Kaska M, Pospísilová B, Slízová D
Department of Surgery, Charles University, Medical Faculty, Hradec Králové, Czech Republic.
Hepatogastroenterology. 2000 Nov-Dec;47(36):1570-4.
BACKGROUND/AIMS: Severe acute pancreatitis is prevalent in Eastern Bohemia (a part of the Czech Republic) and remains a very difficult problem to manage. Recent studies in treatment there are quite frequent but a direct view into the pancreas during its inflammatory process is very rare. Only information about a normal pancreatic microvascular bed appears to be available. This study was designed to explore pathomorphological changes in pancreatic microcirculation at the start and during the development of acute pancreatitis.
A group of 50 laboratory white rats was studied. The acute pancreatitis was induced by the modified method of Siech et al. The method of clamping of biliopancreatic duct and stimulation of external secretory tissue by a cholecystokinin and secretin and oral (orogastric tube) ethanol administration was performed. The pancreatic microvascular patterns were observed by using histochemical and corrosion casts methods.
The study of the corrosion casts of pancreatic microcirculation in the scanning electron microscope and histochemical studies demonstrated the visible reduction of the pancreatic microvascular bed 18 hours after induction of acute pancreatitis. The microvascular bed is not fully destroyed until 48 hours of acute pancreatitis.
The model of acute pancreatitis using postoperative application of ethanol to the digestive tract after stimulation of pancreas by cholecystokinine and secretin in the rats seems to be real and useful. The study of the corrosion casts of microcirculation in the scanning electron microscope and histochemical studies demonstrated the visible reduction of the pancreatic microvascular bed 18 hours after induction of acute pancreatitis. The microvascular bed is not fully destroyed until 48 hours of running acute pancreatitis, as some "islets" of the vital tissue still have undestroyed microvessels at this time. Despite the above-mentioned serious changes, restricted pancreatic microcirculation enables blood and medicament distribution to the still intact pancreatic tissue.
背景/目的:重症急性胰腺炎在东波希米亚(捷克共和国的一部分)较为常见,且仍是一个极难处理的问题。近期在该地进行的治疗研究颇为频繁,但在胰腺炎症过程中直接观察胰腺的情况却极为罕见。目前仅有关于正常胰腺微血管床的信息。本研究旨在探讨急性胰腺炎起始阶段及发展过程中胰腺微循环的病理形态学变化。
对50只实验白鼠进行研究。采用Siech等人改良的方法诱导急性胰腺炎。实施夹闭胆胰管、用胆囊收缩素和促胰液素刺激外分泌组织以及经口(经胃管)给予乙醇的操作。通过组织化学和铸型腐蚀法观察胰腺微血管模式。
在扫描电子显微镜下对胰腺微循环铸型的研究以及组织化学研究表明,急性胰腺炎诱导18小时后胰腺微血管床明显减少。直至急性胰腺炎发作48小时,微血管床才被完全破坏。
在大鼠中,通过胆囊收缩素和促胰液素刺激胰腺后,术后经消化道给予乙醇的急性胰腺炎模型似乎切实可行且有用。在扫描电子显微镜下对微循环铸型的研究以及组织化学研究表明,急性胰腺炎诱导18小时后胰腺微血管床明显减少。在急性胰腺炎发作48小时内微血管床并未被完全破坏,因为此时一些重要组织的“小岛”仍有未被破坏的微血管。尽管有上述严重变化,但受限的胰腺微循环仍能使血液和药物分布到仍完好的胰腺组织。