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
2015年
1期
32-36
,共5页
崔操%李厚成%郭一行%李彬彬
崔操%李厚成%郭一行%李彬彬
최조%리후성%곽일행%리빈빈
关节软骨%股骨头坏死%高压氧%血管内皮生长因子
關節軟骨%股骨頭壞死%高壓氧%血管內皮生長因子
관절연골%고골두배사%고압양%혈관내피생장인자
Capillary vessel%Necrosis of femoral head%Hyperbaric oxygen%Vascular endothelial growth factor
目的 观察兔激素性股骨头坏死过程中关节软骨的变化及在高压氧治疗过程中的病理变化,探讨高压氧治疗促进关节软骨修复的作用机制.方法 健康日本成年大耳白兔60只,按照数字表法随机分模型组(42只)及空白对照组(18只).模型组每周2次肌肉注射醋酸泼尼松龙10 mg/kg,对照组每周2次肌肉注射生理盐水2 ml,共6周.随后将模型组同样按照数字表法随机分为高压氧治疗组(16只)及对照组(16只),治疗组行高压氧治疗,共持续6周.对照组呼吸常压新鲜空气.检测实验后2、4、6、8、10、12周兔血液流变学参数、血管内皮生长因子(VEGF)、组织病理学变化及影像学变化.结果 模型组实验2、4、6周血流变学特性恶化;空白对照组与模型组比较,活化部分凝血活酶时间测定(APTT)第2、4、6周分别为[[(22.68±4.12),(21.68±7.45);(26.38±0.38,20.9±1.23);(27.00±1.21),(13.5±1.60)s];血浆凝血酶原时间测定(PT)第2、4、6周分别为[(7.42±0.13),(7.36±0.20);(7.47±0.24),(4.78 ±0.24);(7.38 ±0.10),(4.19±0.83)s;血小板数量第2、4、6周分别为[(418.75 ±64.23),(584.50±30.87);(396.00±54.49),(656.70 ±33.84);(427.00±45.32),(775.00±64.68)×109/ml].上述3项比较,2组差异均有统计学意义(P＜0.05).模型组兔股骨头微血管内膜断裂、血栓形成,股骨头骨质疏松,光镜下空骨陷窝数增多,脂肪细胞数增多,部分骨小梁断裂,透射电镜股骨头骨细胞体积缩小,核固缩,较多骨细胞已坏死溶解成碎片.高压氧治疗组血流变学特性趋向好转,股骨头软骨下区骨小梁表面的成骨细胞和血管出现大量的VEGF阳性表达,阳性部位主要位于血管内膜;光镜下可发现坏死的骨细胞有修复现象,透射电镜可见新生骨细胞.结论 大剂量激素可造成兔微血管内膜损伤,可能是兔股骨头坏死的重要原因,高压氧通过促进VEGF等细胞因子的分泌加速股骨头的软骨下骨再血管化和再骨化进程,促进软骨修复.
目的 觀察兔激素性股骨頭壞死過程中關節軟骨的變化及在高壓氧治療過程中的病理變化,探討高壓氧治療促進關節軟骨脩複的作用機製.方法 健康日本成年大耳白兔60隻,按照數字錶法隨機分模型組(42隻)及空白對照組(18隻).模型組每週2次肌肉註射醋痠潑尼鬆龍10 mg/kg,對照組每週2次肌肉註射生理鹽水2 ml,共6週.隨後將模型組同樣按照數字錶法隨機分為高壓氧治療組(16隻)及對照組(16隻),治療組行高壓氧治療,共持續6週.對照組呼吸常壓新鮮空氣.檢測實驗後2、4、6、8、10、12週兔血液流變學參數、血管內皮生長因子(VEGF)、組織病理學變化及影像學變化.結果 模型組實驗2、4、6週血流變學特性噁化;空白對照組與模型組比較,活化部分凝血活酶時間測定(APTT)第2、4、6週分彆為[[(22.68±4.12),(21.68±7.45);(26.38±0.38,20.9±1.23);(27.00±1.21),(13.5±1.60)s];血漿凝血酶原時間測定(PT)第2、4、6週分彆為[(7.42±0.13),(7.36±0.20);(7.47±0.24),(4.78 ±0.24);(7.38 ±0.10),(4.19±0.83)s;血小闆數量第2、4、6週分彆為[(418.75 ±64.23),(584.50±30.87);(396.00±54.49),(656.70 ±33.84);(427.00±45.32),(775.00±64.68)×109/ml].上述3項比較,2組差異均有統計學意義(P＜0.05).模型組兔股骨頭微血管內膜斷裂、血栓形成,股骨頭骨質疏鬆,光鏡下空骨陷窩數增多,脂肪細胞數增多,部分骨小樑斷裂,透射電鏡股骨頭骨細胞體積縮小,覈固縮,較多骨細胞已壞死溶解成碎片.高壓氧治療組血流變學特性趨嚮好轉,股骨頭軟骨下區骨小樑錶麵的成骨細胞和血管齣現大量的VEGF暘性錶達,暘性部位主要位于血管內膜;光鏡下可髮現壞死的骨細胞有脩複現象,透射電鏡可見新生骨細胞.結論 大劑量激素可造成兔微血管內膜損傷,可能是兔股骨頭壞死的重要原因,高壓氧通過促進VEGF等細胞因子的分泌加速股骨頭的軟骨下骨再血管化和再骨化進程,促進軟骨脩複.
목적 관찰토격소성고골두배사과정중관절연골적변화급재고압양치료과정중적병리변화,탐토고압양치료촉진관절연골수복적작용궤제.방법 건강일본성년대이백토60지,안조수자표법수궤분모형조(42지)급공백대조조(18지).모형조매주2차기육주사작산발니송룡10 mg/kg,대조조매주2차기육주사생리염수2 ml,공6주.수후장모형조동양안조수자표법수궤분위고압양치료조(16지)급대조조(16지),치료조행고압양치료,공지속6주.대조조호흡상압신선공기.검측실험후2、4、6、8、10、12주토혈액류변학삼수、혈관내피생장인자(VEGF)、조직병이학변화급영상학변화.결과 모형조실험2、4、6주혈류변학특성악화;공백대조조여모형조비교,활화부분응혈활매시간측정(APTT)제2、4、6주분별위[[(22.68±4.12),(21.68±7.45);(26.38±0.38,20.9±1.23);(27.00±1.21),(13.5±1.60)s];혈장응혈매원시간측정(PT)제2、4、6주분별위[(7.42±0.13),(7.36±0.20);(7.47±0.24),(4.78 ±0.24);(7.38 ±0.10),(4.19±0.83)s;혈소판수량제2、4、6주분별위[(418.75 ±64.23),(584.50±30.87);(396.00±54.49),(656.70 ±33.84);(427.00±45.32),(775.00±64.68)×109/ml].상술3항비교,2조차이균유통계학의의(P＜0.05).모형조토고골두미혈관내막단렬、혈전형성,고골두골질소송,광경하공골함와수증다,지방세포수증다,부분골소량단렬,투사전경고골두골세포체적축소,핵고축,교다골세포이배사용해성쇄편.고압양치료조혈류변학특성추향호전,고골두연골하구골소량표면적성골세포화혈관출현대량적VEGF양성표체,양성부위주요위우혈관내막;광경하가발현배사적골세포유수복현상,투사전경가견신생골세포.결론 대제량격소가조성토미혈관내막손상,가능시토고골두배사적중요원인,고압양통과촉진VEGF등세포인자적분비가속고골두적연골하골재혈관화화재골화진정,촉진연골수복.
Objective To observe capillary vessel changes in rabbits with hormone-induced avascular necrosis of femoral head and the possible mechanism involved in the treatment of the disorder with hyperbaric oxygen (HBO).Methods Forty-eight adult Japanese white rabbits were randomly divided into 2 groups:the experimental model group (n =36) and the control group (n =12).The animals in the experimental model group were injected with prednisolone acetate (10 mg/kg),twice a week and the animals in the control group were injected with physiological saline (2 ml) also twice a week for 6 weeks.Then,rabbits in experimental group were randomized into the HBO group (n =18) and the control group (n =18).The HBO group received HBO treatment for 6 weeks,while the control group was treated with normobaric air.Hemorrheology paramcters,vascular endothelial growth factor (VEGF),changes in tissue pathology,as well as changes in radiographic imaging were detected at week 2,4,6,8,10 and 12 following experiment.Results Features of hemorrheology for the model group deteriorated at weeks 2,4 and 6.Endangium in the femoral head capillary vessel of the experimental group was disrupted,and there were thrombosis and osteoporosis in the femoral head.Optical microscopy revealed that the number of empty bone lacunae and fat cells increased,and some bone trabeculae were disrupted.Electron microscopy indicated that cell volume of the femoral head decreased and nuclei shrank,more osteocytes after necrosis occurred were dissolved into fragments.For the HBO treatment group,features of hemorrheology improved,and positive expressions of VEGF in large amounts could be detected in osteogenic cells and blood vessels on thc surface of bone trabeculae in the femoral head,with the positive site being mainly located in endangium.Under optical microscope,repair of necrotic osteocytes could be found,and nascent osteocytes could be detected by transmission microscopy.Conclusions Large dosage of hormones could induce damage to endangium of capillary vessels,which might be an important reason for the necrosis of the femoral head in rabbits.HBO could promote the secretion of such cytokines as VEGF,accelerate revascularization and ossification,which might be an important theoretical evidence for the treatment of hormone-induced avascular necrosis of the femoral head by HBO.
