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To clarify the vasoconstrictory action of leukotriene D4 (LTD4) on the injured coronary arteries, 8 mongrel dogs were denuded by basket balloon catheter (denuded group) and LTD4 (0.33μg) was directly administered into left anterior descending coronary artery. Hemodynamic parameters as well as epicardial ECG were recorded after LTD4 administration. Another 8 non-denuded dogs were served as control.Furthermore, the influence of denudation to LTD4-induced coronary spasm was determined by coronary arteriography (CAG) . In results, a significant reduction of coronary blood flow (from 1.03±0.13 to 0.49±0.05 ml/kg/min. P

Experimental pleurisy in rats was induced by intra-pleural injection of 0.1 ml 2%-λ-carrageenin, as previously reported (1, 2) . The accumulation of pleural fluid continued until the peak volume of 4 ml at 19 hrs after carrageenin injection, involvemen of plasma kallikrein-kinin system in the early phase of the pleurisy was proved with the following series of experiments.(1) The levels of prekallikrein, HMW-and LMW-kininogens in plasma and pleural fluid were measured at 1, 3 and 5 hrs after carrageenin injection. The level of HMW-kininogen in pleural fluid was extremely low, whereas LMW-kininogen level was not reduced. The level of prekallikrein was also low in the pleural fluid, about 1/10 of that in plasma. As the plasma levels of these components in pleurisy rats were not significantly different from those in control rats, the above results suggest that plasma kallikrein-kinin system could be activated at the inflammatory site, but not in circulating blood.(2) Pretreatment with 10 mg/kg intraperitoneal captopril enhanced significantly the accumution of pleural fluid as well as dye exudation.(3) Pretretament with bromelain, 10 mg/kg intravenously, which was shown to exhaust HMW-kininogen and prekallikrein, suppressed the accumulation of pleural fluid and dye exudation, significantly at 1, 3 and hrs after crageenin.