Abstract
Lundsgaard 1 reported that the resting oxygen consumption of the intact frog was unimpaired by brom-acetic acid poisoning while glycolysis was completely inhibited. Fischer 2 using electrical stimulation was unable to find a recovery heat production in isolated frog muscle poisoned with 0.05 to 0.1% brom-acetic acid. Hegnauer 3 stated that 0.01% brom-acetic acid completely inhibited the lactic acid formation which usually followed KCl stimulation but had no effect on the excess oxygen consumption. In view of the apparent contradiction between the work of Fischer and of Hegnnauer a considerable series of experiments was run to determine the excess oxygen consumption and lactic acid production of muscles treated with brom-acetic acid in several concentrations up to 0.2% and then stimulated electrically or chemically. While this work was in progress Hill and collaborators 4 reported a normal recovery heat production in muscles poisoned with 0.004% iodo-acetic acid.
Sartorius muscles were soaked in Ringer's solution containing brom-acetic acid or its sodium salt for half an hour at a temperature of 8°C. They then were placed in a differential volumeter, a resting rate determined (1/2 to 1 hour), stimulated, and the excess oxygen consumption measured. Chemical stimulation was accomplished by dumping 0.9% KCl from a side arm of the experimental bottle. The tension developed by matched muscles similarly treated was recorded on an isometric lever. The excess oxygen consumption and the tension development of electrically stimulated muscles were measured simultaneously on the same muscle. This was accomplished by leading a fine wire from the muscle through a mercury-sealed capillary to an isometric lever. Another respirometer without this mercury seal and containing matched muscles acted as a control on the oxygen consumption. A. H. Hegnauer, to whom I am greatly indebted for his collaboration, made lactic acid determinations on muscles treated and stimulated in an exactly similar manner.
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