FIB)、혈관성혈우병인자(vWF)、응혈인자VⅢ(FⅧ)적활성.이SPSS 11.5진행통계학처리.채용단인소방차분석행조간비교,조내비교채용SNK-q검험.결과 B、C조대서폐조직절편균정현명현폐기종양개변.각조폐병리평분화MLI차이명현(F=520.751、F＝1 037.787,P치균<0.05).B조[(52.00±5.16)%、(91.30+2.26)μm]화C조[(73.30±3.86)%、(99.32±2.81)μm]균고우A조[(16.20±2.53)%、(46.79±3.18)μm,q=28.312、q＝45.157、q＝50.666、q=59.800,P치균<0.053,차C조고우B조(q=16.845、q=9.135,P치균<0.05);각조MAN차이명현(F＝313.304,P<0.05),B조[(103.55±4.45)/mm2]화C조[(83.70±4.72)/mm2]균저우A조[(151.59±8.64)/mm2,q=24.358、q=34.426,P치균<0.053],차C조저우B조(q=10.068.P<0.05).각조대서전혈ATⅢ활성차이명현(F＝25.386.P<0.05).B조[(107.39±8.05)%]화C조[(99.04±3.99)%]ATⅢ활성균저우A조[(116.20±2.53)%.q＝5.173、q=10.076,P치균<0.05].차C조저우B조(q=4.903,P<0.05);각조대서전혈FIB、vWF화FⅧ활성차이명현(F=112.969、F=223.666,F＝70.040.P치균<0.05),B조[(1774.60±72.49)mg/L、(64.45±1.72)%、(227.78±10.38)%]화C조[(1984.00c73.69)mg/L、(71.96±1.85)%、(303.25±32.93)%]FIB균고우A조[(1515.50±62.79)mg/L、(56.02±1.47)%、(200.36±4.88)%,q=11.734、q=21.218、q=15.810、q=29.895,q=4.307、q=16.16l,P치균<0.05],차C조고우B조(q=9.483,q＝14.085、q=11.854.P치균<0.05).결론 본연구성공건립료폐기종합병수면유도저양대서모형.폐조직절편병리제시폐기종대서합병수면유도저양후폐기종정도가중;대서환폐기종후혈액응고성증강,이합병수면유도저양후,해혈액고응상태진일보가중.
Objective To establish a model in rats of pulmonary emphysema with sleep-induced hypoxemia(SIH),and discuss the function changes of coagulation system.Methods According to the different exposure condition,30 Wistar rats were randomly and averagely divided into three groups, 10 each group. Group A (the group of SIH) ,the rats were bred normally for 28 days,then exposed to the mixed gas of 12.5% oxygen for three hours during sleeping time every day (the exposed time was divided into four periods,45 rain each period);group B (the group of emphysema),the rats were exposed to cigarefte smoke two times every day, about 30 min each time; group C (the group of emphysema and SIH), the exposure condition of group B for 28 days,then still exposed to cigarette smoke and also exposed to the mixed gas of 12.5% oxygen for three hours during sleeping time every day (the exposed time was divided into four periods,45 rain each period). All the rats were exposed for 56 days continuously,and then killed. The lungs and whole blood were collected. Lungs were cut and stained with HE. Semiquantitative image analytic method was used to observe the histopathological features, which were quantitatively analyzed hy pathological score of lungs,mean linear intercept(MLI) and mean alveolus number(MAN). And then, AT Ⅲ, FIB,vWF, F Ⅷwere tested. The data were analyzed by SPSS 11.5 system. Group comparison was determined by one-factor analysis of variance. The comparison between two groups was measured by SNK-q test. Results Group B and C got the histopathological changes of emphysema. Pathological score of lungs and MLI were significantly different from groups( F= 520. 751, F= 1037. 787, both P<0.05 ), B[( 52.00±5.16 ) %,(91.30± 2.26) μm] and C [( 73.30±3.86 )%, (99.32±2.81 ) μm] were significantly higher than A [(16.20±2.53)% ,(46. 79±3. 18) μm, q =28. 312, q=45. 157, q =50. 666, q =59. 800,all P<0.05],Cwas significantly higher than B(q= 16. 845, q=9. 135,all P<(0.05);MAN was significantly different from groups(F= 313. 304, P<0.05), B[(103.55+4.45)/mm2] and C [(83.70±4.72)/mm2] were significantly lower than A[(151.59±8.64)/mm2, q=24.358, q=34.426, both P<0.05],C was significantly lower than B(q=10. 068, P<0.05). Levels of AT Ⅲ were significantly different from groups (F=25.386, P<0.05),AT Ⅲ of B[(107.39+8.05)%] and C [(99.04±3.99)%] were significantly lower than A [(116.20 4±2.53) %, q=5.173, q= 10. 076, both P<0.05], C was significantly lower than B (q=4. 903, P<0.05). Levels of FIB, vWF and F Ⅷ were significantly different from groups(F= 112. 969, F=223. 666, F=70.04,all P <0. 05),B[(1774.60+72.49) mg/L,(64.45+ 1.72)%,(227. 78±10. 38) %] and C [(1984.00±73.69) mg/L), (71.96±1.85 )%, (303.25±32.93 )%] were significantly higher than A[(1515. 50+62. 79) mg/L,(56. 02±1.47)%,(200.36±4.88) %, q=11. 734, q=21. 218, q=15. 810, q=29. 895, q=4. 307, q=16. 161 ,all P<0.05],C was significantly higher than B(q =9. 483, q=14.085, q=11. 854, all P<0.05). Conclusions This study established a rat model of pulmonary emphysema with SIH successfully, It was found that the histopathological change of pulmonary emphysema aggravated while the pulmonary emphysema rats were exposed to sleep hypoxemia. The rats of emphysema were in the status of hypercoagulation which was more severe than normal. While exposed to sleep hypoxemia, the status became further more severe.
