1 The involvement of bradykinin (BK) B 2 receptor in acute pancreatitis induced by pancreaticobiliary duct ligation was investigated in rats. 2 The activities of amylase and lipase in the serum, the water content of the pancreas, and vacuolization of the acinar cells were signi®cantly increased 2 h after obstruction of the duct in Sprague-Dawley rats. 3 Elevated serum amylase activity, increased pancreatic oedema, and damage of the pancreatic tissue were signi®cantly less marked in plasma kininogen-de®cient, B/N-Katholiek rats than in the normal strain, B/N-Kitasato rats 2 h after the ligation. 4 Obstruction of the pancreaticobiliary duct augmented the level of (1-5)-BK (Arg 1 -Pro 2 -Pro 3 -Gly 4 -Phe 5 ), a stable BK metabolite, in the blood from 73.0+21.7 pg ml 71 at 0 h to 149.8+38.0 pg ml 71 at 2 h after the induction of pancreatitis in SD rats. 5 Administration of a BK B 2 receptor antagonist, FR173657 (100 mg kg 71 , p.o.) or Hoe140 (100 nmol kg 71 , s.c.), reduced the elevation of amylase and lipase activities in the serum and of pancreatic water content in a dose-dependent manner. The e ective attenuation of oedema formation and vacuolization by the antagonists was also con®rmed light-microscopically. In contrast, treatment with gabexate mesilate or indomethacin did not cause signi®cant suppression of the pancreatitis. 6 These ®ndings suggest a possible involvement of kinin B 2 receptor in the present pancreatitis model. Furthermore, they point to the potential usefulness of the B 2 receptor in clinical acute pancreatitis.

CNS signs and symptoms induced by aseptic meningitis should be considered in cases of glyphosate-surfactant herbicide poisoning.

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We previously reported a 65-year-old man who aspirated an alkaline detergent containing 3.3% w/v (weight of solute per volume of solution) monoethanolamine (MEA) into his lungs, causing asthma-like symptoms. We presently describe the mechanism of MEA-induced bronchoconstriction according to findings in guinea pigs. In anesthetized, artificially ventilated animals, changes in airway opening pressure (P(ao)) were measured as an index of bronchoconstriction. An aerosol of 3.3% MEA solution (0.1 ml kg(-1)) inhaled through a tracheal cannula induced significantly stronger bronchoconstriction than an aerosol of potassium hydroxide (KOH) solution (0.1 ml kg(-1)) at the same pH. MEA-induced bronchoconstriction was significantly suppressed by premedication with intravenously injected atropine sulfate (3 mg kg(-1)), a muscarinic receptor antagonist, or diphenhydramine hydrochloride (10 mg kg(-1)), a histamine-H(1) receptor antagonist. MEA-induced bronchoconstriction was not enhanced by premedication with an intravenous injection of neostigmine (0.1 mg kg(-1)), an acetylcholinesterase inhibitor. When bronchoconstriction was induced by MEA, histamine concentrations in bronchoalveolar lavage fluid (BALF) were not significantly greater than in BALF after KOH-induced bronchoconstriction or in BALF after inhalation of physiologic saline. In vitro, contraction of trachea denuded of epithelium during superfusion with MEA (10 mm) was suppressed by premedication with pyrilamine maleate, a histamine-H(1) receptor antagonist, at 10 and 100 microm. Contraction of trachea denuded of epithelium during superfusion with MEA (10 mm) was suppressed by premedication with atropine sulfate at 10 and 100 microm. These results suggest that asthma-like symptoms may result partly from agonistic MEA effects at histamine-H(1) receptors and muscarinic receptors.

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