EFFECT OF ANOXEMIA, CARBON DIOXIDE AND LACTIC ACID ON ELECTRICAL PHENOMENA OF MYELINATED FIBERS OF THE PERIPHERAL NERVOUS SYSTEM

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Abstract
The effect of anoxemia, CO and lactic acid on nerve is, in general, to raise the threshold, lengthen the absolutely refractory period, decrease conductivity and amplitude of action potential. These effects are reversed in recovery induced by O and washing with isotonic Ringer''s solution. Certain coordinative relationships exist between threshold, refractoriness, conductivity and action potential. Exceptions to the general rule occur and their origin may possibly be attributed to changes in the physical reactance of nerve during depression and recovery. Experimental evidence presented establishes the independent variation of certain of these properties and indicates at least a partial difference in their mechanism. Differential changes in threshold, refractoriness, and conductivity in the different fiber groups are recorded. Depression is most rapid in the smallest or delta fibers and least rapid in the largest or alpha fibers. This differential depression is presumably the result not of fundamental differences or variabilities in the individual fiber group but the physi-cal consequence of the volume area ratio of the fibers. Recovery is most rapid in the large fibers. Further proof of the fundamental similarity of the fiber groups is found in the fact that they acquire the same degree of increase of refractory period before becoming unirri-table. Refractoriness apparently varies with the available O supply and is considered a true index of the nerve''s metabolic state. The action potential recorded near the stimulus is depressed in amplitude. For action potentials definitely below the maximal there occurs a shortening of the crest time and a shortening of the falling phase. Such changes do not occur when maximal action potentials only are compared. For reasons discussed the maximal action potential is considered to approximate more closely to that of the axon action potential than does the submaximal. Consequently no change in the actual form of the axon action potential is considered to occur. "Retention of negativity" has been disregarded as probably not a part of the response process proper. The changes in recorded form, including amplitude of the recorded action potential, may in part be assigned to changes in physical reactance of the nerve. The potential then is not a precise index of the nerve''s metabolic state. Changes in form of the conducted action potential are recorded. They are chiefly due to differential depression of potentials and of conductivity of the fiber groups. Evidence is presented that the detrimental effect of CO2 is pri-marily due to acidity interfering with the use of O and secondarily to the loss of O resulting from changes in partial pressure. The detrimental effect of anoxemia, on the other hand, is principally due to a loss of O physically dissolved or chemically combined. It must in part be due also to changes dependent upon the accumulation of acid products of metabolism. Action potentials recorded practically simultaneously at the stimulus and after conduction showed that conduction with a decrement in nerves depressed by anoxemia and CO2 does not occur. The recording mechanism used was the cathode ray oscillograph.

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