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.     

高压氧对大鼠急性脊髓损伤炎症因子表达的影响

Objective To investigate the effects of early HBO therapy on the expressions of pro inflammatory cytokine mRNA including tumor necrosis factor-α (TNF-α ) and interleukin-10 (IL-10) following spinal cord injury (SCI) in rats. Methods Forty SD rats were randomly divided into 3 groups:the sham operation group (n=4) , the SCI group (n = 18) , and the hyperbaric oxygen group (n = 18). Spinal cord injury model was developed by using the modified Allen impact. Then, the SCI group and the HBO group received HBO therapy 2 hours after injury, once a day. And 3 rats were randomly selected at 6, 12, 24, 72, 120 and 168 h following injury to take samples of injured spinal cord tissue and measure dynamic changes in the expressions of TNF-α, IL-10 mRNA by semi-quantitative RT-PCR method. Results Faint expression of the cytokine mRNA could be noticed in the sham group. The expression of TNF-α mRNA in the injured spinal cord tissue in the SCI group elevated gradually, increased obviously at 12 h after injury and reached peak at 24 h, and its high expression maintained till 72 h after injury. The tendency in the expression of TNF-α mRNA in the HBO group was identical to that of the SCI group, however, the amplitude in the increase of TNF-α mRNA decreased (P＜0. 05). The expression of IL-10 mRNA in the SCI group began to increase at 12 h after injury and increased gradually over time and reached peak at 168 h. The expressions of both TNF-α and IL-10 mRNA were more consistent in the HBO group, with more obvious increase in the expressions of IL-10 mRNA. Conclusions HBO could reduce the release of pro-inflammatory cytokines and increase the expression of anti-inflammatory cytokines,resulting in reduction of secondary spinal cord injury,protection of the damaged nerve cells and promotion of recovery.     

高压氧对局灶性脑缺血再灌注大鼠紧密连接蛋白及血脑屏障通透性的影响

Objective To investigate effects of hyperbaric oxygen (HBO) on the occludin and ZO-1 in the brain tissues and permeability of blood brain barrier (BBB) after cerebral ischemia-reperfusion in mice. Methods Male Wistar mice were randomly divided into 4 groups; the sham group, the ischemia-reperfusion group (IR) , the HBO group and the IR + HBO group. Following development of the cerebral ischemia reperfusion model, 5 sessions of HBO at 0.25 Mpa were applied during the reperfusion period, and 2% Evens blue (EB) was injected into the tail veins an hour before the animals were executed. Following ischemia reperfusion, changes in the permeability of BBB were monitored with the EB method. Following ischemia reperfusion, the distributions of occludin and ZO-1 in the brain tissue were observed with immunohistochemical method, and the expressions of occludin, ZO-1, and the contents of EB were determined by Western Blot and spectrophotometer. Results When compared with that of the sham group, the levels of EB in the brain tissue for the IR group increased significantly, reaching peak at 4 h following IR injury (P＜0. 01). In the IR + HBO group, EB contents in the brain tissue decreased significantly, when compared with those of the IR group ( P＜ 0.01). However, no significant changes in the expression of occludin, ZO-1 and the content of EB in the brain tissue could be noted in the HBO, when compared with those of the sham group (P＞0.05). In the IR group, the expressions of occludin and ZO-1 at 4, 12, 24, 48, 72 h after reperfusion decreased significantly, when compared with those at 0 h( P＜0. 01). However, for the IR + HBO group, the expressions of occludin and ZO-1 at 72 h after reperfusion increased markedly (P＜0. 01). No obvious changes in the expression of occludin and ZO-1 could be noted in the brain tissue in the animals in the HBO group, when compared with those in the sham group (P＞0. 05). Conclusions HBO intervention could increase markedly the expressions of occludin and ZO-1 in the ischemia-reperfusion brain tissue, thus decreasing permeability of BBB.     

急性一氧化碳中毒大鼠脑组织Fas和caspase-3蛋白表达及高压氧的干预作用

目的 观察急性一氧化碳(CO)中毒后大鼠脑组织Fas和caspase-3蛋白表达的改变,为急性CO中毒后迟发性脑病delayed neuropathological sequelae,DNS)的发病机制提供新的证据.方法 50只SD雄性大鼠按数字表法随机分为对照组,染毒后1、3、7 组和高压氧(HBO)治疗7 d组,每组10只.采用HE染色、免疫组织化学染色及Western blot方法,观察染毒后各时间点大鼠脑组织损伤及Fas、caspase-3蛋白表达情况.结果 对照组Fas和caspase-3均表达极低,染毒后1 d,Fas和caspase-3蛋白表达均迅速增加,染毒后3 d达到高峰,3 d与7 d组表达无明显差别,HBO治疗组Fas和caspase-3蛋白表达均较染毒后7 d组显著减少(P<0.01),但仍高于对照组(P<0.05).Fas和caspase-3蛋白表达改变与脑组织损伤程度呈一致变化.结论 Fas蛋白表达和细胞凋亡是CO中毒后DNS的发生机制之一,HBO可能通过减少Fas蛋白表达和抑制细胞凋亡而减轻脑组织的损伤.

Abstract：

Objective To investigate changes in the expression of Fas and caspase-3 in the brain of rats with acute CO poisoning and also to provide new evidence for pathogenic mechanism of delayed neuropathological sequelae (DNS) after CO exposure.Methods Fifty SD male rats were randomly assigned to the control group, the 1, 3, and 7 d CO exposure groups and the 7 d HBO treatment group, each consisting of 10 rats. HE, immunohistochemical staining and Western blot were performed to study the expression of Fas and caspase-3 in the brain tissue, following intoxication at various time points.Results The expression of both Fas and caspase-3 were very low in the control group. One day after CO exposure, the expression of both Fas and caspase-3 increased quickly and reached peak 3 days after exposure. No significant differences in both Fas and caspase-3 expressions could be noted between the 3 d and the 7 d exposure groups. For the HBO treatment group, the expression of both Fas and caspase-3 decreased more significantly (P<0.01) as compared with that of the 7 d exposure group, but was still higher than that of the control group(P<0.05). Changes in the expression of Fas and caspase-3 were closely correlated with the severity of brain injury.Conclusions The expression of Fas and apoptosis might be involved in the mechanism of DNS following CO poisoning. HBO seemed to play an important role in the alleviation of brain damage via decreasing the expression of Fas and inhibiting the apoptosis of cells.     

高压氧对大鼠急性脊髓损伤炎症因子表达的影响

目的 观察大鼠脊髓损伤(spinal cord injury,SCI)后早期高压氧(HBO)治疗对肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)mRNA表达的影响.方法 将36只SD大鼠随机分为2组:SCI组(18只)和HBO组(18只).2组均采用改良的Allen打击法建造大鼠脊髓损伤模型.模型建造成功后,HBO组于损伤2 h后开始行HBO治疗,1次/d.2组分别于损伤后6、12、24、72、120、168 h各取3只大鼠,取损伤部位脊髓组织采用逆转录-聚合酶链式反应(RT-PCR)法测定其中TNF-α、IL-10 mRNA表达的变化.结果 SCI组大鼠脊髓组织中TNF-α mRNA表达逐渐升高,在伤后12h表达明显上调,至24h达高峰,高表达持续至损伤后72 h;HBO组大鼠脊髓组织中TNF-α mRNA表达变化趋势与SCI组一致,但升高幅度降低(P＜0.05);SCI组大鼠IL-10 mRNA表达在损伤后12 h开始升高,并随时间的推移逐渐升高,至168 h达高峰;HBO组表达变化趋势较一致,IL-10 mRNA升高幅度更明显(P＜0.05).结论 HBO能够减少前炎性细胞因子的释放,增加抗炎性细胞因子的表达,从而减少脊髓组织的继发损伤,保护受损的神经细胞,达到促进恢复的作用.

Abstract：

Objective To investigate the effects of early HBO therapy on the expressions of pro inflammatory cytokine mRNA including tumor necrosis factor-α (TNF-α ) and interleukin-10 (IL-10) following spinal cord injury (SCI) in rats. Methods Forty SD rats were randomly divided into 3 groups:the sham operation group (n=4) , the SCI group (n = 18) , and the hyperbaric oxygen group (n = 18). Spinal cord injury model was developed by using the modified Allen impact. Then, the SCI group and the HBO group received HBO therapy 2 hours after injury, once a day. And 3 rats were randomly selected at 6, 12, 24, 72, 120 and 168 h following injury to take samples of injured spinal cord tissue and measure dynamic changes in the expressions of TNF-α, IL-10 mRNA by semi-quantitative RT-PCR method. Results Faint expression of the cytokine mRNA could be noticed in the sham group. The expression of TNF-α mRNA in the injured spinal cord tissue in the SCI group elevated gradually, increased obviously at 12 h after injury and reached peak at 24 h, and its high expression maintained till 72 h after injury. The tendency in the expression of TNF-α mRNA in the HBO group was identical to that of the SCI group, however, the amplitude in the increase of TNF-α mRNA decreased (P＜0. 05). The expression of IL-10 mRNA in the SCI group began to increase at 12 h after injury and increased gradually over time and reached peak at 168 h. The expressions of both TNF-α and IL-10 mRNA were more consistent in the HBO group, with more obvious increase in the expressions of IL-10 mRNA. Conclusions HBO could reduce the release of pro-inflammatory cytokines and increase the expression of anti-inflammatory cytokines,resulting in reduction of secondary spinal cord injury,protection of the damaged nerve cells and promotion of recovery.     

高压氧治疗兔创伤性脑损伤的磁共振观察

Objective To observe the effects of HBO therapy on cerebral edema, blood-brain barrier and neural behavioral scores, induced by brain trauma injury in rabbits with magnetic resonance imaging ( MRI). Methods Twenty-four rabbits were randomly divided into three groups: the sham operation group (n =5), with a skull window of only 8 mm in diameter; the control group (n = 10) , sustained with shock injury (shock intensity of 0.2 Mpa) following skull fenestration; the HBO group(n=90), also sustained with shock injury following skull fenestration, but with HBO treatment. Following the development of the model, MRI scans were made at 6th, 24th, 72nd, and 120th hours to calculate the volume of cerebral edema, apparent diffusion coefficient ( ADC), and neurological behavioral scores. Results After HBO treatment, neurological behavioral scores of the HBO group improved significantly, when compared with that of the control group (P＜ 0. 05). MRI showed that abnormality was not noted in the sham operation group. Before treatment, significant cerebral edema and damage of blood-brain barrier could be seen in both the HBO group and the control group. However, following HBO treatment, cerebral edema and blood-brain barrier damage of the HBO group recovered more rapidly, when a comparison was made between the groups (P＜0. 01) and ADC value of the HBO group was lower than that of the control group (P＜0. 05). Conclusions HBO could hasten recovery of the blood-brain barrier damage induced by cerebral damage with hydraulic impetus, reduce cerebral edema, significantly decrease symptoms of brain injury, and reduce disability rate.     

高压氧对局灶性脑缺血再灌注大鼠紧密连接蛋白及血脑屏障通透性的影响

目的 探讨高压氧(HBO)对局灶性脑缺血再灌注大鼠脑组织中紧密连接蛋白occludin、ZO-1蛋白表达及血脑屏障通透性的影响.方法 雄性Wistar大鼠,随机分成假手术组、脑缺血再灌注组、HBO+脑缺血再灌注组、HBO组.复制局灶性脑缺血再灌注模型,并于再灌注期间行0.25 MPa HBO治疗5次,在处死动物前1 h经尾静脉注射2%伊文思蓝(Evans blue,EB),采用EB法检测缺血再灌注后血脑屏障通透性的变化.应用免疫组织化学的方法观察缺血再灌注后脑组织中occludin蛋白的分布,再采用Western Blot法检测再灌注72 h后脑组织中occludin、ZO-1蛋白表达水平的变化.结果 脑缺血再灌注组较假手术组脑组织EB含量显著增高(P＜0.01),其中EB的渗出以4 h最为明显(1.14±0.07)U/mg.HBO+脑缺血再灌注组较脑缺血再灌注组脑组织中EB含量显著降低(P＜0.01),HBO组与假手术组相比脑组织中EB含量变化不明显(P＞0.05).Occludin蛋白的表达Oh时相比于再灌注后4、12、24、48、72 h时显著降低(P＜0.01).现灌注72 h时,HBO+脑缺血再灌注组较脑缺血再灌注组脑组织中occludin、ZO-1蛋白表达水平于再灌注72 h明显增加(P＜0.01);HBO组与假手术组相比脑组织中occludin、ZO-1蛋白表达变化不显著(P＞0.05).结论 HBO可明显增加脑缺血再灌注脑组织中紧密连接相关蛋白occludin、ZO-1的表达,从而降低血脑屏障通透性.

Abstract：

Objective To investigate effects of hyperbaric oxygen (HBO) on the occludin and ZO-1 in the brain tissues and permeability of blood brain barrier (BBB) after cerebral ischemia-reperfusion in mice. Methods Male Wistar mice were randomly divided into 4 groups; the sham group, the ischemia-reperfusion group (IR) , the HBO group and the IR + HBO group. Following development of the cerebral ischemia reperfusion model, 5 sessions of HBO at 0.25 Mpa were applied during the reperfusion period, and 2% Evens blue (EB) was injected into the tail veins an hour before the animals were executed. Following ischemia reperfusion, changes in the permeability of BBB were monitored with the EB method. Following ischemia reperfusion, the distributions of occludin and ZO-1 in the brain tissue were observed with immunohistochemical method, and the expressions of occludin, ZO-1, and the contents of EB were determined by Western Blot and spectrophotometer. Results When compared with that of the sham group, the levels of EB in the brain tissue for the IR group increased significantly, reaching peak at 4 h following IR injury (P＜0. 01). In the IR + HBO group, EB contents in the brain tissue decreased significantly, when compared with those of the IR group ( P＜ 0.01). However, no significant changes in the expression of occludin, ZO-1 and the content of EB in the brain tissue could be noted in the HBO, when compared with those of the sham group (P＞0.05). In the IR group, the expressions of occludin and ZO-1 at 4, 12, 24, 48, 72 h after reperfusion decreased significantly, when compared with those at 0 h( P＜0. 01). However, for the IR + HBO group, the expressions of occludin and ZO-1 at 72 h after reperfusion increased markedly (P＜0. 01). No obvious changes in the expression of occludin and ZO-1 could be noted in the brain tissue in the animals in the HBO group, when compared with those in the sham group (P＞0. 05). Conclusions HBO intervention could increase markedly the expressions of occludin and ZO-1 in the ischemia-reperfusion brain tissue, thus decreasing permeability of BBB.     

实时荧光定量PCR检测高压氧对实验兔血管内皮素-1及内皮型一氧化氮合酶mRNA表达的影响

目的 检测高压氧(hyperbaric oxygen,HBO)对实验兔颈内动脉和基底动脉内皮素-1(ET-1)及内皮型一氧化氮合酶(eNOS) mRNA表达的影响,探讨HBO暴露致脑血管前循环收缩、后循环扩张的可能机制.方法 健康成年新西兰白兔24只,按数字表法随机分为实验组(n=12)和对照组(n=12).实验组每日持续暴露于0.22 MPa HBO下60 min,连续3d;对照组正常饲养,不予任何处理.实时荧光定量PCR法(FQ-RT-PCR)检测ET-1、eNOS mRNA在2组颈内动脉和基底动脉的表达水平.结果 ET-1、eNOS mRNA在实验兔颈内动脉和基底动脉均有微量表达.与对照组相比,HBO可使实验组颈内动脉ET-1 mRNA表达明显增高[(1.679 ±0.097) vs (1.000±0.017)],eNOS mRNA表达明显下降[(0.571 ±0.039) vs (1.000 ±0.023)];基底动脉ET-1 mRNA表达明显下降[(0.565 ±0.069) vs(1.000±0.034)],eNOS mRNA表达明显增高[(1.667 ±0.134) vs(1.000±0.014)],差异均有统计学意义(P＜0.01).结论 HBO可通过调节ET-1、eNOS mRNA在颈内动脉和基底动脉的相对表达量而发挥收缩前循环、扩张后循环的作用.     

高压氧对激素性股骨头坏死兔血中TF、TNF-α的影响

目的 通过研究激素性股骨头坏死(steroid-induced avascular necrosis of the femoral head,SANFH)兔血组织因子(TF)和肿瘤坏死因子(TNF-α)的动态变化及高压氧(hyperbaric oxygen,HBO)对其影响,探讨SANFH发生机制和高压氧治疗的作用机制.方法 健康新西兰白兔78只,按数字随机表法分为3组:正常对照组(N组)7只,模型组(M组)41只,高压氧组(HBO组)30只.模型组又分为造模即刻组(M0组)10只,造模2周组(M2组)10只、造模4周组(M4组)10只、造模6周组(M6组)11只.HBO组分为: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强龙的方法对模型组及HBO组进行造模处理,HBO组在制模后开始HBO处理,每天1次,并于制模2周、4周、6周分别取静脉血检测TF、TNF-α的变化,于相应取血时间点取血后处死实验动物,取双侧股骨头组织进行组织学观察.结果 M各组TF[M0:(281.42±46.71)pg/ml,M2:(242.25±131.87)pg/ml,M4:(176.39±66.39)pg/ml,M6:(121.32±107.70)pg/ml]、TNF-α[M0:(418.83±75.99)pg/ml,M2:(424.41±57.01)pg/ml,M4:(424.05±136.44)pg/ml,M6:(344.34±112.89)pg/ml]均高于N组[TF:(137.55±21.65)pg/ml,TNF-α:(312.17±31.12)pg/ml],P＜0.05或P＜0.01;而HBO各组与M各组同时间点比较其表达均降低,P＜0.05或P＜0.01;组织学结果:N组股骨头组织形态正常,M组股骨十骺端髓腔内骨髓组织脂肪细胞增多增大、可见变性及片状坏死、炎性细胞浸润、出血、水肿及微小血管血栓、骨髓腔纤维化、造血细胞减少、股骨头萎缩明显;HBO各组脂肪变性、坏死出现率与M组比较明显减少,骨小梁间骨髓炎症反应明显减轻,未见到血栓形成,可见到骨母细胞活跃增生、骨髓纤维化、新生骨形成、股骨头萎缩不明显、骨基质正常.结论 兔SANFH时血中TF、TNF-α含量增高,诱导了体内凝血反应,使股骨头处血栓形成,HBO治疗可抑制实验动物体内TF、TNF-α的释放,从而改善凝血功能的异常,治疗股骨头坏死.

Abstract：

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.     

辛伐他汀预处理减轻缺血再灌注心肌损伤的实验研究

Objective To investigate the effects of pretreatment with simvastatin on iscbemia reperfusion induced myocardial injury, and to further explore related mechanism with respect to inflammation modulation. Methods The rat myocardial ischemia reperfusion model was established by the method of coronary artery ligation. The animals were divided into 3 groups: the sham group, the control group and the simvastatin group. In the simvastatin group, the animals were pretreated with simvastatin (5 mg/kg) one week before by intragastric administration. Ventricular arrhythmia was monitored and scored, infarct size and area at risk of myocardium were determined, and uhrastructural changes were observed. The serum levels of myocardial enzymes and lipids were measured. The content of myocardial inflammatory cytokines [tumor necrosis factor (TNF) -α、interleukin(IL) -6, and monocyte chemoattractant protein(MCP) - 1]were also evaluated. Results When compared with those of the control group, the amount and duration of ventricular arrhythmia in simvastatin group were less and score of ventricular arrhythmia was significantly lower. When pretreated with simvastatin, the serum levels of CK-MB and LDH in simvastatin group were significantly lower than those of the control group. The infarct size/area at risk ratio of the simvastatin treated group was significantly less than those of the control group. The uhrastructures of myocardial cells were better maintained in simvastatin group. No significant differences were observed in the serum concentrations of total cholesterol, triglycerides, low density lipoprotein and high density lipoprotein when comparisons were made each other among the three groups. However, the levels of TNF-α,IL-6 and MCP-1 in heart tissue of the treated animals were significantly lower than those of the control group. Conclusions Pretreatment with simvastatin ameliorates ischemia reperfusion induced myocardial injury, which is partly related with the down-regulation of inflammatory cytokines expression in heart tissue but independent of its role of lipids modulation.     

高渗造影剂对肾血管内皮合成和分泌NO及ET-1的影响

目的 通过体内和体外实验探讨高渗造影剂泛影葡胺对肾血管内皮功能的影响,旨在为造影剂肾病的发病机制提供实验依据。方法 大鼠肾动脉内皮血管环在含不同剂量高渗造影剂泛影葡胺的培养液中孵育1h,检测培养液中一氧化氮（nitric oxide,NO）和内皮素（endothelin-1,ET-1）的含量。通过免疫组织化学染色分析大鼠尾静脉注射泛影葡胺24h后,肾小球毛细血管内皮细胞内皮型一氧化氮合成酶（endothelia nitric oxide synthase,eNOS）和ET-1的表达变化。结果 泛影葡胺对NO分泌没有影响,而ET-1分泌增加,且呈剂量依赖性。大鼠尾静脉注射泛影葡胺24h后,肾小球内皮细胞ET-1表达显著增强;而eNOS表达没有变化。结论 高渗造影剂泛影葡胺可以影响肾血管内皮功能,导致ET-1合成和分泌增加,这一作用可能与造影剂引起的肾血管收缩和急性肾功能不全有关。     

高压氧对成年大鼠脑缺血再灌注损伤后脑血管内皮生长因子表达的影响

目的 探讨脑缺血模型大鼠经30 d高压氧(HBO)治疗后大脑血管内皮生长因子(VEGF)表达的变化.方法 24只成年SD大鼠随机分为3组:对照组(C组)8只、缺血再灌注组(IR组)8只、HBO治疗组(HBO组)8只.C组为正常大鼠,IR组和HBO组大鼠经大脑中动脉栓塞(MCAO)1.5 h后再灌注,HBO组行HBO治疗.HBO治疗(0.28 MPa,60 min)30 d,1次/d,于31 d麻醉处死,取脑组织切片,VEGF和CD34免疫组化染色,光镜观察并于损伤区取图,进行相关分析.结果 VECF广泛分布,缺血区表达强烈,3组间有明显差异(P＜0.05),HBO组(13497.14±397.44)低于IR组(22.097.7±616.89);C组未见CD34表达,其他2组集中表达于缺血区;HBO组(5571.16±603.63)表达少于IR组(5349.72±390.88),但差异无统计学意义(P＞0.05).结论 长期HBO治疗抑制大鼠缺血脑组织VEGF的表达,可能对神经细胞具有保护作用,有利于促进脑组织自我修复.     

High false-negative rate of the anterior spinal artery by intercostobronchial trunk arteriography alone compared to CT during arteriography

ObjectivesThis study aimed to assess the frequencies of the anterior spinal arteries identified by CT during arteriography (CTA) and arteriography alone.MethodsThis retrospective study included 137 vessels in 83 patients who performed both bronchial arteriography and CTA and categorized them into three groups based on the catheter tip locations: intercostobronchial trunk (ICBT), bronchial artery (BA), and intercostal artery (ICA). The frequencies of anterior spinal artery identified by CTA and arteriography alone were compared for each group.ResultsICBT, BA, and ICA groups were evaluated by CTA in 46, 79, and 12 vessels, respectively. By CTA evaluation, anterior spinal artery was identified in seven vessels (15.2%) in ICBT group, 0 in BA group and two (16.7%) in ICA group. The frequencies of anterior spinal artery were significantly higher (p < 0.05) in ICBT and ICA groups than in BA group. By arteriography evaluation alone, a faint anterior spinal artery was identified in two vessels (4.3%) in ICBT group, 0 in BA group, and 1 (8.3%) in ICA group.ConclusionsAnterior spinal artery branched only from the ICBT or ICA and not from the BA in both arteriography and CTA assessments. There was high false-negative rate (71%) of the anterior spinal artery by ICBT arteriography alone assessment compared to CTA assessment. This result explains one of the reasons that spinal ischemia occurs in arteriography-negative spinal artery cases.Advances in knowledgeFalse-negative rate of anterior spinal artery was 71% (5/7) by intercostobronchial trunk arteriography alone assessment.     

高压氧对大鼠心脑肺超微结构的影响

目的　探讨高压氧（ＨＢＯ）对心、脑、肺超微结构的影响。方法　１６只大鼠随机分为ＨＢＯ组及对照组,将ＨＢＯ组鼠一次暴露于纯氧舱内,于０．２５ ＭＰａ（２．５ ＡＴＡ）压力下停留２ 小时,总暴露时间为３ 小时,对照组鼠则暴露于常压空气中３ 小时。然后分别观察两组动物心、脑、肺超微结构的变化。结果　ＨＢＯ组动物心肌细胞线粒体肿胀、细胞核固缩、核周膜性空泡;大脑皮质神经元细胞核固缩和核周间隙增宽;肺上皮细胞内质网扩张。对照组动物未见明显变化。结论　ＨＢＯ可引起大鼠心、脑、肺超微结构轻度变性     

ACOP对大鼠血中NO、ET-1和CEC的影响及高压氧的作用

目的 探讨急性一氧化碳中毒（ACOP）对大鼠血管内皮及其细胞功能的影响和高压氧治疗（HBOT）的作用。方法 参照Jiang式染毒法制成ACOP大鼠模型,有相应对照地、分别对中毒后即刻和次日起每日1次HBOT的第1,3,7,14天后,血中一氧化氮（NO）、内皮素－1（ET－1）水平和循环内皮细胞（CEC）计数进行测定。结果（1）ACOP后即刻机体血中NO水平显著降低,ET－1水平和CEC计数显著升高（P＜0．05）;（2）HBOT后中毒大鼠血中NO水平显著回升（P＜0．05）,ET－1水平和CEC计数显著回降;其后上述指标都趋于恢复到正常水平。结论 （1）ACOP可导致机体严重的血管内皮及其细胞功能的损伤;（2）0．2MPa（绝对压）HBOT对ACOP导致的血管内皮及其功能损伤具有显著的改善和作用;（3）血中NO、ET－1水平和CEC计数指标的单独或联合检测,可作为临床上判断ACOP患者血管内皮及其功能损伤程度、评估疗效、预测预后的重要手段。     

临床高压氧下新生仔兔视网膜变化的观察

目的　观察足月正常体重新生仔兔在模拟临床高压氧治疗 (hyperbaric oxygen therapy,HBOT)下视网膜组织结构的变化和检测视网膜组织中血管内皮生长因子 (vascular endothelial growthfactor,VEGF)的表达 ,来推断足月正常体重的新生儿在临床 HBOT下是否产生同早产儿视网膜病变(retinopathy of prem aturity,ROP)一样的病变。从而了解能否应用高压氧 (hyperbaric oxygenation,HBO)来治疗新生儿疾病。方法　足月产正常体重 12 d龄新生仔兔 116只 ,随机分成 HBO实验组 (A组 )、常氧高压氮组 (B组 )、空气对照组 (C组 )。 A、B组分别经不同实验压力、实验次数及喂养时间后取眼球与同龄 C组眼球病理切片进行显微镜下比较 ,按 1984年国际眼科学术大会制定的 ICROP诊断标准进行诊断 ,并采用 S- P免疫组化标记法进行 VEGF表达的检测。结果　全部 116只仔兔共 2 32只眼 ,经观察均未发现 ROP病理改变。 A、B、C组兔眼球视网膜组织中 VEGF的表达无显著性差异 (P>0 .0 5 )。结论　足月产正常体重新生仔兔在模拟临床 HBOT下没有发现产生 ROP。临床对足月产正常体重新生儿直接或间接性缺氧性疾病的治疗 ,可参考这一结果运用 HBO进行综合治疗 ,以提高其疗效。     

高压氧综合治疗对严重烧伤患者血浆一氧化氮、内皮素-1含量的影响

目的研究严重烧伤患者血浆一氧化氮（NO）、内皮素-1（ET-1）含量的变化及高压氧（HBO）的影响。方法选择烧伤总面积（TBSA）≥30％或Ⅲ度面积≥10％的患者84例，分为高压氧组（HBO组）和非高压氧组（non—HBO组），分别于伤后10个时相点抽取静脉血，分别用硝酸还原酶法，放免分析法测定血浆NO，ET-1含量的变化。结果non—HBO组患者伤后各时相点平均血浆ET-1含量明显高于正常对照组（P〈0．01），而NO的含量则显著降低（P〈0．01）；HBO组治疗后NO接近正常对照组（P〉0．05），但ET-1显著低于non—HBO组（P〈0．01）。结论严重烧伤患者血浆NO的降低及ET-1的升高参与烧伤后机体变化的全过程；HBO可显著改变严重烧伤患者血浆NO，ET-1含量，故对烧伤治疗有益。     

高压氧对兔内毒素血症治疗的实验研究

目的 观察高压氧(HBO)治疗对兔内毒素血症系统症状、周围血细胞及肺脏病理变化的影响.方法 46只新西兰兔静脉注射内毒素150μg/kg后,随机分成2组:对照组22只,不给予任何处理;HBO组24只,采用HBO治疗(每8 h 1次,共6次).2组分别于汴射内毒素后2、6、24、48 h采耳动脉血1 ml,检测白细胞和血小板,48 h后处死兔,观察肺组织变化.结果 与注射内毒素前相比,对照组兔白细胞和血小板在实验后2、6、24 h明显下降,48 h仍未恢复正常(P＜ 0.01或＜0.05).HBO组2、24h白细胞和血小板分别高于对照组(P＜0.01,P＜0.05),48 h后几乎完全恢复到实验前水平(P＞0.05).与对照组相比,HBO组兔肺组织内炎症反应较轻,且无微血栓及出血灶,48 h死亡率显著降低(P＜0.05).结论 HBO治疗能够显著减轻兔内毒素血症症状及白细胞、血小板的下降,减轻肺组织的炎症反应与出血,并显著降低死亡率(P＜0.05).     

高压氧对急性一氧化碳中毒患者血浆一氧化氮、内皮素-1含量的影响

目的　观测急性一氧化碳 (CO)中毒患者血浆一氧化氮 (NO)、内皮素 - 1(ET- 1)含量的变化及高压氧 (HBO)的影响。方法　 6 6例 CO中毒的患者被分为轻、中、重度三组 ,分别用硝酸还原酶法、放免分析法测定治疗前后三组患者及对照组的 NO、ET- 1含量的变化。结果　 HBO治疗前不同中毒程度组患者的血浆 ET- 1的含量较对照组明显升高 ,而 NO的含量则显著降低 (P<0 .0 1) ,同时各组间差异均有显著性 ;HBO治疗前后比较发现 ,HBO治疗 1次后 NO、ET- 1较治疗前有明显变化 ,但仍明显高于对照组 ;而 10次 HBO治疗后接近对照值。结论　急性 CO中毒患者血浆 ET- 1的升高及 NO的降低参与 CO造成的意识障碍的发生过程 ;这两个指标的变化可用于判断 CO中毒意识障碍程度及 HBO的疗效 ;HBO治疗对 NO、ET- 1含量的变化有有益的调节作用 ,可改善 CO的病理损害作用。     

诱生型一氧化氮合酶和内皮素-1在内毒素休克家兔血管反应性变化中的作用

目的了解诱生型-氧化氮合酶（iNOS）和内皮素-1（ET-1）在内毒素休克后家兔血管反应性变化中的作用。方法家兔128只,随机分为3组：脂多糖（LPS）对照组（n=48）,氨基胍（AG）＋LPS组（n=40）,PD-142893＋LPS组（n=40）。LPS对照组再分为6亚组：正常对照组、给LPS后0．5、1、2、4、6小时组（n=8）,测各组肠系膜上动脉（SMA）、腹腔动脉（CA）和左肾动脉（LRA）的血管反应性及组织iNOS、ET-1mRNA水平。AG＋LPS组和PD-142893＋LPS组均再分为5亚组：正常对照组、给LPS后1、2、4、6小时组（n：8）,测各组SMA、CA、LRA的血管反应性。结果内毒素休克早期CA的血管收缩和舒张反应性增加要多于SMA和LRA,且CA组织iNOSmRNA水平升高明显高于SMA和LRA,而3根血管ET-1mRNA水平均无明显变化;休克晚期SMA和LRA的血管收缩和舒张反应性的丢失均要多于CA,且SMA和LRA血管组织中iNOS和ET—1mRNA水平升高要高于CA。使用AG和PD．142893抑制iNOS和ET-1后各血管的反应性得到明显恢复。结论内毒素休克后iNOS和ET-1在各器官血管的差异表达可能参与了血管低反应性器官差异的形成。