医药前沿
醫藥前沿
의약전연
YIAYAO QIANYAN
2013年
34期
64-66
,共3页
张建华%林洪%刘升湘%俞雄杰%郁毅刚
張建華%林洪%劉升湘%俞雄傑%鬱毅剛
장건화%림홍%류승상%유웅걸%욱의강
兔%火炮打击%肺脏%爆震伤%P38
兔%火砲打擊%肺髒%爆震傷%P38
토%화포타격%폐장%폭진상%P38
rabbit%artil ery%strike%lung blast injury%P38
目的:探讨实弹演习火炮打击后兔肺爆震伤的病理变化及P38表达特点。方法闽南山地师团进攻实弹演习,设置6组。远离演习场的空白对照实验兔组(A组),火炮打击区域设置炮火覆盖山体反角隐蔽组(B组)和迎面角隐蔽组(C1-C3组),各组均含实验兔6只。火炮打击后6 h,各组存活兔处死后取肺中叶近肺门处组织,HE染色观察其病理损伤形态,免疫组化染色观察P38的组织表达。结果与A组比较,B组和C组兔肺组织均可见肺膜下点片状出血和明显的组织水肿,H E染色示后两组肺泡细胞局灶性坏死、肺泡壁破坏及间质水肿伴炎细胞浸润,C组病理损伤明显强于B组。免疫组化结果示后两组肺组织内P38染色强度、范围和阳性细胞率均高于A组,且C组P38免疫反应程度高于B组。结论火炮打击后兔肺组织呈明显的出血、水肿、细胞坏死等爆震伤病理表现。反角掩体保护有助于减轻肺脏损伤。P38过表达与肺脏损伤病理程度显著相关,它参与了兔肺爆震伤的分子病理调控,是该型损伤治疗的潜在靶标。
目的:探討實彈縯習火砲打擊後兔肺爆震傷的病理變化及P38錶達特點。方法閩南山地師糰進攻實彈縯習,設置6組。遠離縯習場的空白對照實驗兔組(A組),火砲打擊區域設置砲火覆蓋山體反角隱蔽組(B組)和迎麵角隱蔽組(C1-C3組),各組均含實驗兔6隻。火砲打擊後6 h,各組存活兔處死後取肺中葉近肺門處組織,HE染色觀察其病理損傷形態,免疫組化染色觀察P38的組織錶達。結果與A組比較,B組和C組兔肺組織均可見肺膜下點片狀齣血和明顯的組織水腫,H E染色示後兩組肺泡細胞跼竈性壞死、肺泡壁破壞及間質水腫伴炎細胞浸潤,C組病理損傷明顯彊于B組。免疫組化結果示後兩組肺組織內P38染色彊度、範圍和暘性細胞率均高于A組,且C組P38免疫反應程度高于B組。結論火砲打擊後兔肺組織呈明顯的齣血、水腫、細胞壞死等爆震傷病理錶現。反角掩體保護有助于減輕肺髒損傷。P38過錶達與肺髒損傷病理程度顯著相關,它參與瞭兔肺爆震傷的分子病理調控,是該型損傷治療的潛在靶標。
목적:탐토실탄연습화포타격후토폐폭진상적병리변화급P38표체특점。방법민남산지사단진공실탄연습,설치6조。원리연습장적공백대조실험토조(A조),화포타격구역설치포화복개산체반각은폐조(B조)화영면각은폐조(C1-C3조),각조균함실험토6지。화포타격후6 h,각조존활토처사후취폐중협근폐문처조직,HE염색관찰기병리손상형태,면역조화염색관찰P38적조직표체。결과여A조비교,B조화C조토폐조직균가견폐막하점편상출혈화명현적조직수종,H E염색시후량조폐포세포국조성배사、폐포벽파배급간질수종반염세포침윤,C조병리손상명현강우B조。면역조화결과시후량조폐조직내P38염색강도、범위화양성세포솔균고우A조,차C조P38면역반응정도고우B조。결론화포타격후토폐조직정명현적출혈、수종、세포배사등폭진상병리표현。반각엄체보호유조우감경폐장손상。P38과표체여폐장손상병리정도현저상관,타삼여료토폐폭진상적분자병리조공,시해형손상치료적잠재파표。
Objective: To investigate the pathological characteristics and histological expression of P38 in rabbit pulmonary blast injury induced by artil ery strike. Method: When the mountain division in South Fujian lanched a military exercise, we used 30 rabbits for the fol owing experiments by equal y al ocating them into blank control group (Group A) which was far away from the exercise field,reverse-shelter-protecting group (Group B), and forward-shelter-protecting group (Group C). Six hours after artil ery strike, the surviving rabbits were sacrificed for their lung middle lobe lung tissues nearing the pulmonary hilar. HE staining was performed to observe the pathological morphous, and immunohistochemical study to investigate the histological expression of P38. Results: Compared with the rabbit lung tissues in Group A, those in Group B and C exhibited focal to broad hemorrhage underneath the lung membrane and obvious parenchymatous edema. HE staining showed that lung tissues in the latter two groups experienced focal necrosis of alveolar cell, disruption of alveolar wal , and interstitial edema with extensive infiltration of inflammatory cell, the pathological injury was markedly severer in Group C than that in Group B. Immunohistochemical results showed that the intensity and scope of P38 expression and the percentage of positive cells in lung tissues from Group B and C were significantly higher than those from Group A. In addition, the immunoreactivity of P38 was much higher in Group C than that in Group B. Conclusion: Rabbit lung exhibits obvious pathological alterations of pulmonary blast injury such as hemorrhage, edema, cellular necrosis, etc., after artil ery strikes. Reverse-shelter-protection helps the al eviation of lung injury. Overexpression of P38 significantly correlates with the pathological degree of lung injury and potential y involves in the molecular regulation of pulmonary blast injury of rabbit, suggesting that it is a potential therapeutic target.