不同时间脑室注射脑源性神经营养因子治疗新生大鼠缺氧缺血性脑损伤效果的比较

目的　比较新生大鼠缺氧缺血性脑损伤后不同时间脑室注射脑源性神经营养因子 (BDNF)对脑损伤的影响。方法　 7d龄SD大鼠左侧颈总动脉结扎后行 8%低氧吸入 2 5h形成缺氧缺血性脑损伤 ,伤后 0、1和 4h分别向脑室注射0 5 μgBDNF ,观察对脑水肿、皮层和海马脂质过氧化物(MDA)水平和细胞凋亡的影响。结果　伤后即刻给予BD NF减轻脑水肿、防止MDA过量产生和细胞凋亡增加的效果最为显著 ,伤后 4h给予效果较差。结论　BDNF对新生大鼠缺氧缺血性脑损伤后的皮层和海马具有显著的保护作用 ,以早期应用效果较为明显     

缺氧程度的判断

氧气吸入可用于各种原因引起的缺氧,血气分析检查是用氧指标,当患者动脉血氧分压低于6.67kPa(50mmHg)时,则应给予吸氧。1)轻度低氧血症:PaO2>6.67kPa(50mmHg),SaO2>80%,无发绀,一般不需氧疗。2)中度低氧血症:PaO2为4～6.67kPa(30～50mmHg),SaO260%～80%,有发绀、呼吸困难,需氧疗。     

氨气致呼吸道损伤护理教训

氨气致呼吸道损伤早期,呼吸道损伤征象往往不足以表现呼吸道的损伤程度。我们曾遇到2例氨气致呼吸道损伤死亡患者。例1男,30岁。因制冷设备爆炸氨溢漏,在密闭条件下吸入含高浓度氨气空气6s左右致伤,伤后未做任何处理,20h后入科。体表无烧伤,T37℃,P78次/min,R24次/min,Bp110/80mmHg(1mmHg=0.133kPa)。WBC5.8×109/L,RBC22×1012/L,血小板165×109/L,呼吸道分泌物较多且粘稠,鼻咽部黏膜充血。入院后32h因呼吸道粘膜脱落,出血,引出呼吸道梗阻而死亡。例2女,28岁。因储氨罐爆炸致伤,伤后11h入科,有密闭条件下高浓度氨吸入史,吸入时间约7…     

气管切开在原发性脑干损伤治疗中的作用

目的 探讨气管切开在原发性脑干损伤治疗中的作用.方法 我科于1998年1月～2006年12月共收治20例原发性脑干损伤的患者,其中伤后24h内切开1例,伤后24～72h内切开5例,72h～7d内切开4例,10例未切开.结论 在原发性脑干损伤治疗中,早期气管切开预防痰液堵塞气道,有效改善呼吸功能,降低脑耗氧量,纠正低氧血液,减轻继发性脑损害及全身多脏器功能衰竭,降低死亡率.     

椎基底动脉缺血／再灌注对豚鼠听功能和耳蜗形态学影响

目的 探讨椎基底动脉缺血／再灌注耳蜗损伤后耳蜗病理形态学和听功能改变。方法经颅底径路建立豚鼠椎基底动脉缺血／再灌注耳蜗损伤模型。68只豚鼠随机分成6组：正常组、缺血1h组、缺血再灌注组（按再灌注时间分12h、24h、48h．7d,4组）。各组动物分别于手术前和处死前行听性脑干反应（auditory brainstem response,ABR）测定,观察ABR各波潜伏期、Ⅰ-Ⅲ波间期和Ⅲ波阈值,部分动物观察了缺血时ABR变化。耳蜗组织切片HE染色技术观察组织细胞形态变化。结果血管阻断缺血时ABR表现波形不典型,重复性差,在缺血10～20min后波形逐渐稳定;缺血组与再灌注（12h、24h、48h、7d）各组ABR各波潜伏期和Ⅰ-Ⅲ波间期较正常组延长,Ⅲ波阈值升高,尤以再灌注24h变化最为显著,48h和7d后ABR阈值有所恢复,但不能恢复正常。耳蜗病理形态学改变发现缺血组毛细胞变形肿胀,再灌注（12h、24h、48h．7d）各组损伤进一步加重,再灌注24—48h损伤最重,可见明显外毛细胞缺损,螺旋神经元胞体和神经纤维较正常组减少,血管纹变薄,均以基底转为明显。结论豚鼠椎基底动脉缺血／再灌注时可致耳蜗损伤,表现为听功能和耳蜗组织形态学改变。     

烧冲复合伤临床特征和救治

烧冲复合伤系因爆炸导致体表烧伤、爆炸伤、吸入伤和冲击波所致的多脏器和多部位损伤的一种内外伤并存的特殊损伤类型[1],其特点是伤情复杂,相互加强和恶化、外伤掩盖内伤、诊断困难以及治疗矛盾等[2].     

新生儿胎粪吸入综合征伴肺动脉高压5例护理体会

胎粪吸入综合征（MAS）多因胎儿宫内慢性缺氧所致,如缺氧时间较长或程度较重可使肺小动脉平滑肌增生或痉挛,导致出生后持续的胎儿循环,血液通过动脉导管和卵圆孔发生右向左分流,使婴儿发生严重青紫和呼吸困难,形成新生儿持续肺动脉高压（PPHN）和低氧血症,若不及时处理或护理不当,可能危及生命。我中心自2006年5月至2007年9月共收治MAS伴PPHN患儿5例,现将护理体会总结如下。     

弥漫性脑外伤对大鼠内耳超微结构及听功能影响的实验研究

目的探讨弥漫性脑外伤对大鼠内耳超微结构及听功能的影响。方法建立弥漫性脑外伤大鼠模型并完全随机分成正常对照组及外伤1、2、3、4周组,每组各30例。采用听性脑干反应测定及光镜、电镜观察等手段,记录各波波峰潜伏期（PL）及各波峰间潜伏期（IPL）,观察各组动物耳蜗超微结构及听功能的变化。结果正常对照组大鼠耳蜗结构正常,外伤后各组内耳超微结构有明显损伤变化。外伤1、2、3、4周组V波阈值均高于正常对照组[分别为（18．50±7．83）、（17．83±8．35）、（16．00±7．12）、（15．42±7．21）dB比（1．17±2．13）dB],差异均有统计学意义（均P〈0．05）。同时外伤1、2、3、4周组I波、Ⅲ波、Ⅳ波PL及I-Ⅲ、Ⅲ-V、I-V IPL均明显高于正常对照组,差异均有统计学意义（P〈0．05）。结论弥漫性脑外伤对内耳超微结构及听功能均有不同程度的影响,听功能变化可能与耳蜗超微结构损伤有关。     

利多卡因氯霉素复合液持续冲洗治疗眼烧伤的临床观察

目的观察利多卡因氯霉素复合液持续结膜囊冲洗治疗眼烧伤的疗效.方法对56例共105只眼,致伤因素分别为电弧伤、化学伤、火焰伤、热水(油)烫伤,给予利多卡因氯霉素复合液持续结膜囊冲洗治疗.结果总有效率为92.3%,仅有4例6只眼发生角膜穿孔、真菌性角膜炎等严重并发症,1例出现视网膜部分剥落.结论利多卡因氯霉素复合液持续结膜囊冲洗治疗眼烧伤是一种简单易行、效果满意的方法,值得临床推广应用.     

神经内科压疮的护理

压疮,原称为褥疮,传统医学称为"席疮",主要是皮肤或皮下组织由于压力,复合剪切力,摩擦力作用而发生在骨隆突处的局限性损伤。经测定一个持续达14.4kPa的压力就可使皮肤组织发生坏死,9.33kPa压力持续2h即可造成不可逆皮肤组织细胞变性[1]。压疮也是长期卧床患者,特别是老年、昏迷、瘫痪、营养不良的常见并发症。神经内科老年中风患者的皮肤的反应力、移动能力、活动能力及营养等都较差,加之尿失     

Halothane-induced liver injury in outbred guinea pigs: role of trifluoroacetylated protein adducts in animal susceptibility

Halothane causes a mild form of liver injury in guinea pigs that appears to model the hepatotoxicity seen in approximately 20% of patients treated with this drug. In previous studies, it was concluded that the increased susceptibility of some outbred guinea pigs to halothane-induced liver injury is not caused by their inherent ability to metabolize halothane to form toxic levels of trifluoroacetylated protein adducts in the liver. In this study, we reevaluated the role of trifluoroacetylated protein adducts in halothane-induced liver injury in guinea pigs. Male outbred Hartley guinea pigs were treated with halothane intraperitoneally. On the basis of serum alanine aminotransferase levels and liver histology, treated animals were designated as being susceptible, mildly susceptible, or resistant to halothane. Immunoblot studies with the use of anti-trifluoroacetylated antibodies showed that susceptible guinea pigs for the most part had higher levels of trifluoroacetylated protein adducts in the liver 48 h after treatment with halothane than did less susceptible animals. In support of this finding, the level of trifluoroacetylated protein adducts detected immunochemically in the sera of treated guinea pigs correlated with sera levels of alanine aminotransferase activity. In addition, the levels of cytochrome P450 2A-related protein but not those of other cytochrome P450 isoforms, measured by immunoblot analysis with isoform-specific antibodies, correlated with the amount of trifluoroacetylated protein adducts detected in the livers of guinea pigs 8 h after halothane administration. The results of this study indicate that the susceptibility of outbred guinea pigs to halothane-induced liver injury is related to an enhanced ability to metabolize halothane in the liver to form relatively high levels of trifluoroacetylated protein adducts. They also suggest that cytochrome P450 2A-related protein might have a major role in catalyzing the formation of trifluoroacetylated protein adducts in the liver of susceptible guinea pigs. Similar mechanisms may be important in humans.     

Comparison of hepatotoxicity and metabolism of butyltin compounds in the liver of mice,rats and guinea pigs

The hepatotoxicity of tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) was compared among mice, rats and guinea pigs in vivo. Further, the metabolism of these butyltin compounds in the liver was also investigated in these species. The oral administration of TBTC and DBTC to mice induced obvious liver injury, as demonstrated by both serodiagnosis and histopathological diagnosis. The concentrations of TBTC and DBTC that induced hepatotoxicity in mice at 24 h after oral administration were 180 and 60 micro mol/kg, respectively. In the case of rats, the liver injury induced by TBTC and DBTC was detected at 24 h by the serodiagnosis, but not by histopathological diagnosis. On the other hand, in guinea pigs, TBTC and DBTC administration did not produce any clear liver injury at 24 h, as evaluated by these two diagnostic methods. Thus, the following ranking was obtained with regard to increasing order of sensitivity to liver injury caused by TBTC and DBTC: mice, rats and guinea pigs. The total butyltin contents in the liver of mice were equivalent at 3 h and 24 h after the administration of TBTC or DBTC; however, the contents in the liver of rats and guinea pigs were relatively lower at 3 h and higher at 24 h than those of mice, although there were no differences between rats and guinea pigs in the total liver butyltin content. Concerning the liver metabolism of these butyltin compounds, the main form of butyltin compounds in these animals treated with TBTC was DBTC within 3 h after oral administration, while the main metabolites at 24 h were different in each species, indicating that the liver metabolism of TBTC might vary by animal type. When the animals were treated with DBTC orally, DBTC was hardly metabolized in the livers of these animals even at 24 h, and the liver levels of DBTC were two times greater in mice and guinea pigs than in rats at 3 h and were lower in mice at 24 h than in rats and guinea pigs. The analysis of cellular distributions of DBTC in the liver at 3 h after the administration showed that the levels of DBTC in the nuclear, microsomal and mitochondrial fractions of mice hepatocytes were relatively higher than in those of rats, which were greater than in those of guinea pigs. These results suggest differences in the sensitivity of mice, rats and guinea pigs to hepatotoxicity caused by butyltin compounds and demonstrate that the difference in the sensitivity of these animals to the hepatotoxicity induced by TBTC and DBTC may be partly due to differences in hepatic metabolism of TBTC and in the distribution of DBTC within cell organelles, respectively.     

Biochemical effects of combined gases of nitrogen dioxide and ozone. III. Synergistic effects on lipid peroxidation and antioxidative protective systems in the lungs of rats and guinea pigs

Rats and guinea pigs were exposed continuously to 0.4 ppm NO2, 0.4 ppm O3 or a combination of the two gases for 2 weeks. The concentration of lipid peroxides in lungs of rats and guinea pigs exposed to NO2 alone or O3 alone did not change. The lipid peroxide level of rats inhaling the combined gases also did not change. However, the level of lipid peroxides in guinea pigs exposed to a combination of the two gases was increased to 2.2 times of the control level, showing a synergistic interaction. No increases of antioxidative protective enzyme activities and of antioxidants (such as NPSH, VE, VC) in guinea pigs exposed to NO2, O3 or the combined gases were found. In rats, no changes in enzyme activities and of the antioxidant contents were observed after NO2 alone, but O3 exposure produced slight increases of NPSH, VC, and GPx-H2O2. On the other hand, in rats exposed to the combined gases, marked synergistic increased of many antioxidative factors such as NPSH, VC, G6PD, GPx-cum.OOH and GPx-H2O2 were found. The results show that those animals which are able to increase antioxidative protective factors in the lung following exposure to the combined gases do not respond with a significant increase in lipid peroxides. On the other hand, in animals with poor induction-ability of these factors lipid peroxides are formed. This might explain why guinea pigs were the most sensitive to the effects of the combined gases. Furthermore, it was shown that in guinea pigs the increased level of lipid peroxides and that in rats the increased activities of antioxidative enzymes and the increased contents of the antioxidants were synergistic following exposure to the combined gases.     

Biochemical effects of combined gases of nitrogen dioxide and ozone. II. Species differences in lipid peroxides and antioxidative protective enzymes in the lungs

Changes in lipid peroxide (thiobarbituric acid reactant) levels, in the content of non-protein sulfhydryls (NPSH) and total proteins, and in the activities of antioxidative protective enzymes were examined in the lungs of four animal species exposed to a mixture of NO2 and O3 for 2 weeks. Male mice, hamsters, rats and guinea pigs were used. Thiobarbituric acid (TBA) reactant levels were increased significantly in the lungs of mice and guinea pigs, but not in hamsters and rats. NPSH contents were increased markedly in hamsters, mice and rats, but not in guinea pigs. The activities of antioxidative protective enzymes also changed with the exposure. The most characteristic change was the significant increase in glutathione peroxidase (GPx-H2O2) activity in hamsters and rats - species which did not exhibit increases in their TBA reactant levels. The increase in this enzyme activity in mice was significant, but not very large. Furthermore, guinea pigs were genetically deficient in this enzyme, and the increase in glycolytic enzymes for regenerating NADPH was also lowest in guinea pigs. The glutathione S-transferase (GSH-Tase) activity in mice and guinea pigs was decreased by exposure to the combined gases. These results suggest that the increases in lipid peroxide levels in mice and guinea pigs may be due to a lesser ability to regenerate protective reducing substances, such as NPSH and NADPH, than that of hamsters and rats. Induction of protective enzyme activities on exposure to the combined gases was also poor in mice and guinea pigs.     

长期应用地西泮对豚鼠耳蜗微音器电位的影响

目的观察长期应用地西泮对豚鼠耳蜗微音器电位的影响。方法采用逐渐增加剂量的方法皮下注射地西泮3个月后停药,10d后用不同强度的短声刺激诱发微音器电位产生,测量诱发微音器电位产生的阈值,用共聚焦显微镜测量耳蜗毛细胞内Ca2+浓度的变化。结果应用地西泮3个月后停药,与对照组相比,引起豚鼠微音器电位产生的阈值明显降低,微音器电位的幅度显著增加,记录出自发的微音器电位,毛细胞内Ca2+浓度降低。结论长期应用地西泮后豚鼠耳蜗对声刺激的敏感性增加可能与毛细胞内Ca2+浓度降低有关。     

高温气体吸入致豚鼠急性肺损伤动物模型制备的实验研究

目的 制备高温气体吸入致豚鼠急性肺损伤(ALI)动物模型.方法 选择20只雄性豚鼠随机分为2组,每组10只,其中健康豚鼠为对照组、急性肺损伤豚鼠为实验组.实验组吸入150℃ 高温气体制作豚鼠ALI动物模型,然后处死2组豚鼠并取豚鼠右肺的大体标本,称重计算豚鼠肺湿/干重比(W/D),选取2组豚鼠左上肺组织进行HE染色,利用光学显微镜观察肺组织病理变化情况,及时记录其病理变化的结果 ;对豚鼠动脉血液进行血气分析并比较.结果实验组豚鼠肺组织病理结构呈现明显的急性炎症性改变;实验组豚鼠肺W/D比值显著高于对照组[(5.72±0.31)vs(4.88±0.11),P<0.05];实验组豚鼠pH、PaO2显著低于对照组[(7.02±0.12)vs(7.38±0.04),(98.80±62.60)mmHg vs(177.30±24.70)mmHg,P<0.05],而PaCO2显著高于对照组[(74.70±23.23)mmHg vs(31.10±8.77)mmHg,P<0.05].结论 成功制作豚鼠ALI实验动物模型.该模型达到ALI要求,仿真性能高、重复性好、稳定性高,为今后研究高温气体吸入致ALI的临床及基础研究提供了可靠的动物模型.     

Adrenaline reveals the torsadogenic effect of combined blockade of potassium channels in anaesthetized guinea pigs

BACKGROUND AND PURPOSE: Torsade de pointes (TdP) can be induced in several species by a reduction in cardiac repolarizing capacity. The aim of this study was to assess whether combined I(Kr) and I(Ks) blockade could induce TdP in anaesthetized guinea pigs and whether short-term variability (STV) or triangulation of action potentials could predict TdP. EXPERIMENTAL APPROACH: Experiments were performed in open-chest, pentobarbital-anaesthetized, adrenaline-stimulated male Dunkin Hartley guinea pigs, which received three consecutive i.v. infusions of either vehicle, the I(Kr) blocker E-4031 (3, 10 and 30 nmol kg(-1) min(-1)), the I(Ks) blocker HMR1556 (75, 250, 750 nmol kg(-1) min(-1)) or E-4031 and HMR1556 combined. Phenylephrine-stimulated guinea pigs were also treated with the K(+) channel blockers in combination. Arterial blood pressure, ECGs and epicardial monophasic action potential (MAP) were recorded. KEY RESULTS: TdP was observed in 75% of adrenaline-stimulated guinea pigs given the K(+) channel blockers in combination, but was not observed in guinea pigs treated with either I(K) blocker alone, or in phenylephrine-stimulated guinea pigs. Salvos and ventricular tachycardia occurred with adrenaline but not with phenylephrine. No changes in STV or triangulation of the MAP signals were observed before TdP. CONCLUSIONS AND IMPLICATIONS: Combined blockade of both I(Kr) and I(Ks) plus the addition of adrenaline were required to induce TdP in anaesthetized guinea pigs. This suggests that there must be sufficient depletion of repolarization reserve and an appropriate trigger for TdP to occur.     

Effect of liposome-encapsulated recombinant human superoxide dismutase (liposome-r-h-SOD) on the lung injury induced by Forssman antiserum in guinea pigs

We investigated the effect of liposome-r-h-SOD on the lung injury induced by Forssman antiserum in guinea pigs. Intravenous injection of Forssman antiserum produced a biphasic increase in pulmonary resistance in guinea pigs. Liposome-r-h-SOD blocked this biphasic increase in a dose-dependent manner. Exudate and hemorrhage in the alveolar spaces and connective tissues were blocked by liposome-r-h-SOD. Liposome-r-h-SOD was more effective when it was injected 30 min prior to challenge than 5 min prior to challenge. On the other hand, free r-h-SOD or a mixture of free r-h-SOD and empty liposome did not block the lung injury. SOD activity in porcine endothelial cells cultured with liposome-r-h-SOD increased in a dose-dependent and time-dependent manner, while it did not increase with free r-h-SOD. Exogenous SOD was detected by immunoperoxidase staining in endothelial cells of arterioles and capillaries and in alveolar epithelial cells of the lung of guinea pigs injected with liposome-r-h-SOD. These findings suggest that superoxide radical may take part in the lung injury induced by Forssman antiserum. Liposome-r-h-SOD, which adheres to and/or is endocytosed by endothelial cells, may protect the lung from oxygen radicals.     

Biochemical effects on combined gases of nitrogen dioxide and ozone. I. Species differences of lipid peroxides and phospholipids in lungs

In the present study, changes of lipid peroxides, phospholipids and antioxidant levels in lungs of 4 animal species exposed to the combined gases of NO2 and O3 were compared. Male mice, hamsters, rats and guinea pigs were used. Lipid peroxides were increased significantly in the lungs of mice and guinea pigs exposed to the combined gases, but not in hamsters and rats. Changes of alpha-tocopherol (VE) contents were slight. On the other hand, non-protein sulfhydryl (NPSH) contents were increased strikingly, especially in hamsters, but were not increased in guinea pigs. Phosphatidylcholine (PC) contents were increased and phosphatidylethanolamine (PE) contents were decreased by the exposure to the combined gases, with the order guinea pig greater than mouse greater than rat. In hamsters no changes were seen. The changes of fatty acid composition in guinea pigs and mice were marked, the increases of palmitate and palmitolate and the decreases of polyunsaturated fatty acid were especially characteristic. These changes in phospholipid class and fatty acid composition may be a "a kind of adaptation phenomenon" to avoid further lipid peroxidation. On the other hand, the changes in hamsters and rats were small. The results show the existence of species differences in lipid peroxide formation by exposure to the combined gases of NO2 and O3. They were found to be related to the contents of antioxidants and the compositions of phospholipids and their fatty acids.     

小儿哮喘宁平喘作用的研究

目的初步评价小儿哮喘宁的平喘作用,为临床应用提供科学的实验依据。方法运用乙酰胆碱及组胺致豚鼠哮喘模型、内毒素（lipoplysaccharides,LPS）致小鼠急性肺损伤模型、卵白蛋白（ovalbumin,OVA）致豚鼠过敏性哮喘模型及OVA加LPS致小鼠过敏性哮喘模型,评价小儿哮喘宁的平喘作用。结果小儿哮喘宁20、10、5 g/kg均能延长乙酰胆碱＋组胺所致豚鼠化学刺激性哮喘的引喘潜伏期及OVA致豚鼠过敏性哮喘的引喘潜伏期并减少跌倒动物数;20 g/kg小儿哮喘宁能降低LPS致小鼠急性肺损伤程度;对嗜酸粒细胞（eosinophil,EOS）浸润型过敏性哮喘动物模型的作用优于对中性粒细胞（neutrophil,NEU）浸润型过敏性哮喘动物模型的作用。结论小儿哮喘宁有平喘的作用,该作用可能与其抑制肺水肿、降低气道EOS浸润有关。