Papp M, Makara G B, Folly G
Lymphology. 1975 Dec;8(4):148-53.
Pancreatic oedema was induced by physiological saline infused into the superior pancreatico-duodenal artery of 34, chloralose anaesthetized dogs. Both lymph flow from cannulated pancreatico-duodenal lymphatics and intralymphatic pressure in the non-transected ones increased significantly. The increase in pressure may be due to the regional lymph nodes obstructing increased lymph flow. The development of gross pancreatic oedema preceded the peak values of pancreatico-duodenal lymph flow and pressure. This suggested impeded fluid movement along tissue interstices and from tissue interstices into the pancreatic lymphatics. The progression of the oedema ran roughly parallel with the increase in fluid pressure measured by a perforated capsule implanted two weeks earlier into pancreatic tissues supplied by the artery. The results suggest that both the rise in lymph flow and pressure during the development of oedema in lobular organs like the pancreas are rather the consequences and not the causes of oedema.
在34只经水合氯醛麻醉的犬中,通过向胰十二指肠上动脉注入生理盐水诱导胰腺水肿。来自插管的胰十二指肠淋巴管的淋巴流量以及未横断淋巴管的淋巴内压均显著增加。压力升高可能是由于局部淋巴结阻碍了淋巴流量增加所致。大体胰腺水肿的出现先于胰十二指肠淋巴流量和压力的峰值。这表明沿组织间隙以及从组织间隙进入胰腺淋巴管的液体移动受阻。水肿的进展大致与两周前植入由该动脉供血的胰腺组织中的穿孔胶囊所测得的液压升高平行。结果表明,在胰腺等小叶器官水肿形成过程中,淋巴流量和压力的升高是水肿的结果而非原因。