Morel Denis R, Frossard Jean-Louis, Cikirikcioglu Banu, Tapponnier Maxime, Pastor Catherine M
Hôpitaux Universitaires de Genève, Division d'Investigations Anesthésiologiques, Geneva, Switzerland.
Intensive Care Med. 2006 Nov;32(11):1872-80. doi: 10.1007/s00134-006-0264-9. Epub 2006 Jul 15.
Lung injury is a severe complication of acute pancreatitis that increases the mortality rate of the disease. The pathophysiology of acute pancreatitis has been studied in several experimental models, but the kinetics of pulmonary complications in relation to the pancreatic disease is not completely understood. We then studied the severity of acute pancreatitis-associated lung injury over 18h in rats that had taurocholic acid injection in the pancreatic duct and determined whether blood collected from rats with pancreatitis is toxic enough to induce injury in normal lungs.
Prospective, randomized, and controlled animal study in an animal research laboratory in a university hospital.
We isolated lungs from rats with acute pancreatitis 2, 6, and 18h after taurocholic acid injection in the biliopancreatic duct and perfused them with blood collected from the same rats. Additionally, blood collected from rats with acute pancreatitis (time-points: 2 and 6h) was perfused in normal lungs.
Taurocholic acid injection induced a severe pancreatic injury that started as early as 2h after the injection and persisted without recovery over the 18-h study period. In contrast, the pulmonary injury was transient, appearing at the 6-h time point with recovery by the end of the study. Pulmonary injury was moderate and evidenced mostly during lung reperfusion. Interestingly, blood collected at the 2-h time point in pancreatic rats induced pulmonary injury in normal lungs while blood collected at the 6-h time-point was not toxic.
While pancreatic injury persists over the full experimental period, pulmonary injury is transient in our experimental model. The recovery of lung injury by 18h might be explained by a decrease in the overall toxicity of pancreatic blood over time.
肺损伤是急性胰腺炎的一种严重并发症,会增加该疾病的死亡率。急性胰腺炎的病理生理学已在多种实验模型中进行了研究,但肺部并发症与胰腺疾病相关的动力学尚未完全明确。我们随后研究了在胰管注射牛磺胆酸的大鼠中,18小时内急性胰腺炎相关性肺损伤的严重程度,并确定从胰腺炎大鼠采集的血液是否毒性足以诱导正常肺脏损伤。
在大学医院的动物研究实验室进行的前瞻性、随机对照动物研究。
在胆胰管注射牛磺胆酸后2、6和18小时,我们从患有急性胰腺炎的大鼠中分离出肺脏,并用从同一只大鼠采集的血液进行灌注。此外,将从患有急性胰腺炎的大鼠(时间点:2小时和6小时)采集的血液灌注到正常肺脏中。
牛磺胆酸注射诱导了严重的胰腺损伤,最早在注射后2小时开始,并在18小时的研究期间持续且未恢复。相比之下,肺损伤是短暂的,在6小时时间点出现,并在研究结束时恢复。肺损伤为中度,主要在肺再灌注期间表现出来。有趣的是,在胰腺炎大鼠2小时时间点采集的血液在正常肺脏中诱导了肺损伤,而在6小时时间点采集的血液则没有毒性。
在整个实验期间胰腺损伤持续存在,而在我们的实验模型中肺损伤是短暂的。18小时时肺损伤的恢复可能是由于胰腺血液的总体毒性随时间降低所致。