Karanjia N D, Singh S M, Widdison A L, Lutrin F J, Reber H A
Department of Surgery, VA Medical Center, Sepulveda, California 91343.
Dig Dis Sci. 1992 Feb;37(2):268-73. doi: 10.1007/BF01308182.
We investigated the etiology of interstitial hypertension in chronic pancreatitis by examining the relationship between pancreatic ductal and interstitial pressures in cats. The main pancreatic duct was cannulated in the tail of the gland and perfused at 1, 2, or 5 ml/hr, to simulate pancreatic secretion. Intraductal and interstitial pressures were measured in four groups of animals: (1) normal cats; (2) normal cats after acutely narrowing the main duct to 25% of its original diameter; (3) normal cats after encasing the body and tail in a rigid latex capsule; and (4) cats with chronic pancreatitis created by narrowing the main duct five weeks earlier. Duct perfusion increased intraductal pressure in all of the cats, but significantly more in groups 2, 3, and 4 compared to group 1. Pancreatic interstitial pressure was unchanged by duct perfusion in groups 1 and 2, but increased in groups 3 and 4. We concluded that the compliant tissue of the normal pancreas expanded to effectively dissipate the increase in duct pressure associated with duct perfusion. In chronic pancreatitis, the inelastic parenchyma and capsule limited the distensibility of the gland, which resulted in elevated interstitial pressures during duct perfusion.
我们通过研究猫的胰管压力与间质压力之间的关系,来探究慢性胰腺炎中间质高压的病因。在胰腺尾部将主胰管插管,并以每小时1、2或5毫升的速度灌注,以模拟胰腺分泌。在四组动物中测量了导管内压力和间质压力:(1)正常猫;(2)将主胰管急性狭窄至其原始直径的25%后的正常猫;(3)将胰腺体部和尾部包裹在硬乳胶胶囊中的正常猫;(4)五周前通过狭窄主胰管而诱发慢性胰腺炎的猫。导管灌注使所有猫的导管内压力升高,但与第1组相比,第2、3和4组升高得更显著。在第1组和第2组中,导管灌注未改变胰腺间质压力,但在第3组和第4组中升高。我们得出结论,正常胰腺的顺应性组织会扩张,以有效消散与导管灌注相关的导管压力升高。在慢性胰腺炎中,无弹性的实质和包膜限制了腺体的扩张性,这导致在导管灌注期间间质压力升高。