NO、NOS与宫缩乏力性产后出血关系的研究

目的:探讨血清NO及NOS在预测宫缩乏力性产后出血发生发展中的作用。方法:选择剖宫产终止妊娠的孕妇180例,因臀位、社会因素、骨盆狭窄、胎儿宫内窘迫等行剖宫产术,按产后24 h内出血量≥500 m l分为产后出血组(n=47)及非产后出血组(n=133)。所有孕妇于剖宫产术麻醉前30 m in及术后2 h测血清NO及NOS,术中娩出胎儿后于子宫切缘上缘及胎盘母体面中央无钙化区分别取子宫肌组织及胎盘组织各一,切片作免疫组织化学分析iNOS的表达,准确收集剖宫产术中出血量及产后24 h出血量。结果:产后出血组术前、术后血清NO及NOS含量较非产后出血组明显增高,差异有显著性意义(P<0.05);血清NOS预测产后出血的灵敏度、特异度、阳性预测值、阴性预测值均高于血清NO值;从SABC免疫组化结果可见在子宫肌及胎盘均有iNOS表达,产后出血组子宫肌和胎盘的iNOS阳性表达率均显著高于非产后出血组,P<0.05;经等级相关检验,子宫肌、胎盘组织iNOS的表达强度随术前血清NO、NOS水平的升高而增加,均呈正相关。结论:血清NO、NOS水平可以正确反映子宫、胎盘NOS的活性,可作为预测宫缩乏力性产后出血的1项有效的指标。

NO与牙周病周期性发病关系的研究

目的:临床上牙周病总是活动与静止期交替发生,经研究牙周病患者中NO含量及其牙周病有显著相关性。本研究目的系为了阐明NO在牙周病中的调节机制。方法:通过对牙周炎患者不同时期的唾液NO含量进行分析,来检测其活动期与静止期NO含量变化。结论:数据表明,NO在高浓度状态下可以导致炎症加重,在低浓度状态下可以抗炎。

分娩发动对NO、NOS水平及产后出血的影响

目的探讨剖宫产孕妇术前临产状态对其血清NO、NOS水平的影响以及在产后出血防治中的作用。方法选择剖宫产终止妊娠的孕妇180例,因臀位、社会因素、骨盆狭窄、胎儿宫内窘迫等行剖宫产术,按剖宫产术前临产与否分为临产组(n=88):阴道试产6小时以上者;未临产组(n=92):未经阴道试产直接行剖宫产术者;所有孕妇分别于剖宫产术麻醉前30分钟及术后2小时测血清NO及NOS,术中娩出胎儿后于子宫切缘上缘及胎盘母体面中央无钙化区分别取子宫肌组织及胎盘组织各一,切片作免疫组织化学分析iNOS的表达,准确收集剖宫产术中出血量及产后24小时出血量。结果未临产组产后24小时出血量及产后出血的发生率均大于临产组;无论是临产组还是未临产组,术前到术后血清NO及NOS水平均呈逐渐下降的趋势,而且未临产组术前、术后血清NO及NOS含量较临产组明显增高,差异有显著性意义(P<0.05);未临产组子宫肌和胎盘的iNOS阳性表达率均显著高于临产组(P<0.05);术前、术后血清NO、NOS含量与产后24小时出血量均呈显著正相关。结论分娩发动且经过充分阴道试产的孕妇,随着其体内NO、NOS水平及表达下降,剖宫产产后出血的发生率也下降。

2型糖尿病血管并发症患者血脂及血浆NO水平的临床研究

目的:评价2型糖尿病(DM)血管并发症患者血脂及血浆NO水平的状况。方法:对203例临床诊断为2型DM的住院患者(男性103例,女性100例)的空腹血脂及血浆NO水平做出分析。结果:A组总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、甘油三酯(TG)、载脂蛋白A1、载脂蛋白B及NO分别为:(4.83±0.87)mmol/L,(2.67±0.42)mmol/L,(1.75±0.65)mmol/L,(1.53±0.19)g/L,(0.88±0.17)g/L及(8.12±1.96)mmol/L。A组高密度脂蛋白胆固醇(HDL-C)的均值为(1.34±0.18)mmol/L,高于C组(P<0.01),NO降低的检出率B组高于C组(P<0.01),血浆NO水平较差的C组显著低于A组(P<0.01)。结论:2型DM患者血糖的控制程度会导致其血脂及NO水平的差异,血糖控制较差会导致血脂代谢紊乱程度增加,并使NO生成减少,要防止血管并发症的发生应该重视及时评价糖代谢问题。

Nitric Oxide:from a mysterious labile factor to the molecule of the Nobel Prize Recent progress in nitric oxide research

NO is now known to be an important messenger molecule in biology.It regulates a variety of functions within cells and tissues including vasodilation, neurotransmission and immunological process. This review will focus on the nitric oxide synthase gene family and recent progress on molecular genetic analysis of NOS1, NOS2 and N0S3 genes.

How to protect liver graft with nitric oxide

Organ preservation and ischemia reperfusion injury associated with liver transplantation play an important role in the induction of graft injury. One of the earliest events associated with the reperfusion injury is endothelial cell dysfunction. It is generally accepted that endothelial nitric oxide synthase （e-NOS） is cell-pro- tective by mediating vasodilatation, whereas inducible nitric oxide synthase mediates liver graft injury after transplantation. We conducted a critical review of the literature evaluating the potential applications of regulating and promoting e-NOS activity in liver preservation and transplantation, showing the most current evidence to support the concept that enhanced bioavailability of NO derived from e-NOS is detrimental to ameliorate graft liver preservation, as well as preventing subse- quent graft reperfusion injury. This review deals mainly with the beneficial effects of promoting ＂endogenous＂ pathways for NO generation, via e-NOS inducer drugs in cold preservation solution, surgical strategies such as ischemic preconditioning, and alternative ＂exogenous＂ pathways that focus on the enrichment of cold storage liquid with NO donors. Finally, we also provide a basic bench-to-bed side summary of the liver physiology and cell signalling mechanisms that account for explaining the e-NOS protective effects in liver preservation and transplantation.