CAJ | 학술논문

目的研究甲强龙(甲泼尼龙)对出血性休克大白鼠的影响并探讨其机制.方法大白鼠经动脉放血,造成失血性休克模型,随后用自体血和生理盐水从静脉回输,进行复苏.复苏前大白鼠随机分成三组:假休克组,休克组和甲强龙治疗组.结果复苏后72 h,休克组的生存率降至20%,而甲强龙治疗组的生存率达80%,差异显著(P＜0.01).复苏后18h器官病理取材,H-E染色,光镜下显示:休克组大白鼠的心、肺、肾、肝组织出现不同程度水肿、细胞变性、间质炎性细胞浸润等.甲强龙治疗组大白鼠的上述脏器的病理改变明显减轻.复苏后18 h,CK、Cr、ALT、AST、ALKP检测,休克组明显升高,而甲强龙治疗组只有轻度增高,差异非常显著(P＜0.01).复苏后2 h,肝脏枯否细胞用LPS刺激后,休克组的细胞内Ca2+浓度和TNF-α产量明显增高,而甲强龙治疗组轻度增高,差异显著(P＜0.01).结论甲强龙可以通过抑制kupffer细胞内Ca2+升高和激活,阻止TNF-α的过度产生,降低机体系统性炎症反应程度,最终减轻出血性休克大白鼠脏器的损伤和降低死亡率.
목적연구갑강룡(갑발니룡)대출혈성휴극대백서적영향병탐토기궤제.방법대백서경동맥방혈,조성실혈성휴극모형,수후용자체혈화생리염수종정맥회수,진행복소.복소전대백서수궤분성삼조:가휴극조,휴극조화갑강룡치료조.결과복소후72 h,휴극조적생존솔강지20%,이갑강룡치료조적생존솔체80%,차이현저(P＜0.01).복소후18h기관병리취재,H-E염색,광경하현시:휴극조대백서적심、폐、신、간조직출현불동정도수종、세포변성、간질염성세포침윤등.갑강룡치료조대백서적상술장기적병리개변명현감경.복소후18 h,CK、Cr、ALT、AST、ALKP검측,휴극조명현승고,이갑강룡치료조지유경도증고,차이비상현저(P＜0.01).복소후2 h,간장고부세포용LPS자격후,휴극조적세포내Ca2+농도화TNF-α산량명현증고,이갑강룡치료조경도증고,차이현저(P＜0.01).결론갑강룡가이통과억제kupffer세포내Ca2+승고화격활,조지TNF-α적과도산생,강저궤체계통성염증반응정도,최종감경출혈성휴극대백서장기적손상화강저사망솔.
Objective: To investigate the effect of methylprednisolone (MP) on hemorrhagic shock in rats and elucidate the underlying mechanisms. Method: Wistar rats were bled to induce the shock and subsequently resuscitated with shed blood and normal saline. Just prior to resuscitation, the rats were divided into three groups: sham group, shock group and shock+MP groups. Results: 72 h after resuscitation, the survival rate of shock group decreased to 20%, while the survival rate of shock+MP group was 80%, the difference was significant (P ＜0.01). 18 h after resuscitation, pathologic alterations of organs showed: in shock group, pulmonary edema, leukocyte infiltration in interstitial tissue and cellular degeneration occurred. MP reduced these pathological alterations significantly. 18 h after resuscitation, creatine phosphokinase, transaminases and creatinin were elevated significantly in shock group,while these in shock+MP group were elevated slightly, the differences were significant (P ＜0.01). Increases in intracellular calcium and production of TNF-α by isolated kupffer cells stimulated by endotoxin were elevated significantly by hemorrhagic shock, which were totally prevented by MP (P ＜0.01). Conclusion: Methylprednisolone reduces organ injury and mortality caused by hemorrhagic shock by blocking increase of intracellular calcium, activation and production of TNF-α of kupffer cells and preventing systemic progressive inflammation responses.