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成人呼吸窘迫综合征发病机制中的弥散性血管内凝血:2. 实验研究。

Disseminated intravascular coagulation in the pathogenesis of adult respiratory distress syndrome: 2. Experimental study.

作者信息

Ogawa R, Takano Y, Fujita T

出版信息

Jpn J Surg. 1977 Dec;7(4):223-9. doi: 10.1007/BF02469354.

Abstract

The role of disseminated intravascular coagulation (DIC) in the pathogenesis of adult respiratory distress syndrome (ARDS) was studied in the experimental animals. ARDS was simulated in dogs by the administration of various doses of Escherichia coli endotoxin (Difco). The alveolar surface activity in the group which received lethal dose of endotoxin (3 mg/kg) exhibited no significant alterations with mild pulmonary insufficiency and little pathologic change five hours after the induction of shock. On the other hand, a significant decrease in alveolar surface activity was found to develop in the group which received sublethal dose of endotoxin (1 mg/kg) accompanying enlarged alveolar-arterial oxygen tension differences (A-aDO2) and elevated pulmonary vascular resistance after 24 hours. These changes occurred concomitantly with pathologic findings of DIC, interstitial edema and atelectasis. The disturbance in ventilatory function observed in prolonged shock appeared to be related to the impairment of pulmonary microcirculation caused by DIC and subsequent hypoxia of lung tissue which led to a loss of alveolar surfactant.

摘要

在实验动物中研究了弥散性血管内凝血(DIC)在成人呼吸窘迫综合征(ARDS)发病机制中的作用。通过给予不同剂量的大肠杆菌内毒素(Difco)在犬身上模拟ARDS。接受致死剂量内毒素(3mg/kg)的组,在休克诱导后5小时,肺泡表面活性无明显改变,仅有轻度肺功能不全且病理变化轻微。另一方面,接受亚致死剂量内毒素(1mg/kg)的组,在24小时后发现肺泡表面活性显著降低,同时伴有肺泡-动脉氧分压差(A-aDO2)增大和肺血管阻力升高。这些变化与DIC、间质水肿和肺不张的病理表现同时出现。在长时间休克中观察到的通气功能障碍似乎与DIC引起的肺微循环损害以及随后肺组织缺氧导致肺泡表面活性物质丧失有关。

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