实验性颅脑损伤后脑组织NO的变化

CHANGES OF NITRIC OXIDE LEVEL IN BRAIN TISSUES AFTER EXPERIMENTAL FOCAL INJURY

目的 探讨脑损伤后急性期局部一氧化氮 (NO)含量变化及其与脑水肿的关系。方法 采用自由落体法制造大鼠脑损伤后 ,于相应时间点取出脑组织测定其含水量、NO及Ca2 + 浓度。结果 在损伤后急性期脑组织含水量、NO及Ca2 + 含量均升高 ,其中Ca2 + 浓度和NO含量分别于损伤后 4h、8h达高峰 ,且Ca2 + 升高趋势持续时间长。经检验 ,NO含量与脑组织含水量呈正相关。

Objective To explore the changes of nitric oxide (NO) level and its relationship with brain edema in acute brain injury.Methods After acute brain injury model was produced by free dropping of rats, brain tissues were obtained and its water concentration,Ca 2+ and NO were measured.Results After brain injury,the water content, NO level and Ca 2+ were all increased. The peak levels of Ca 2+ and NO emerged 4 hours and 8 hours after the injury respectively, and the increasing of Ca 2+ tended to last for a longer time. Tests showed that No concentration was positively correlated with the water content in brain tissues.Conclusion NO is involved in the occurrence of brain edema after acute brain injury.盚Z]Methods Methods Linkage analysis of EH were performed in 95 Chinese nuclear families with 477 subjects using the technique of fluorescence based gene scan with microsatellite markers. Markers were selected in 11 chromosomal regions containing 18 candidate genes regulating blood glucose and lipid metabolism. The two locus, non parametric linkage analysis (NPL), maximum LOD score and transmission/disequilibrium test (TDT) with GENEHUNTER program were used in this study. Results No significant linkages were found by NPL and LOD score analysis ( P >0.05 or LOD score <1) at all loci. The results of TDT showed significant linkage with EH at D8S261 and D11S1347 (χ 2 =11.92, P <0.001 and χ 2 =7.37, P <0.01, respectively). Near these loci, there were a few candidate genes including lipoprotein lipase (LPL) and a cluster of apolipoprotein (apoA1 C3 A4). Conclusion TDT suggests significant linkage with EH at D8S261 and D11S1347. Whether the genes located at or near the two loci, such as LPL and apoA1 C3 A4, are susceptibility genes of EH need to be verified. Key words Essential hypertension; Linkage (genetics); Glycolipids; Genes,regulator