高压氧对脑梗死患者血浆蛋白C与蛋白S的影响

目的观察高压氧(HBO)对脑梗死患者血浆蛋白C(PC)与蛋白S(PS)的影响,探讨HBO治疗脑梗死的作用和机制.方法将脑梗死急性期患者分为常规治疗组及HBO治疗组,用酶免法分别测定两组患者治疗前及治疗后血浆蛋白C与蛋白S水平,观察HBO治疗前后的变化.结果脑梗死急性期治疗前两组患者血浆PC、PS水平均明显下降,治疗后HBO治疗组患者血浆PC、PS水平明显高于常规治疗组,并且恢复正常,而常规治疗组患者血浆PC、PS水平仍低.结论HBO可促进脑梗死患者血浆PC、PS水平恢复正常,减轻神经系统损伤,对脑梗死有治疗作用.     

高压氧对脑缺血再灌注大鼠的海马诱导型一氧化氮合酶mRNA表达的影响

目的　观察高压氧对脑缺血再灌注大鼠的海马诱导型一氧化氮合酶信使核糖核酸 (iNOSmRNA)表达的影响。方法　将 5 4只大鼠随机分为脑缺血再灌注组 (IR组 )、脑缺血再灌注加高压氧处理组(HBO组 )和对照组 ,建立脑缺血再灌注大鼠动物模型。应用荧光定量逆转录 聚合酶链反应 (RT PCR )技术检测各组在再灌注 6h、2 4h、48h、96h时相点大鼠的海马iNOSmRNA表达。结果　再灌注各时相点的IR组和HBO组的海马iNOSmRNA表达均显著高于对照组 (均P <0 .0 1) ;HBO组大鼠再灌注 2 4h、48h、96h时海马iNOSmRNA表达均显著低于IR组 (P <0 .0 5 ,P <0 .0 1,P <0 .0 1)。结论　高压氧治疗可以显著抑制再灌注后大鼠海马iNOSmRNA表达 ,从而减少延迟性NO的产生 ,有助于减轻脑缺血再灌注损伤。     

一氧化碳中毒临床治疗指南(一)

急性一氧化碳中毒(acute carbon monoxide poisoning,ACOP)是常见的中毒之一,也是急性中毒死亡的最主要原因.为指导我国现场救治及临床医生及时、规范、有效地抢救治疗ACOP患者,减轻缺氧性损伤,减少迟发脑病发生率,笔者通过收集和分析已经完成的国内外有关ACOP抢救治疗文献,以循证医学证据为基础,采用国际通用的方法,多次与临床医生反复认真讨论,并经有关专家审议,做出了比较客观科学的结论,以期规范ACOP诊断和治疗.指南中的推荐意见依据2001年国际感染论坛提出的Delphi分级标准(表1),将指南中涉及的文献按照研究方法和结果分成Ⅰ～Ⅴ级5个层次,推荐意见的推荐级别分为A～E级,A级为最高.     

骨科常见护理纠纷原因分析及防范对策

随着社会的进步,医学知识和法制观念的普及,人们的法律意识和维权意识越来越强,医疗护理纠纷呈不断上升趋势。骨科属于重建医学,病种复杂,患者年龄跨度大,康复时间长,是医疗护理纠纷的高危科室。本文征对骨科护理中易发生纠纷的几个环节进行原因分析及防范策略探讨。     

高压氧预处理对扩张皮瓣成活的影响

皮肤软组织扩张术是通过皮肤软组织的定期扩张达到局部组织增量的目的,已成为一种常用的创面修复方法.由于扩张可造成局部血供状态的改变,因此扩张皮瓣坏死在临床上有较高的发生率.高压氧(hyperbaric oxygen,HBO)是一种成熟的临床治疗方法,在整形外科领域,HBO曾被用于皮片移植、皮瓣移植术后及创面的治疗[1-2 ].2000年以来,一些学者研究发现HBO预处理可以提高脑和脊髓组织的缺血耐受,减轻损伤[3-4],也可以提高皮瓣的缺血耐受[5].本研究的目的是探讨其对扩张皮瓣成活的作用.     

兔激素性股骨头坏死模型的建立

目的： 建立兔激素性股骨头坏死的模型。方法: 新西兰大白兔24只,分为正常对照组（N）、模型2周（M2)组和模型4周(M4)组。使用内毒素+激素建立股骨头坏死的动物模型。给药后2周和4周取双侧股骨头观察骨小梁和髓腔的组织形态学变化。结果: 模型组骨小梁内骨细胞核固缩,空骨陷窝增加,小梁间脂肪细胞增多、增大;髓腔内脂肪细胞增多、增大,造血组织明显减少。结论: 小剂量内毒素+激素成功诱导兔股骨头坏死模型,这种动物模型操作简单,稳定可靠,重复性好,为研究激素性股骨头坏死的发病机制和治疗方法提供了帮助。     

高压氧对急性一氧化碳中毒大鼠血清蛋白脂质蛋白质抗原、抗体的影响

目的 观察急性一氧化碳中毒(acute carbon monoxide poioning,ACOP)大鼠血清中蛋白脂质蛋白质(proteolipid protein,PLP)抗原、抗体的变化,探讨免疫机制在ACOP中的作用以及高压氧(HBO)治疗可能的作用机制.方法 202只大鼠按随机数字表法分为3组:染毒组(CO组),高压氧组(HBO组),常压氧组(NBO组).采用静态一氧化碳吸入法建立ACOP大鼠模型.染毒前及染毒后即刻、100 min和3、7、10、20 d取腹主动脉血,用ELISA法测定血清PLP抗原、抗体的含量.结果 染毒后即刻CO组、HBO组和NBO组PLP抗原及抗体均较染毒前升高(P＜0.05).HBO组100 min时PLP抗原低于CO组(P＜0.05);3、7 d时PLP抗体低于CO组(P＜0.05);3、10 d时HBO组PLP抗体低于NBO组(P＜0.05);7、20 d时NBO组PLP抗体低于CO组(P＜0.05).结论 ACOP后大鼠存在自身免疫反应及髓鞘损伤,及时、规律的HBO治疗可减轻髓鞘损伤.     

氧疗在一氧化碳中毒现场的应用

一氧化碳(carbon monoxide,CO)为无色、无嗅、无刺激性的窒息性气体,通常由含碳物质在不完全燃烧时产生,是工业生产和生活环境中最常见的窒息性气体.     

Effects of hyperbaric oxygen on TF、TNF-α in the rabbit model of steroid-induced avascular osteonecrosis of femoral head

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.     

高压氧对激素性股骨头坏死兔血中骨保护素变化的影响

目的 研究激素性股骨头坏死( steroid - induced avascular osteonecrosis of femoral head,SANFH)兔血骨保护素(osteoprotegerin,OPG)含量的变化及高压氧(hyperbaric oxygen,HBO)对OPG含量的影响.方法 78只健康新西兰白兔按数字表法随机分为3组:正常对照组(N组)7只、制模组(M组)41只、HBO组30只.M组又分为制模完成组(M0组)10只、制模2周组(M2组)10只、制模4周组(M4组)10只、制模6周组(M6组)11只.HBO组又分为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基强的松龙龙的方法对M组及HBO组进行制模处理.HBO组在制模完成后予HBO处理,1次/d,并分别于制模2、4、6周抽取静脉血检测OPG含量,于相应取血时间点取血后处死动物,取双侧股骨头进行组织形态学观察.结果 M0组[(4.69±3.01) ng]较N组[(13.2 ±9.25) ng]OPG水平降低(P ＜0.05)；HBO2组较N组OPG水平升高(P ＜0.05);HBO4组与HBO2组比较OPG水平无明显变化；HBO6组OPG水平达到高峰,与HBO2及HBO4组比较差异有统计学意义(P ＜0.05)；HBO各组与其相应M各组比较OPG均提高,差异均有统计学意义(P＜0.05).结论 HBO可提高OPG含量,抑制破骨细胞成熟与分化,加速成骨细胞的增殖、分裂,促进坏死股骨头的修复.