氨氯地平并苯那普利对高血压患者血浆一氧化氮与内皮素的影响

目的:评价氨氯地平、苯那普利单独和联合治疗对高血压患者血浆一氧化氮(NO)和内皮素(ET)的影响。方法:选择126例高血压患者随机分为3组,氨氯地平组(A组,41例,接受氨氯地平治疗);苯那普利组(B组,45例,接受苯那普利治疗);联合治疗组(C组,40例,接受氨氯地平和苯那普利治疗)。于治疗前、后行血压及血浆NO、ET测定,并与40例正常对照组血浆NO、ET水平对照。结果:较之对照组,三组高血压患者NO水平显著降低(P<0.01),ET水平显著升高(P<0.01)。三组治疗后血压、ET水平均有显著下降(P均<0.01),A组及B组下降幅度无显著差异,C组下降幅度明显高于A组和B组的(P<0.05);三组血浆NO水平均有显著升高(P均<0.01);A组及B组血浆NO水平升高无显著差异(P>0.05),C组NO升高幅度明显高于A组和B组的(P<0.05)。结论:氨氯地平和苯那普利单独治疗均可明显降低血压和血浆ET水平,同时升高血浆NO水平,而两药联用疗效更佳。     

丁苯酞及针刺联合高压氧治疗急性一氧化碳中毒后迟发性脑病的疗效观察

目的探讨丁苯酞及针刺联合高压氧治疗急性一氧化碳中毒后迟发性脑病的临床疗效。方法将符合标准的120例患者随机分为研究组和对照组,每组60例。研究组在高压氧等常规治疗的基础上加用丁苯酞及针刺治疗,对照组给予高压氧等常规治疗。观察和比较两组治疗效果及治疗前后MMSE评分、脑电图变化。结果研究组简易智能精神量表评分及脑电图与对照组比较差异有统计学意义（P〈0．05）,研究组能明显改善MMSE评分且脑电图异常率比对照组低;研究组在痊愈率和总有效率方面显著优于对照组,差异有统计学意义（P〈0．05）。结论丁苯酞及针刺联合高压氧治疗急性一氧化碳中毒后迟发性脑病可以提高患者的治疗效果和生存质量,有良好的临床应用价值。     

水通道蛋白4对一氧化碳中毒后迟发性脑病大鼠神经损伤的影响

目的 探讨水通道蛋白4(Aquaporin 4,AQP4)对一氧化碳(Carbon monoxide,CO)中毒后迟发性脑病(Delayed encephalopathy,DEACMP)大鼠神经损伤的影响。方法 将210只雄性SD大鼠随机分为空白对照(Blank control,BC)组、CO中毒(CO)组、钠-钾-氯共转运体(Na⁺-K⁺-Cl^- cotransporter,NKCC)抑制剂处理(布美他尼)组、p38-丝裂原活化蛋白激酶(Mitogen activated protein kinase,MAPK)抑制剂处理(MAPK)组和AQP4特异性抑制剂处理(AQP4抑制剂)组,每组各42只; 根据造模后不同时间点将每组大鼠进一步分为染毒3、6、12、24、48、72 h和7 d后共7个亚组,每亚组各6只; 取大鼠脑前额叶皮质组织,计算脑皮质含水量,采用HE法观察脑皮质形态; 采用免疫组化链霉菌抗生物素蛋白-过氧化物酶(Streptavidin-perosidase,SP)染色法测定大鼠脑皮质AQP4,p38 MAPK,NKCC1、胶质纤维酸性蛋白(Glial fibrillary acidic protein,GFAP)和S100钙结合蛋白B(S100 calcium binding protein B,S100B)蛋白表达水平。结果 与BC组比较,CO组大鼠在染毒3、6、12、24、48、72 h后尾静脉COHB水平和脑皮质含水量显著升高,脑皮质AQP4,p38 MAPK,NKCC1,GFAP和S100B蛋白表达水平显著升高,染毒7 d后恢复正常(P<0.05); 与CO组比较,布美他尼组、MAPK组和AQP4抑制剂组大鼠脑皮质含水量显著降低,脑皮质AQP4,p38 MAPK,NKCC1,GFAP和S100B蛋白表达水平显著降低,且AQP4抑制剂组变化更明显(P<0.05)。结论 p38-MAPK/NKCC信号通路可能参与调控CO中毒DEACMP大鼠脑皮质AQP4表达,抑制AQP4表达可有效减轻大鼠脑水肿并改善预后,有望成为预防和治疗DEACMP的新靶点。     

Mild carbon monoxide poisoning impairs left ventricular diastolic function

Rationale:

Carbon monoxide (CO) poisoning is associated with direct cardiovascular toxicity. In mild CO poisoning in which cardiovascular life support is not required, the effects of CO on left and right ventricular functions are unknown in patients without cardiac failure.

Objectives:

Echocardiography was used to determine whether or not mild CO poisoning impairs ventricular function. Twenty otherwise healthy patients with CO poisoning and 20 age- and gender-matched controls were studied. Echocardiographic examinations were performed at the time of admission and 1 week after poisoning.

Results:

The impairment observed in the left and right ventricular diastolic function at the time of admission was greater than the impairment 1 week after poisoning. Mild CO poisoning did not have a significant effect on systolic function. Carboxyhemoglobin levels were positively correlated with left ventricular diastolic dysfunction, whereas the levels were not correlated with right ventricular diastolic function.

Conclusions:

In CO intoxication, the development of left and right ventricular diastolic dysfunction precedes systolic abnormality. Patients with mild CO poisoning do not manifest cardiovascular symptoms; however, it should be borne in mind that most of these patients have myocardial involvement.     

Bone mineral density improvement after lung volume reduction surgery for severe emphysema

BACKGROUND: In patients with severe emphysema, bone mineral density (BMD) is reduced and the risk of osteoporosis is increased. STUDY OBJECTIVES: To identify the impact of lung volume reduction surgery on BMD. DESIGN: Prospective cohort study. SETTING: University hospital. PATIENTS AND INTERVENTIONS: Forty emphysematous patients, all receiving oral steroid therapy, underwent bilateral lung volume reduction surgery. Thirty similar patients, who refused the operation, followed a standard respiratory rehabilitation program. MEASUREMENTS: All subjects were evaluated pretreatment and 12 months posttreatment for respiratory function, nutritional status, and bone-related biochemical parameters. BMD was assessed by dual-energy radiograph absorptiometry. RESULTS: After surgery, we observed significant improvements in respiratory function (FEV1, + 18.8% [p < 0.01]; residual volume [RV], -29.6% [p < 0.001]; diffusing capacity of the lung for carbon monoxide [Dlco], + 21.6% [p < 0.01]) nutritional parameters (fat-free mass, + 6.0% [p < 0.01]), levels of bone-related hormones (free-testosterone, + 20.5% [p < 0.01]; parathormone, -11.2% [p < 0.01]), bone turnover markers (osteocalcin, -12.7% [p < 0.05]; bone-alkaline-phosphatase, -14.0% [p < 0.05]; beta-crosslaps, -33.6% [p < 0.001]), BMD (lumbar, + 8.8% [p < 0.01]; femoral, + 5.5% [p < 0.01]), and T-score (lumbar, + 21.0% [p < 0.01]; femoral, + 12.4% [p < 0.01]) with reduction in osteoporosis rate (50 to 25%). Nineteen patients who had undergone surgery were able to discontinue treatment with oral steroids. These subjects showed a more significant improvement in BMD (lumbar, + 9.6%; femoral, + 6.8%; p < 0.001) and T-score (lumbar, + 27.3%; femoral, + 14.3%; p < 0.001). The remaining 21 patients who had undergone surgery experienced significant improvement compared to respiratory rehabilitation subjects despite continued therapy with oral steroids (BMD: lumbar, + 4.5% vs -0.7%, respectively [p < 0.01]; femoral, + 2.7% vs -1.1%, respectively [p < 0.05]; T-score: lumbar, + 14 vs -2.1, respectively [p < 0.01]; femoral, + 7.4 vs -2.7, respectively [p < 0.01]). The increase in lumbar BMD was correlated with the surgical reduction of RV (p = 0.02) and with the increase in Dlco (p = 0.01) and fat-free mass (p = 0.01). CONCLUSIONS: Lung volume reduction surgery significantly improves BMD compared to respiratory rehabilitation therapy, even in patients requiring oral steroids. The increase in BMD correlates with RV, Dlco, and fat-free mass, suggesting that the restoration of respiratory dynamics, gas exchange, and nutritional status induces improvement in bone metabolism and mineral content.     

CORM-3介导小胶质细胞ICAM-1抑制放射性脑损伤炎症反应

目的本研究旨在探讨水溶性一氧化碳分子释放剂(CORM-3)对放射性脑损伤炎症反应的影响及其分子机制。方法 BV2系小胶质细胞,随机分为正常对照组、单纯照射组和照射加CORM干预组,通过ELISA法测定各组照射后24 h炎症因子TNF-α、IL-1β的表达情况;采用免疫荧光法判断各组小胶质细胞激活形态,TUNEL染色比较各组共培养后原代神经元凋亡情况,并用Western blot法检测P38 MAPK通路对CORM干预放射后细胞间黏附分子1(ICAM-1)蛋白表达的影响。结果 BV2细胞放射后24 h TNF-α、IL-1β表达明显增高;CORM-3可减轻放射后小胶质细胞活化程度及炎症表达,降低了放射后TUNEL阳性细胞百分比;CORM-3抑制了放射后BV2细胞磷酸化P38及ICAM-1蛋白的表达增加,而P38抑制剂进一步下调放射后BV2细胞ICAM-1的表达。结论 CORM-3通过P38 MAPK-ICAM-1通路抑制内源性小胶质细胞活化和外源性白细胞趋化的双重调控方式改善放射后脑损伤炎症反应,进而减轻放射后炎症所致神经元损伤,这为改善鼻咽癌放疗后脑损伤的治疗提供了有潜在前景的新途径。     

不同细胞构筑在高压氧治疗迟发型脑病中的功能研究

目的：通过研究高压氧（ HBO）治疗急性CO中毒大鼠皮层不同细胞构筑在神经细胞凋亡中的差别,探讨HBO治疗急性CO中毒的机制及靶向定位。方法利用雄性SD大鼠,建立急性CO中毒模型。应用免疫组织化学以及免疫荧光的方法,测定在CO中毒和HBO治疗1 d、3 d、7 d、14 d和21 d后Caspase－3、NeuN和MMP－9的表达变化。结果急性CO中毒后,皮层神经细胞凋亡随中毒后时间延长而加重;不同细胞构筑发生凋亡程度不同,内颗粒层和内锥体细胞层最明显;Caspase－3与MMP－9在内颗粒层与内锥体细胞层变化最明显,在1 d开始增多,3 d达到最大值,7 d开始减少;HBO治疗后,MMP－9和Caspase－3降低,尤其以内颗粒层与内锥体细胞层最明显;且HBO治疗7 d后,降低最明显。结论急性CO中毒后,皮层各层神经细胞均发生凋亡现象,内颗粒层和内锥体细胞层最明显;凋亡可能与MMP－9降解神经细胞周围的基质, Caspase－3促进凋亡有关;HBO治疗可能是通过调控复杂的蛋白表达机制,调节MMP－9以及Caspase－3的表达水平,最终抑制神经细胞的凋亡;HBO治疗7 d对凋亡的作用最明显。