CAJ | 학술논문

目的对急性脑梗死(acute cerebral infarction,ACI)患者CD11b、CD11c和CD54作动态观察,找出其变化规律及高压氧(hyperbaric oxygen,HBO)对该规律的影响,并进一步阐明HBO对ACI患者脑血管的保护作用；同时对ACI患者治疗前CD11b、CD11c和CD54与近、远期神经功能恢复程度相关性进行探讨.方法 64例ACI患者分2组:HBO组31例,常规治疗联合HBO治疗；治疗对照组33例,仅行常规治疗.2组分别在治疗前(发病≤72 h)及治疗第7、10、12、20天晨抽取外周静脉血测定CD11b、CD11c和CD54,并在相同治疗时间进行神经功能缺损程度评分(neural functional damage scores,NDS).另外选取正常对照组25人,仅抽取周围静脉血测定CD11b、CD11c和CD54.结果 HBO组和治疗对照组治疗前CD11b、CD11c和CD54表达明显升高,达到高峰,2组各指标差异无统计学意义(P＞0.05),第7天均开始下降.HBO组CD11b、CD11c高峰持续时间为7d,治疗对照组持续10 d；HBO组CD54高峰持续时间为10 d,治疗对照组持续12d.经相关性和线性回归分析发现,发病第20天时NDS水平(近期疗效)和发病半年、1年时NDS的水平(远期疗效)分别为97.2％、96.7％及97.6％,可用CD11b和/或CD11c和/或CD54的上调水平以及其他相关因素解释.结论 HBO治疗后可缩短ACI患者CD11b、CD11c和CD54高峰持续时间.说明HBO可干预细胞黏附分子的变化过程,缩短其异常时限,减少它们的表达,对ACI患者有保护作用,并减少白细胞的黏附.同时治疗前CD11b、CD11c和CD54的表达可预测病情的轻重,影响近、远期疗效,为研究如何调控或抑制CD11b、CD11c和CD54的表达、减少对血管的损伤及早期制定更全面的治疗方案提供依据.
목적 대급성뇌경사(acute cerebral infarction,ACI)환자CD11b、CD11c화CD54작동태관찰,조출기변화규률급고압양(hyperbaric oxygen,HBO)대해규률적영향,병진일보천명HBO대ACI환자뇌혈관적보호작용；동시대ACI환자치료전CD11b、CD11c화CD54여근、원기신경공능회복정도상관성진행탐토.방법 64례ACI환자분2조:HBO조31례,상규치료연합HBO치료；치료대조조33례,부행상규치료.2조분별재치료전(발병≤72 h)급치료제7、10、12、20천신추취외주정맥혈측정CD11b、CD11c화CD54,병재상동치료시간진행신경공능결손정도평분(neural functional damage scores,NDS).령외선취정상대조조25인,부추취주위정맥혈측정CD11b、CD11c화CD54.결과 HBO조화치료대조조치료전CD11b、CD11c화CD54표체명현승고,체도고봉,2조각지표차이무통계학의의(P＞0.05),제7천균개시하강.HBO조CD11b、CD11c고봉지속시간위7d,치료대조조지속10 d；HBO조CD54고봉지속시간위10 d,치료대조조지속12d.경상관성화선성회귀분석발현,발병제20천시NDS수평(근기료효)화발병반년、1년시NDS적수평(원기료효)분별위97.2％、96.7％급97.6％,가용CD11b화/혹CD11c화/혹CD54적상조수평이급기타상관인소해석.결론 HBO치료후가축단ACI환자CD11b、CD11c화CD54고봉지속시간.설명HBO가간예세포점부분자적변화과정,축단기이상시한,감소타문적표체,대ACI환자유보호작용,병감소백세포적점부.동시치료전CD11b、CD11c화CD54적표체가예측병정적경중,영향근、원기료효,위연구여하조공혹억제CD11b、CD11c화CD54적표체、감소대혈관적손상급조기제정경전면적치료방안제공의거.
Objective To observe dynamically the CD11b,CD11c and CD54 in patients with acute cerebral infarction (ACI),to find out the change pattern and the effect of HBO on the change pattern,to illustrate the protective effects of HBO on cerebrovascular lesion in patients with ACI,and to explore the correlation between the CD1 1b,CD1 1c and CD54 before therapy and near and long-term effects on neurological recovery.Methods Sixty-four cases of ACI were divided into the HBO + routine therapy group (31 cases) and the therapy control group with only routine therapy (33 cases).CD11b,CD11c and CD54 in the subjects of both groups were measured in 72 hours,and on the 7th,10th,12th and 20th days respectively following acute infarction,and neural functional damage scores (NDS) were also evaluated at the same time.CD1 1b,CD11c and CD54 of the subjects in the normal control group (25 cases) were also measured by taking blood samples from peripheral veins.Results The expression of CD11b,CD11c and CD54 in the HBO group and the control group increased obviously within 72 hours of onset,and reached peak value within 72 hours.No significant differences could be seen between the two groups (P ＞ 0.05).Then,the above data declined on the 7th day.CD11b,CD11c in the HBO group maintained at peak level for7 days,while those in the control group maintained for 10 days.CD54 peak value kept for 10 days in the HBO group,while peak value maintained for 12 days in the therapy control group.Correlation analysis and linear regression analysis indicated that NDS on the 20th day (short-term curative effect) and NDS within half a year and a year (long-term effect) were 97.2％,96.7％,97.6％ respectively,which could be explained with the up-regulation of CD11b and/or CD1 1c and/or CD54 and other related factors.Conclusions The duration of peak levels of CD11 b,CD1 1 c and CD54 in ACI patients could be shortened,following hyperbaric oxygen therapy.HBO might intervene in the changing process of intercellular adhesion molecule,shorten the duration of abnormal time,reduce their expression,protect ACI patients and reduce the adhesion of leukocytes.The expression of CD11b,CD11c and CD54 could predict the severity and prognosis of the disease,interfere with the short or long- term curative effects on the patients before therapy and reduce the damage of blood vessels.In addition,they could provide scientific basis for the regulation and control of CD11b,CD11c and CD54 expression,and the early development of a comprehensive treatment profile of the disease.