Further evidence about the mechanism of the inhibition of contractions caused by cadmium ions (Cd2+) in guinea-pig taenia coli has been sought. Cd2+ at a concentration of 0.5 mM completely inhibited the high-K (40 mM)-induced contraction within 3-5 min. Cd2+ did not shift the Ca2+-induced concentration-response curve to the right in Ca2+-free K+ depolarized muscle, although it reduced the Ca2+ response size. The K+-induced increase in tissue calcium content and 45Ca uptake determined by the lanthanum method was significantly reduced in the presence of Cd2+ (0.5 mM) and the contractions of the glycerolated taenia coli were inhibited with increasing Cd2+ (0.001-0.5 mM). Muscle strips, incubated in a medium containing 0.5 mM Cd2+, accumulated greater amounts of cadmium than within the extracellular space. It is suggested that the inhibitory action on tension produced by Cd2+ in taenia coli may result from the interference of calcium permeability at the cell membrane. There is the possibility that Cd2+ acts on the contractile system of the muscle.

The anti-platelet aggregating action of minidose aspirin and its combined effect with dilazep were examined in healthy male volunteers. A quantitative and dose-dependent decrease in platelet aggregability was observed on a single oral administration of 30 mg, 100 mg and 300 mg of aspirin and also on the repeated oral administration of 10 mg and 30 mg three times a day for 5 days. Administration of 100 mg of dilazep in combination with 30 mg or 100 mg of aspirin produced an anti-platelet effect equivalent to a 3-fold dose of aspirin alone. In the repeated administration test, the t. i. d. admin istration of aspirin 10 mg+ dilazep 100 mg was confirmed to be close to the ideal in the balance between anti-platelet action and the reduced production of PGI2.

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