Failure of acetyl salicylic acid (aspirin) to reduce experimental myocardial ischaemic damage.

Rats fed on acetylsalicylic acid (aspirin) 1.5 mg/100 g body weight for a period of three weeks were subjected to myocardial infarction by s.c. administration isoprenaline hydrochloride 8.5 mg/100 g of body weight on two consecutive days. Heart specimens were taken for histological examination at 24 hr, on 5th day and 12th day. An equal number of rats were given saline to serve as control. As compared to controls aspirin-treated rats were found to have macroscopically bigger infarcts and microscopically showed persistent oedema on the 12th day. Further, no histological evidence of favourable action of aspirin was seen on the fifth day and after twenty-four hr.

Modification of the toxicity of acetylcholine by prior atropinization in mice.

The potentiation of acetylcholine (Ach) toxicity in mice with prior atropinization was tested. The experiments were carried out with three doses of 200 mg, 300 mg, and 400 mg/kg of Ach administered ip. Prior atropinization was observed to potentiate the Ach toxicity at all dose levels of atropine except the highest in the group that received Ach 200 mg/kg and the results were variable in the other two groups.

Local anaesthetic activity of some new substituted acylamides II.

Six new substituted acylamides, chemically related to lignocaine were studied for local anaesthetic activity and toxicity in mice, frogs and guinea pigs. Only one of these compounds, w-pyrrolidino 2, 3, 5, 6 tetramethyl acetanilide was found to possess potency comparable to lignocaine with a slightly higher therapeutic index. Study of the S.A.R. of this group indicated that by removal of two methyl groups at position 3 and 5 in the above compound, a local anaesthetic with greater potency than lignocaine may be obtained. Further exploration of the potentialities of a compound having pyrrolidine group as a part of basic side chain is indicated.