心房钠尿肽对家兔急性呼吸窘迫综合征的作用及机制

Effect of atrial natriuretic peptide on acute respiratory distress syndrome of rabbit and the possible mechanism

目的:研究心房钠尿肽(ANP)对急性呼吸窘迫综合征中肺泡Ⅱ型上皮细胞(AT-Ⅱ)的保护作用。方法:24只家兔随机等分为对照组、内毒素(ET)组、ANP组。通过耳缘静脉给药,给药3h后处死动物,收集肺泡灌洗液(BALF),测定BALF表面张力和总磷脂(TPL)、丙二醛(MDA)、总蛋白(TP)含量及乳酸脱氢酶(LDH)、碱性磷酸酶(AKP)活性。结果:与对照组比较,ET可使BALF中LDH活性[(618±174)U/Lvs(1104±294)U/L]及TP含量[(38±17)g/Lvs(110±32)g/L]升高(P<0.05),ANP可逆转此现象;ANP能逆转ET引起的MDA含量升高;ET可使BALF中TPL含量[(0.53±0.07)μg/kgvs(0.31±0.10)μg/kg]明显降低(P<0.05)、表面张力[(20.8±3.0)mN/mvs(26.3±3.9)mN/m]升高(P<0.05),ANP治疗后TPL[(0.45±0.08)μg/kg]升高、表面张力[(20.2±3.2)mN/m]降低;与对照组比较,ET组AKP活性[(0.10±0.08)U/Lvs(0.36±0.10)U/L]升高(P<0.05),ANP治疗后AKP[(0.14±0.09)U/L]明显降低。结论:ANP能减轻ET引起的急性呼吸窘迫综合征,其机制可能与ANP保护AT-Ⅱ并促进其分泌表面活性物质有关。

Objective To explore the protective effects of atrial natriuretic peptide （ANP）on alveolar type Ⅱ cells （AT-Ⅱ） in rabbets with acute respiratory distress syndrome（ARDS） induced by endotoxin（ET） . Methods Twenty-four rabbits were divided into 3 groups ： Control group （ n = 8）, ET group （ n = 8） and ANP group （ n = 8）, each group was injected only physiological saline, ET and physiological saline, and ET and ANP through ear-veln. Three hours later, the rabbits was sacrificed and the bronchoalveolar lavage fluid（BALF） was collected. Surface tension（ST）, total phospholipids（TPL）, total protein（TP）, maleic dialdehyde（MDA） contents, and the activity of lactate dehydrogenase（LDH） and alkaline phosphatase （AKP） in the BALF were measured. Result Compared with control group, ET could increase the content of TP, and the activity of LDH[ （618 ± 174） U/L vs （ 1 104 ± 294 U/L） ]in BALF（ P 〈 0. 05） ,which could be reversed by ANP. ET could also increase the content of TPL（0. 53 ±0. 07 vs 0. 31 ±0. 10 μg/kg） ,and decreased surface tension [ （20. 8 ± 3. 0） mN/m vs （26.3 ± 3.9 mN/m） ] （ P 〈 0. 05） ,but there were no significant differences between ANP group and control group. ANP could prevent the increasing of the activity of AKP and the content of MDA in BALF（ P 〈 0. 05）induced by ET. Conclusions ANP can effcetively protect the lung injury from ARDS induced by ET. One of the most important mechanisms is possibly that ANP can protect the AT-Ⅱ and facilitate the secretion of pulmonary surfactant.