中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
2011年
2期
78-81
,共4页
赵立明%高春锦%杨晋才%武连华%梁方%吕彧
趙立明%高春錦%楊晉纔%武連華%樑方%呂彧
조립명%고춘금%양진재%무련화%량방%려욱
股骨头缺血坏死%激素%组织因子%肿瘤坏死因子%高压氧
股骨頭缺血壞死%激素%組織因子%腫瘤壞死因子%高壓氧
고골두결혈배사%격소%조직인자%종류배사인자%고압양
Avascular necrosis of the femoral head%Hormone%Tissue factor%Tumor necrosis factor%Hyperbaric oxygen
目的 通过研究激素性股骨头坏死(steroid-induced avascular necrosis of the femoral head,SANFH)兔血组织因子(TF)和肿瘤坏死因子(TNF-α)的动态变化及高压氧(hyperbaric oxygen,HBO)对其影响,探讨SANFH发生机制和高压氧治疗的作用机制.方法 健康新西兰白兔78只,按数字随机表法分为3组:正常对照组(N组)7只,模型组(M组)41只,高压氧组(HBO组)30只.模型组又分为造模即刻组(M0组)10只,造模2周组(M2组)10只、造模4周组(M4组)10只、造模6周组(M6组)11只.HBO组分为:2周HBO组(HBO2组)7只、4周HBO组(HBO4组)11只、6周HBO组(HBO6组)12只.采用注射内毒素加甲强龙的方法对模型组及HBO组进行造模处理,HBO组在制模后开始HBO处理,每天1次,并于制模2周、4周、6周分别取静脉血检测TF、TNF-α的变化,于相应取血时间点取血后处死实验动物,取双侧股骨头组织进行组织学观察.结果 M各组TF[M0:(281.42±46.71)pg/ml,M2:(242.25±131.87)pg/ml,M4:(176.39±66.39)pg/ml,M6:(121.32±107.70)pg/ml]、TNF-α[M0:(418.83±75.99)pg/ml,M2:(424.41±57.01)pg/ml,M4:(424.05±136.44)pg/ml,M6:(344.34±112.89)pg/ml]均高于N组[TF:(137.55±21.65)pg/ml,TNF-α:(312.17±31.12)pg/ml],P＜0.05或P＜0.01;而HBO各组与M各组同时间点比较其表达均降低,P＜0.05或P＜0.01;组织学结果:N组股骨头组织形态正常,M组股骨十骺端髓腔内骨髓组织脂肪细胞增多增大、可见变性及片状坏死、炎性细胞浸润、出血、水肿及微小血管血栓、骨髓腔纤维化、造血细胞减少、股骨头萎缩明显;HBO各组脂肪变性、坏死出现率与M组比较明显减少,骨小梁间骨髓炎症反应明显减轻,未见到血栓形成,可见到骨母细胞活跃增生、骨髓纤维化、新生骨形成、股骨头萎缩不明显、骨基质正常.结论 兔SANFH时血中TF、TNF-α含量增高,诱导了体内凝血反应,使股骨头处血栓形成,HBO治疗可抑制实验动物体内TF、TNF-α的释放,从而改善凝血功能的异常,治疗股骨头坏死.
目的 通過研究激素性股骨頭壞死(steroid-induced avascular necrosis of the femoral head,SANFH)兔血組織因子(TF)和腫瘤壞死因子(TNF-α)的動態變化及高壓氧(hyperbaric oxygen,HBO)對其影響,探討SANFH髮生機製和高壓氧治療的作用機製.方法 健康新西蘭白兔78隻,按數字隨機錶法分為3組:正常對照組(N組)7隻,模型組(M組)41隻,高壓氧組(HBO組)30隻.模型組又分為造模即刻組(M0組)10隻,造模2週組(M2組)10隻、造模4週組(M4組)10隻、造模6週組(M6組)11隻.HBO組分為:2週HBO組(HBO2組)7隻、4週HBO組(HBO4組)11隻、6週HBO組(HBO6組)12隻.採用註射內毒素加甲彊龍的方法對模型組及HBO組進行造模處理,HBO組在製模後開始HBO處理,每天1次,併于製模2週、4週、6週分彆取靜脈血檢測TF、TNF-α的變化,于相應取血時間點取血後處死實驗動物,取雙側股骨頭組織進行組織學觀察.結果 M各組TF[M0:(281.42±46.71)pg/ml,M2:(242.25±131.87)pg/ml,M4:(176.39±66.39)pg/ml,M6:(121.32±107.70)pg/ml]、TNF-α[M0:(418.83±75.99)pg/ml,M2:(424.41±57.01)pg/ml,M4:(424.05±136.44)pg/ml,M6:(344.34±112.89)pg/ml]均高于N組[TF:(137.55±21.65)pg/ml,TNF-α:(312.17±31.12)pg/ml],P＜0.05或P＜0.01;而HBO各組與M各組同時間點比較其錶達均降低,P＜0.05或P＜0.01;組織學結果:N組股骨頭組織形態正常,M組股骨十骺耑髓腔內骨髓組織脂肪細胞增多增大、可見變性及片狀壞死、炎性細胞浸潤、齣血、水腫及微小血管血栓、骨髓腔纖維化、造血細胞減少、股骨頭萎縮明顯;HBO各組脂肪變性、壞死齣現率與M組比較明顯減少,骨小樑間骨髓炎癥反應明顯減輕,未見到血栓形成,可見到骨母細胞活躍增生、骨髓纖維化、新生骨形成、股骨頭萎縮不明顯、骨基質正常.結論 兔SANFH時血中TF、TNF-α含量增高,誘導瞭體內凝血反應,使股骨頭處血栓形成,HBO治療可抑製實驗動物體內TF、TNF-α的釋放,從而改善凝血功能的異常,治療股骨頭壞死.
목적 통과연구격소성고골두배사(steroid-induced avascular necrosis of the femoral head,SANFH)토혈조직인자(TF)화종류배사인자(TNF-α)적동태변화급고압양(hyperbaric oxygen,HBO)대기영향,탐토SANFH발생궤제화고압양치료적작용궤제.방법 건강신서란백토78지,안수자수궤표법분위3조:정상대조조(N조)7지,모형조(M조)41지,고압양조(HBO조)30지.모형조우분위조모즉각조(M0조)10지,조모2주조(M2조)10지、조모4주조(M4조)10지、조모6주조(M6조)11지.HBO조분위:2주HBO조(HBO2조)7지、4주HBO조(HBO4조)11지、6주HBO조(HBO6조)12지.채용주사내독소가갑강룡적방법대모형조급HBO조진행조모처리,HBO조재제모후개시HBO처리,매천1차,병우제모2주、4주、6주분별취정맥혈검측TF、TNF-α적변화,우상응취혈시간점취혈후처사실험동물,취쌍측고골두조직진행조직학관찰.결과 M각조TF[M0:(281.42±46.71)pg/ml,M2:(242.25±131.87)pg/ml,M4:(176.39±66.39)pg/ml,M6:(121.32±107.70)pg/ml]、TNF-α[M0:(418.83±75.99)pg/ml,M2:(424.41±57.01)pg/ml,M4:(424.05±136.44)pg/ml,M6:(344.34±112.89)pg/ml]균고우N조[TF:(137.55±21.65)pg/ml,TNF-α:(312.17±31.12)pg/ml],P＜0.05혹P＜0.01;이HBO각조여M각조동시간점비교기표체균강저,P＜0.05혹P＜0.01;조직학결과:N조고골두조직형태정상,M조고골십후단수강내골수조직지방세포증다증대、가견변성급편상배사、염성세포침윤、출혈、수종급미소혈관혈전、골수강섬유화、조혈세포감소、고골두위축명현;HBO각조지방변성、배사출현솔여M조비교명현감소,골소량간골수염증반응명현감경,미견도혈전형성,가견도골모세포활약증생、골수섬유화、신생골형성、고골두위축불명현、골기질정상.결론 토SANFH시혈중TF、TNF-α함량증고,유도료체내응혈반응,사고골두처혈전형성,HBO치료가억제실험동물체내TF、TNF-α적석방,종이개선응혈공능적이상,치료고골두배사.
Objective To investigate dynamic changes in serum TF and TNF-α in the rabbit model of steroid-induced avascular osteonecrosis of femoral head ( SANFH) and also to explore the mechanism of SANFH, as well as effects of hyperbaric oxygen ( HBO) on SANFH. Methods Seventy-eight New Zealand male rabbits were randomly divided into 3 groups:the normal control (group N) (7 animals), the model group (group M) (41 animals) and the HBO group (group H) (30 animals). The model group was subdivided into the immediate model group (the M0 group) (10 animals), the two-week model group (the M2 group) (10 animals), the four-week model group (the M4 group) (10 animals) and the six-week model group (the M6 group) (11 animals). The HBO group was further divided into the 2-week HBO therapy group (HBO2) (7 animals), the 4-week HBO therapy group (HBO4) (11 animals) and the 6-week HBO therapy group (HBO6) (12 animals). Through injection of endotoxin and methyl-prednisolone, rabbits in the group HBO2, HBO4 and HBO6 received HBO therapy 1 hour daily from the second day of the experiment. The durations of HBO therapy were 2 weeks ( HBO2), and 4 weeks respectively. The animals were sacrificed after blood samples were taken at respective blood collection time. Then, levels of TF, TNF-α in the serum were measured and the histological changes in the femoral heads were observed. Results Levels of TF and TNF-α in group M0 increased significantly, when compared with those of group N (P ＜0. 05 or P ＜0.01), while for the HBO subgroups the expression of TF and TNF-α measured at the same time points all decreased, when compared with that of the model subgroups (P＜0. 05 or P ＜0.01). To elaborate, TF levels in group M2 and M4 were much higher than those in group HBO2 and HBO4 ( P＜0. 01 ). TF level in group M6 was higher than that in group HB06 ( P ＜ 0.05). TNF-α in group M0 also increased significantly, when compared with that in group N( P ＜0.01). TNF-α levels in group M2 and M6 were also much higher than those in group HBO2 and HBO6 ( both P ＜0. 01 ). TNF-α in group M4 was higher than that in group HBO4 (P＜0.01). Histological examination revealed that tissues of the femoral heads in group N were normal, osteonecrosis and thrombus could be noted in group M2 and M4, hyperplasia fibrosis could be found in group M6, and osteonecrosis in HBO2 and HB04 groups seemed less severer than that in M2 and M4 groups, no thrombi in HBO2, HBO4 groups were noted, and growth of new bones were detected in HBO4 and HBO6. Conclusions The levels of TF and TNF-α levels increased in the rabbit model of SANFH, inducing blood coagulation. Thrombosis at the femoral heads was one of the causes of SANFH. HBO therapy could inhibit the release of TF and TNF-α, thus improving the abnormality of blood coagulation and enhancing treatment of osteonecrosis.
