Exhaled nitric oxide and its long‐term variation in healthy non‐smoking subjects

Exhaled nitric oxide (NOexp) is an indicator of inflammation in the airways. Reference values obtained from healthy adults or information on long‐term variation of NOexp are not yet available. The aims of this pilot study were to collect values of NOexp from a selected group of healthy adults and to assess their long‐term variation. We studied 26 healthy subjects (age 21–48, 16 male, 10 female) with normal findings in flow‐volume spirometry, pulmonary diffusing capacity, relative amount of blood eosinophils, chest X‐ray and ECG at rest. NOexp was determined according to the European Respiratory Society guidelines during slow expiration against an airflow resistance. The measurements were repeated after 7 (n=13) and 23 days (n=17). The mean value of NOexp (n=26) was 6·9 ng g^–1 (95% confidence interval, 6·0–7·9 ng g^–1). The upper limit of intra‐individual variation (+2 SD) was 11·9 ng g^–1 and the lower limit (–2 SD) 1·9 ng g^–1, respectively. The mean (SD) value of NO production (NO output) was 39·1 pmol s^–1 (20 pmol s^–1). We found no correlation between NOexp and age (r=–0·06, P=0·78) and no association of NOexp with the gender (male vs. female, P=0·40). The intraindividual coefficient of variation (CoV) was 15·8% of NOexp and 20·7% of NO output within the interval of 7 days. CoV was 16·8% of NOexp and 18% of NO output within the interval 23 days. The results suggest that NOexp values over 12 ng g^–1 are abnormally high in healthy subjects. According to the results the change of NOexp by 30–35% or more within the interval of 1–3 weeks would be abnormal.     

谷氨酸诱导体外培养的鸡胚脊髓神经细胞释放NO

用鸡胚脊髓神经细胞的原代培养,测定细胞中亚硝酸盐的含量,研究了谷氨酸(Glu)对原代培养神经细胞中NO的影响。结果表明,谷氨酸作用于原代培养的鸡胚脊髓神经细胞,在诱导神经细胞释放乳酸脱氢酶(LDH)的同时,还可诱导细胞释放一氧化氮(NO)。如先用NO合成酶抑制剂L-NOARG作用细胞,再加入Glu,则发现L-NOARG能降低Glu导致的培养液中LDH活性升高。提示NO可能参与介导Glu的神经毒性作用。     

从自由基生物学角度评价鸡肉质量的实验研究

本文把外观健康和非健康的活鸡各20只分成两组,宰后测其肝、腿肌中超氧化物歧化酶(SOD)含量和脂质过氧化产物丙二醛(MDA)水平,发现两组中上述指标值差异显著(P<0.050 ;同时对两组实验鸡胴体在宰后4小时做了感官鉴别,也判断出其品质存在差异。提示体内SOD活性和MDA水平可以反映鸡肉质量,比感官鉴别更具敏感性,同时也可以反映宰前鸡的健康状况。     

Changes of circulating TNF and its effects on Pseudomonas aeruginosa septic shock in rabbits

Itiswellknownthatcertaincytokinesplayapivotalroleinthedevelopmentoftraumaandshock.Tumornecrosisfactor(TNF)isapolypep-tiedcytokinesynthesizedinmonocytesandmacrophagesinresponsetolipopolysaccharide(LPS)stimulation-TherelationshipbetweenTNFandendotoxic-septicshockbecomesafocusoftheresearchofshockmediators[1'2].Alargeamountofexperimentalandclinicaldata[3-9JsuggestthatTNFplaysanimportantroleinthepathogenesisofendotoxic-septicshockbuttheprecisemechanismandtherelationshipofTNFtoshockseverityrem…     

茶多酚对老化相关酶GSH－Px、SOD及代谢产物过氧化脂质的影响

本实验研究了连续服用茶多酚２０天，对１４月龄小鼠血及肝中ＳＯＤ、ＧＳＨ－Ｐｘ和ＬＰＯ的影响。结果表明茶多酚能提高血及肝中ＳＯＤ及ＧＳＨ－Ｐｘ活性，与正常对照组比较Ｐ＜０．０１，同时能降低血及肝中ＬＰＯ含量，与正常对照组比较Ｐ＜０．０１。提示茶多酚可通过降低机体自由基水平，起到抗衰老作用。     

Chronic vitamin E treatment prevents defective endothelium-dependent relaxation in diabetic rat aorta

Summary We examined the effect in rats of 2 months of streptozotocin-induced diabetes mellitus on relaxation and contraction of aortas in vitro. A further diabetic group was treated from time of diabetes induction with a 1% dietary supplement of vitamin E. Diabetes caused a 26.5% deficit (p<0.001) in maximum endothelium-dependent relaxation to acetylcholine in phenylephrine-precontracted aortas. This was 64.3% attenuated (p<0.01) by vitamin E treatment; maximum relaxation was not significantly altered compared to non-diabetic rats. Vitamin E treatment of non-diabetic rats did not significantly affect acetylcholine-induced relaxation. Diabetes or treatment did not significantly alter acetylcholine sensitivity. Endothelium-independent relaxation response to glyceryl trinitrate was not affected by diabetes or vitamin E treatment, indicating that vascular smooth muscle responses to nitric oxide remained unaltered. There was a 35.4% reduction in the maximum contractile response to phenylephrine with diabetes (p<0.05) which was unaffected by vitamin E treatment. The data suggest that the chronic deficit in nitric oxide-mediated endothelium-dependent relaxation in diabetes depends largely upon excess activity of reactive oxygen species. Treatment with vitamin E to increase free radical scavenging specifically protected vascular endothelium although it had no effect on deficits in vascular smooth muscle contractile responses.Abbreviations NO Nitric oxide - ARI aldose reductase inhibitor - ACH acetylcholine - GTN glyceryl trinitrate - GSH reduced form of glutathione - EC₅₀ effective concentration for 50% of the maximal response     

Production of nitrite by primary rat astrocytes in response to pneumococci

Recent studies using a rat model of pneumococcal meningitis have shown that nitric oxide synthase (NOS) inhibitors greatly attenuated microvascular changes and brain edema formation. The site of NO production during bacterial meningitis is unknown. In this study we tested whether primary astrocyte cultures from neonatal rat cortex can be induced to release NO upon stimulation with pneumococci. NO production was assessed by measuring nitrite in the cell culture supernatant using the Griess reaction. Stimulation with heat-killed unencapsulated pneumococci (HKP) increased nitrite concentrations in astrocyte culture supernatants in a dose-dependent fashion. Administration of AT-nitro-L-arginine (L-NA), aminoguanidine, L-canavanine, cycloheximide, and dexamethasone prevented the increase in nitrite concentrations. Addition of L-arginine, but not of o-arginine, partially reversed the inhibitory effect of L-NA. Administration of SOD increased nitrite accumulation. Moreover, at 72 h after stimulation with heat-killed pneumococci (10⁷ cfu/ml) astrocytes showed an inducible NOS-like immunoreactivity. Accumulation of nitrite was also observed when rat cerebellar neurons and microglia were stimulated with HKP, whereas there was only a slight increase of nitrite in media of rat C6 glioma cells, but no increase of nitrite when the human glioblastoma cell line LN-229 was stimulated with HKP. There was a stronger increase in nitrite levels when astrocytes from Lewis rats were used compared to that from Wistar rats. In conclusion, our study indicates that astrocytes, neurons and microglia are inducible for NO production upon stimulation with pneumococci.     

NO对兔局灶脑缺血脑水肿和脑梗塞灶的影响

本文在兔MCAO局灶脑缺血模型基础上,利用外源性一氧化氮(NO)前体物质L-精氨酸和NOS抑制剂L-NNA研究NO对脑缺血后脑水肿和脑梗塞的影响。NZW兔42只随机分为7组,每组6只,计对照组、假手术组、MCAO组、MCAO+NS组、MCAO+L-Arg组、MCAO+D-Arg组及MCAO+L-Arg+L-NNA组。结果提示:与单纯MCAO组比较,L-Arg组的脑组织H_2O、Na~+、Ca~(2+)含量明显下降(P<0.01),脑梗塞灶亦明显缩小(P<0.01)。从而显示L-Arg系通过产生NO促使血管舒张而减轻脑水肿和缩小梗塞灶,为临床改进脑缺血的治疗提供依据。     

热休克反应对大鼠感染性脑水肿脑组织诱生型一氧化氮合酶mRNA表达的影响

:探讨热休克反应 (HSR)对百日咳杆菌所致的大鼠感染性脑水肿诱生型一氧化氮合酶 (iNOS)mRNA表达的影响。方法 :从大鼠左侧颈内动脉注入百日咳菌液制备感染性脑水肿 (感脑 )模型 ,采用组织细胞原位杂交技术检测脑组织iNOSmRNA的表达。结果 :生理盐水组、4h感脑组及 4h热休克处理组均未见iNOSmRNA表达 ,8h ,2 4h时感染性脑水肿组均有明显的杂交信号 ,以 2 4h更为明显 ;而 8h ,2 4h热休克处理组仅有少数细胞有阳性信号。结论 :热休克反应对感染性脑水肿的保护作用可能与抑制iNOSmRNA的表达有关     

高龄初产妊高征孕妇过氧化反应的研究

目的：探讨高龄初产妊高征孕妇体内过氧化反应。方法：测定正常初产妇、妊高征孕妇妊娠晚期母血过氧化脂质（LPO）、超氧化物歧化酶（DOD）的含量。结果：1．高龄初产妇母血LPO较非高龄初产妇明显升高，SOD明显下降，P＜0．05。孕妇年龄与母血LPO呈明显正相关，与SOD呈明显负相关，P均＜0．05。2．妊高征孕妇LPO较正常孕妇显著增高，SOD显著下降，P＜0．05，并随病情加重LPO水平升高、SOD水平下降更为显著，P＜0．05。3．高龄初产妊高征孕妇母血LPO含量较非高龄初产妊高征孕妇明显增高，P＜0．05，而SOD则无显著变化，P＞0．05。4.妊高征孕妇胎儿宫内生长发育迟缓（IUGR）发生率较正常孕妇显著升高，P＜0．025，各组脐血清LPO、SOD含量无显著差异，P＜0．05。结论：高龄初产妊高征孕妇体内过氧化作用明显增强，LPO水平的升高可能为高龄初产妇妊高征发生率及IUGR发生率增加的原因之一。