No abstract

No abstract

The antiallergic activities of synthetic acrophylline [1] and acrophyllidine [2] have been demonstrated. Both compounds 1 and 2 at 30 mumol/kg reduced the plasma leakage in mouse ear in a passive cutaneous anaphylactic (PCA) reaction. In addition, compound 1 suppressed mast cell degranulation in a dose-dependent manner, while compound 2 at 100 microM produced no significant inhibition of the release of preformed inflammatory mediators. These results suggest that the antiallergic effect of compound 1 probably occurs through the suppression of mast cell degranulation, and that of compound 2 by protection of the vasculature against challenge by mediators of inflammation.

A series of new N‐alkyl‐2,3,4,9‐tetrahydrofuro[2,3‐b]quinoline‐3,4‐dione and N‐alkyl‐4,9‐dihydrofuro[2,3‐b]‐quinolin‐4‐one derivatives were prepared and evaluated for their anti‐inflammatory activity by the carrageenin hind paw edema method and antiallergic activity by the rat passive cutaneous anaphylaxis method. Among those tested compounds, N‐ethyl‐2,3,4,9‐tetrahydrofuro[2,3‐b]quinoline‐3,4‐dione was the most promising agent which could provide a novel structural prototype for antiallergic agents.

We studied the electrophysiological and antiarrhythmic actions of 3,4,quinoline-3,4-dione], a furoquinoline alkaloid derivative, in guinea pig heart preparations. In the perfused whole heart model, HA-7 caused a prolongation in the basic cycle length, ventricular repolarization time, and the atrioventricular (AV) nodal Wenckebach cycle length and prolonged the refractory period of the atrium, AV node, and His-Purkinje system. The atrioventricular conduction interval was also prolonged in a frequency-dependent manner. In isolated hearts, HA-7 significantly raised the threshold for experimental atrial fibrillation and reduced the occurrence of reperfusion-induced ventricular fibrillation. Conventional microelectrode-recording study shows that HA-7, but not d-sotalol, prolonged the action potential duration (APD) and decreased the maximum rate of depolarization in isolated atrial strips. In ventricular papillary muscles, higher concentrations of HA-7 caused a prolongation of APD 90 in a frequency-independent manner, whereas d-sotalol exerted a reverse frequency-dependent action on this parameter. Whole-cell patch clamp results on ventricular myocytes indicate that HA-7 decreased both the slow (I Ks ) (IC 50 ϭ 4.8 M) and fast component (I Kr ) (IC 50 ϭ 1