Karanjia N D, Widdison A L, Lutrin F J, Reber H A
Department of Surgery, VA Medical Center, Sepulveda, CA 91343.
Pancreas. 1991 Jul;6(4):392-7. doi: 10.1097/00006676-199107000-00003.
Perfusion of the main pancreatic duct in cats with a dilute solution of bile salts increases ductal permeability. Subsequent perfusion of a permeable duct with activated pancreatic enzymes results in acute edematous pancreatitis. Simultaneous infusion of 16-16 dimethyl-PgE2 converts edematous pancreatitis to acute hemorrhagic pancreatitis (AHP). AHP may be associated with a reduction in pancreatic blood flow; it is certainly associated with increases in microvascular permeability. Low dose dopamine is a splanchnic vasodilator and may also reduce pancreatic microvascular permeability through beta agonist effects. In these studies, we investigated the effect of dopamine in an established feline model of biliary AHP. We also studied its effect on blood flow in both normal pancreas and after induction of AHP. We found that dopamine significantly reduced the degree of pancreatic inflammation, even when administered up to 12 h after onset of biliary AHP. However, the drug had no significant effect on blood flow either in normal pancreas or in the gland affected by hemorrhagic pancreatitis. We concluded that the effect of dopamine was most likely due to its ability to reduce pancreatic microvascular permeability.
用稀释的胆盐溶液灌注猫的主胰管会增加导管通透性。随后用活化的胰酶灌注通透性增加的导管会导致急性水肿性胰腺炎。同时输注16,16-二甲基前列腺素E2可将水肿性胰腺炎转变为急性出血性胰腺炎（AHP）。AHP可能与胰腺血流减少有关；它肯定与微血管通透性增加有关。低剂量多巴胺是一种内脏血管扩张剂，也可能通过β激动剂作用降低胰腺微血管通透性。在这些研究中，我们研究了多巴胺在已建立的猫胆源性AHP模型中的作用。我们还研究了其对正常胰腺以及诱导AHP后胰腺血流的影响。我们发现，即使在胆源性AHP发作后12小时给药，多巴胺也能显著减轻胰腺炎症程度。然而，该药物对正常胰腺或受出血性胰腺炎影响的腺体的血流均无显著影响。我们得出结论，多巴胺的作用很可能是由于其降低胰腺微血管通透性的能力。
