摘要
一氧化氮(NO)合酶mRNA表达减少,使NO合酶活性降低、NO生成减少,是高原肺水肿(HAPE)最重要的因素;其次是肺动脉高压-毛细血管壁高压,造成毛细血管内皮和肺泡表皮层断裂,液体及内含物渗漏;胃肠黏膜损伤,细菌及内毒素入血,引发炎性介质释放,形成肺部炎症及水肿。脑毛细血管压升高和血管内皮生长因子的作用,使毛细血管通透性增加是高原脑水肿(HAPE)主要因素;其次是缺氧使Na+-K+ATP酶活性降低,脑细胞内Na+、Cl-和水分增加;肺通气量增加,H+下降,以及炎性介质释放亦是引起脑水肿的因素。治疗:吸入低浓度的NO,用于治疗HAPE;口服硝苯地平;静脉给氨茶碱或口服β2-受体激动剂;口服乙酰唑胺或呋噻米利尿脱水,严重的HACE用高渗葡萄糖或甘露醇静脉滴注脱水;地塞米松口服或静脉滴注,HAPE和HACE都适用;预防或轻症可选用中药单方或复方。
The main important factor resulting in high altitude pulmonary is the decreased genesis of NO, which is caused by decreased activity of NO synthase resulting from decreased expression of NOS mRNA.The other factors are hypertension of pulmonary artery and capillary wall, which results in break of caoillary endothelium and alveolar euticular plate and leakage of liquid and contents as well as stomach intestinal mucous membrane injury, which results in pulmonary inflammatory and edema resulting from releasing of inflammatory medators because of bacteria and endotoxin entered blood. The main factors of high altitude cerebral edema are increased permeability of blood capillary,the other factors are inereasion of Na^＋ ,Cl^- and H20 in brain resulting from deereasion of hypoxia performed Na^＋ -K^＋ ATPase activity acitivity, as well as releasing of inflammatory mediators resulting from decreased H^＋ induced by increased pulmonary ventilation volume, Their therapy includes NO inhalation with low concentration for HAPE, nifedipine, by oral aminophylline by venoclysis or β2- receptor agonists by oral; diuretic acetasolamide or furosemide by oral, As for severe HACE, it needs dehydration by intravenous drip of hypertonic glucose and mannitol. Hexadecadrolin oral or injection is feasible to HAPE and HACE. The single or compound prescription of chinese herbal medicine can be used. for their prevention and therapy of their mild one.
出处
《医学综述》
2007年第21期1623-1625,共3页
Medical Recapitulate
关键词
高原肺水肿
高原脑水肿
一氧化氮
利尿剂
Β2-受体激动剂
缺氧
High altitude pulmonary edema
High altitude cerebral edema
Nitric oxide
Diuretic
β2-receptor agonists
Hypoxia
