3 In rat mesenteric arteries, there were no significant differences between portal hypertensive and sham-operated animals in endothelium-dependent relaxations to acetylcholine (ACh). The difference between portal hypertensive and sham-operated rats in the maximum response to U46619 was maintained following a combination of methylene blue (1 M) and N0-monomethyl-L-arginine (100 gM), suggesting that any differences in endothelial function do not explain differences in the response to vasoconstrictors. 4 In rat aorta, there were no significant differences between portal hypertensive and sham-operated animals in the contractile response to NA or KCl or in the endothelium-dependent relaxations to ACh. 5In pithed rats, there was no difference between portal hypertensive and sham-operated animals in the pressor potency of NA. 6 It is concluded that portal hypertension produces an increase in the contractile response to the vasoconstrictors NA, U46619 and KCl in rat mesenteric arteries but not in the aorta. This suggests that the diminished responsiveness to vasoconstrictors reported in portal hypertensive rats in vivo is not due to a diminished responsiveness at the level of the vascular smooth muscle.

Hereditary pancreatitis is a genetically transmitted condition usually presenting in childhood or adolescence. The natural history of the condition is that recurrent episodes of pancreatitis may be followed by the development of pancreatic exocrine and endocrine failure. Treatment options are limited, usually consisting of surgical drainage procedures whose efficacy is uncertain and whose effect on disease progression is unknown. We report a child with hereditary pancreatitis treated by means of a pancreatic duct stent placed via endoscopic retrograde cholangiopanctreatography resulting in long-term control of symptoms and speculate that earlier intervention may alter the disease course.

There were no differences between mesenteric arteries from sham or 14-day portal hypertensive (PH) rats in the potency of or maximum endothelium-dependent relaxations (EDR) to acetylcholine. There were no differences between sham-operated and PH rats in the effects of the combination of the nitric oxide synthase inhibitor N^G-monomethyl-L-arginine (100 µmol/l) and methylene blue (10 µmol/l) in causing a significant reduction in the EDR to acetylcholine. The degree of portal-systemic shunting, as measured by ⁵⁷Co-labeled microspheres, was unaffected by acute administration of N^G-monomethyl-L-arginine (50 mg/kg) or methylene blue (5 mg/ kg). In conclusion, nitric oxide is the main mediator of EDR in rat mesenteric artery, and no evidence was found for an increased role for endothelial-derived nitric oxide in PH rats.

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