Protective effects of prostaglandin E1 on acute lung injury of caerulein-induced acute pancreatitis in rats.

Protective effects of prostaglandin E1 on acute lung injury of caerulein-induced acute pancreatitis in rats.
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前列腺素E1对雨蛙素诱导的急性胰腺炎大鼠急性肺损伤的保护作用。

DOI:
10.1152/ajpgi.1997.272.1.g23
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发表时间:
1997
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Steer,ML
Steer,ML
中科院分区:
--
文献类型:
--
作者:
Yamanaka,K;Saluja,AK;Brown,GE;Yamaguchi,Y;Hofbauer,B;Steer,ML

文献摘要

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输注超最大刺激剂量的胰腺促分泌素雨伞素(10微克·公斤-1·小时-1)4小时可诱发大鼠间质性水肿性急性胰腺炎。这种急性胰腺炎模型与急性肺损伤的证据相关,包括肺微血管内隔离的中性粒细胞、微血管通透性增加和间质性肺水肿。前列腺素 E1(PGE1;50 ng.kg-1.min-1)与雨蛙素一起输注不会改变促分泌素诱发的胰腺炎的严重程度,但确实会减轻胰腺炎相关的急性肺损伤的严重程度。伴随促分泌素诱发的胰腺炎,肺重量、肺水含量、肺微血管通透性的增加以及中性粒细胞在肺微血管内的隔离均通过输注PGE1而减少。 PGE1 的输注不会干扰胰腺中多形核中性粒细胞的隔离,也不会减少循环中性粒细胞上 CD11b/c 受体的增强表达。我们的观察表明,PGE1 通过防止中性粒细胞在肺内隔离来减轻胰腺炎相关的急性肺损伤的严重程度。我们推测 PGE1 通过扩张肺血管、增加肺流量以及减少中性粒细胞与内皮细胞的相互作用和附着来干扰中性粒细胞隔离。
Infusion of a supramaximally stimulating dose of the pancreatic secretagogue caerulein (10 micrograms.kg-1.h-1) for 4 h induces interstitial edematous acute pancreatitis in rats. This model of acute pancreatitis is associated with evidence of acute lung injury, including sequestered neutrophils within the pulmonary microvasculature, increased microvascular permeability, and interstitial pulmonary edema. Infusion of prostaglandin E1 (PGE1; 50 ng.kg-1.min-1) along with caerulein does not alter the severity of secretagogue-induced pancreatitis, but it does reduce the severity of pancreatitis-associated acute lung injury. The rise in lung weight, lung water content, and pulmonary microvascular permeability and the sequestration of neutrophils within the pulmonary microvasculature that accompany secretagogue-induced pancreatitis are all reduced by infusion of PGE1. Infusion of PGE1 does not interfere with polymorphonuclear neutrophil sequestration in the pancreas or reduce the enhanced expression of CD11b/c receptors on circulating neutrophils. Our observations indicate that PGE1 reduces the severity of pancreatitis-associated acute lung injury by preventing neutrophil sequestration within the lung. We speculate that PGE1 interferes with neutrophil sequestration by dilating pulmonary vasculature, increasing pulmonary flow rate, and reducing neutrophil-endothelial cell interaction and attachment.