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Lior Lowenstein, Laszlo Dezsi
Med Sci Monit 1997; 3(3): BR290-293
The goal of this study was to determine the alterations in contractile and dilatory responses of dog mesenteric arteries after acute necrotizing pancreatitis. The study was designed to determine whether deformed red blood cells (rbc) and/or toxins released during acute pancreatitis had a damaging effect on the endothelium contributing to the multiple organ failure observed in pancreatitis. Pancreatitis was induced by injecting vegetable oil into the canine pancreatic duct. Rings of arteries were mounted for isometric tension recording in organ chambers. Cumulative norepinephrine (NE) doses were used to elicit vasoconstriction. To induce vasorelaxation several doses of the endothelium dependent dilator acetylcholine (ACh), or somatostatin (ST) were added to the precontracted rings. Vascular reactions were tested in a control group and a pancreatitic group (1 hr after induction of the pancreatitis), and in both groups the effect of the NO inhibitor NG-nitro-L-arginine (L-NAME) was also studied. Norepinephrine resulted in an increase in tension in a dose dependent manner in both groups. Norepinephrine in its highest dose (10-6 M) elicited 1770+/- 782 mg and 1597 &plusm; 590 mg increases in tension in the control and pancreatitic group, respectively. Acetylcholine induced vasorelaxation also in a dose dependent manner in both groups studied. Acetylcholine in its highest dose (10-6 M) relaxed the rings by 434 +/- 215 mg and 468 +/-238 mg in the control and the pancreatitic group, respectively. Somatostatin, as well, induced a dose dependent vasorelaxation. In its highest dose (10-8 M), somatostatin relaxed the rings by 174 +/- 28 mg and 153 +/- 27 mg in the control and pancreatitic group, respectively. None of the differences between groups were significant. The endothelium-dependent relaxation by ACh was abolished in both groups after treatment with L-NAME. Although toxins released during acute pancreatitis cause rbc deformation (echinocytosis), no vascular smooth muscle or endothelial damage was observed. This does not exclude the possibility that vascular damage at a later phase of pancreatitis contributes to the development of multiple organ failure.