THE PHARMACOLOGY OF DENERVATED MAMMALIAN MUSCLE II. SOME PHENOMENA OF ANTAGONISM, AND THE FORMATION OF LACTIC ACID IN CHEMICAL CONTRACTURE

¹ From the National Institute for Medical Research, Hampstead, London

The following are the main conclusions to be drawn from the above experiments.

1. The stimulating effect of acetyl-choline, and of other bases of the nicotine-choline group, on denervated mammalian muscle is not definitely affected by curari in doses sufficient to abolish the indirect excitability of normal muscle, or by atropine in doses sufficient to abolish the parasympathetic effects of acetyl-choline.

2. Adrenaline completely abolishes the action of these bases in doses sufficient, in its absence, to produce maximal contracture. Other vasoconstrictors have not this action. Ergotamine, in doses which reverse the vasoconstrictor effect of adrenaline, reduces, but does not abolish its antagonism to acetyl-choline, etc.

3. The stimulating effect of acetyl-choline, and of other bases of the nicotine-choline group, on denervated mammalian muscle, is evanescent. Increase of dose, beyond the minimum needed to produce maximal tension, does not prolong the effect.

4. One dose of any of these substances, renders the muscle temporarily insensitive not only to the chemical stimulus, but also to maximal, direct electrical stimulation. Fatigue by direct electrical stimulation leaves the muscle still excitable by the chemical stimulus. In both these respects the denervated mammalian muscle differs from the normal avian and amphibian muscle.

5. The contracture produced by the bases in denervated mammalian muscle, or normal avian muscle, is accompanied by the production of lactic acid, which is of the same dimensions as that observed in a tetanus producing equivalent tension. There is no ground for suggesting that the contracture depends on an alternative contractile metabolism, or that it corresponds to a second, parasympathetic innervation (see part I).

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