N-乙酰半胱氨酸在呼吸系统疾病中的应用

目的:评价N-乙酰半胱氨酸(NAC)在呼吸系统疾病中的应用。方法:通过查阅国外近期相关文献进行综述。结果:(1)NAC能减少COPD患者急性发作的发生率,改善临床症状,可能有助于肺功能的改善;(2)初步临床试验结果表明,长时间大剂量的NAC治疗有助于肺间质纤维化患者肺功能的改善;(3)NAC可以通过抗氧化作用,保护急性肺损伤及ARDS肺组织免受氧化作用损伤,从而减轻临床症状,改善氧合。结论:NAC是一种具有广泛前景的治疗急性和慢性呼吸道疾病的药物。     

肺表面活性物质-呼气末正压治疗血浆诱导的急性呼吸窘迫综合征

目的研究在急性呼吸窘迫综合征(ARDS)时,联合应用肺表面活性物质(PS)和呼气末正压(PEEP)治疗的效果,并探讨两者之间的关系。方法45只健康SD大鼠,体重为200~312g,麻醉后进行机械通气,气管内滴注血浆至PaO2<200mmHg,将实验动物随机分为PEEP4.0(4 cmH2O)和PEEP7.5(7.5 cmH2O)条件下对照组、PS100(100mg/kg)组和PS200(200mg/kg)组共6组,分别在滴注血浆前、急性肺损伤制成后、给药后30、60、90、120、150和180分钟测定大鼠血气分析、静态比胸肺顺应性(Cst)。实验后取左肺用于病理检查和计算肺指数(LI)。结果经过血浆滴注后,各组实验动物PaO2和Cst分别下降到79.8±19.8mmHg和0.42±0.07m l/(cmH2O.kg)。PEEP7.5PS200组和PS100组的PaO2回升至383±57mmHg和398±51mmHg,明显高于其他4组(P<0.01),此两组比较,PaO2无显著差别。PEEP7.5水平下的3个组,PaO2和LI均显著高于PEEP4.0各对应组(P<0.05)。PEEP7.5PS 100组和PS200组大鼠肺透明膜形成显著少于其他四组(P<0.05),PEEP7.5PS100组肺透明膜形成显著少于PEEP4.0PS200组(P<0.05)。结论在滴注血浆诱导的大鼠ARDS时,高剂量PS较低剂量PS能更有效对抗血浆蛋白的抑制作用;使用合适的较高PEEP与低剂量PS联合治疗能有效改善肺氧合功能和胸肺顺应性,并节省PS用量。     

人工肾与呼吸机治疗急性呼吸窘迫综合征临床对比研究

目的探讨人工肾(代替人工肺)治疗急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)的临床疗效,并论证在ARDS早期其替代呼吸机的可行性。方法24例ARDS患者,随机分为两组:人工肾(代替人工肺)治疗研究组(n=12)和呼吸机治疗对照组(n=12),两组均持续治疗6h,观察治疗前后临床症状、全胸片、血气分析、血常规、凝血四项、电解质及中心静脉压(CVP)的变化,判断疗效。结果研究组治疗前后动脉血氧分压PaO2和CVP差异有显著性(P<0.01),而对照组治疗前后动脉血氧分压PaO2和CVP差异无显著性(P>0.05),研究组与对照组治疗后动脉血氧分压PaO2、CVP比较差异有显著性(P<0.01)。结论人工肾(代替人工肺)显著纠正了ARDS患者的低氧血症和心功能衰竭,可减轻肺水肿、缓解肺部和全身炎症反应,提高疗效,在早期可完全替代呼吸机。     

Cardiac Beriberi (Shoshin Beriberi) Caused by Excessive Intake of Isotonic Drink

A 21 month old female had voluntarily ingested 0.5–1.51 of isotonic sports drink daily from 10 months of age. She developed hyponatremia and beriberi heart disease, which resulted in metabolic acidosis and cardiogenic shock (shoshin beriberi). Mechanical ventilation was applied for pulmonary edema. Right heart failure was improved after administering vitamin Bi. However, 5 days after the shock, hypoxemia and diffuse radiographic infiltrates progressed, and a diagnosis of adult respiratory distress syndrome (ARDS) was made. After the occurrence of an air leak, the patient died of respiratory failure. The cardiogenic shock and pulmonary edema due to cardiac beriberi may have triggered the ARDS.     

Chronic ethanol ingestion increases expression of the angiotensin II type 2 (AT2) receptor and enhances tumor necrosis factor-alpha- and angiotensin II-induced cytotoxicity via AT2 signaling in rat alveolar epithelial cells

BACKGROUND: Alcohol abuse increases the risk of acute lung injury in critically ill patients. We have shown that alveolar epithelial cell (AEC) apoptosis in response to inflammatory mediators, including tumor necrosis factor-alpha (TNF-alpha), parallels endotoxin-mediated acute lung injury in ethanol-fed rats. Although angiotensin II mediates TNF-alpha-induced apoptosis of AECs in vitro, its role in ethanol-mediated susceptibility to AEC apoptosis is unknown. METHODS: Adult male rats were fed the Lieber-DeCarli diet for 6 weeks. AECs were isolated, and TNF-alpha- and angiotensin II-induced cytotoxicity (by terminal transferase-mediated dUTP nick end labeling staining) was determined with or without the addition of the angiotensin-converting enzyme inhibitor (lisinopril) or a selective blocker of the angiotensin II type 1 receptor (AT(1)) or type 2 receptor (AT(2)). Finally, the relative expression of the AT(1) and AT(2) receptors in AECs was determined by Western blot analysis. RESULTS: TNF-alpha-induced cytotoxicity, but not angiotensin II-induced cytotoxicity, was prevented by lisinopril, indicating that de novo angiotensin II synthesis is required for TNF-alpha-induced apoptosis in these cells. Both TNF-alpha- and angiotensin II-induced cytotoxicity in AECs from control-fed and ethanol-fed rats were inhibited by the selective AT(2) blocker, PD123319, but not by the selective AT(1) blocker, losartan. In parallel, ethanol ingestion doubled AT(2) expression in AECs (by Western blot) but had no significant effect on AT(1) receptor expression. CONCLUSIONS: Chronic ethanol ingestion increases AT(2) expression in the alveolar epithelium and enhances TNF-alpha- and angiotensin II-induced cytotoxicity, both of which act via AT(2). Together, these findings suggest that selective AT(2) receptor inhibition could limit the development of acute lung injury in alcoholic patients.     

儿科ICU中急性呼吸窘迫综合征的临床回顾性分析

目的总结我院儿科重症监护室中(PICU)收治的急性呼吸窘迫综合征(ARDS)患儿的临床流行病学特点,以期提高ARDS的诊治水平。方法回顾性总结2002年6月～2004年2月我院PICU的14例确诊为ARDS患儿的特点。结果ARDS的发病率为2.3%。诱发ARDS的因素有体外循环、肺炎、脓毒症、休克等,其中以体外循环为最多见(占发病人数的42.9%)。确诊时急性肺损伤指数和PaO2FiO2分别为(3.2±0.6)和(86.5±23.8)。机械通气时最高吸气峰压和呼气终末正压分别是(33.8±8.4)cmH2O、(8.3±4.8)cmH2O。ARDS平均住院时间为18.1d,占PICU危重病人总住院时间的21.2%。因多器官功能衰竭、呼吸衰竭死亡6例(病死率42.9%),占PICU死亡总数的21.5%。结论积极去除高危因素预防ARDS、探讨ARDS更有效的治疗方法、降低病死率仍是我们今后工作的重点。     

肾上腺皮质激素在氨中毒性ARDS抢救治疗中的应用

氨中毒为氨吸入和刺激皮肤及粘膜而引起的多器官功能损害.主要表现为眼部、皮肤及呼吸道粘膜的化学性灼伤.当氨吸入肺并发弥漫性肺组织损伤导致肺水肿和急性吸吸衰竭时称氨中毒性成人型呼吸窘迫综合征,简称氨中毒性ARDS.其病情凶险,缺乏特效治疗,病死率较高.临床上表现为呼吸频率增加和呼吸窘迫.因此,合理应用肾上腺皮质激素(简称激素)治疗氨中毒性ARDS,对提高病人的生成率,减少死亡率.预防并发症有着及其重要的作用.     

重症胰腺炎合并呼吸道窘迫综合症的护理

急性胰腺炎是指胰腺分泌的消化酶被激活后对自身器官产生消化所引起的炎症,是常见的急腹症.分单纯性和出血坏死型(重症)胰腺炎2种,后者是急性胰腺炎的严重类型.由于发病突然,临床表现复杂,病情进展迅速,易引起全身多器官功能障碍,病死率高达30%～60%[1],故治疗相当棘手.临床工作者不断探索,使本病的治疗在近年来有较大进展,护理上也发生了很大变化,现将川北医学院附属医院2003-01/2004-10收治的11例重症胰腺炎合并ARDS患者护理体会总结如下.     

急性呼吸窘迫综合征患者肺机械通气的监护

探讨46例患者肺保护性机械通气的监护作用与意义。通过监护46例急性呼吸窘迫综合征(ARDS)患者所起的作用证明及时调节机械通气辅助呼吸参数,对治愈ARDS患者具有重要的作用与意义,可以减少并发症的发生。对ARDS患者,肺保护性机械通气的监护必不可少。     

双水平气道正压通气治疗早期ARDS护理体会

近年来，双水平气道正压通气（BiPAP）作为一种无创通气模式，以其无创性、安全性、有效性和高依从性，已较广泛应用于早期ARDS患者中，我院2000年1月-2004年12月采用BiPAP呼吸机共治疗早期ARDS患者86例，取得较好效果。现将护理体会总结如下。