Abstract

cell (galvanic skin response) varies, ceteris paribus, with the degree to which the sweat ducts are filled.' This being so, change in amplitude of action potentials so enigendered can, in suitable circumstances, be utilized as an indication of secretory activity due to some other agency. If one is concerned with the question of whether or not the sweat gland cells are active in the sense of forming sweat rather than with the question of sweat emergence, which is to say, sweating, then the method of action potential recording, herein employed, is the method of choice. One drawback, of no present concern, is that once the ducts are filled, sweat formation may continue unabated, or even vary in intensity, unreflected by any change in the action potential indicator unless the variation be such as to deplete the ducts to some degree through reabsorption. The action potential test in carefully arranged circumstance thus is a subtle test of action in subtle degree. It is usually a simple matter to measure decrease (such as that caused by the action of transmission blocking agents) of action by sweat gland cells,2 for then it is sufficient to fill the ducts initially, thus obtaining easily a control value. One may then let matters take their course. If, however, an excitatory action of a given agent is anticipated, or sought for, anticipated or not, the technical problem is in some measure compounded. An equilibrium between secretion and reabsorption must be established so that one achieves a constant control amplitude of response prior to experimental maneuver. And that equilibrium must be established with the ducts less than full in order that an excitatory action upon the sweat gland cells may find expressioni, through duct filling, in iniereased response amplitude. In some experiments, these mandata cannot be fulfilled, and the day is wasted. The specific problem herein assayed is whether or not aspirin (in the form of sodium acetylsalicylate) might cause sweating by a peripheral action, which is to say, by direct action at the sweat gland rather than through the coiitrolling centers in the central nervous system. The question arises as a sequel to the many observations by Dr. Robert K. S. Lim to the effect that aspirin, in contrast to narcotic analgesics, acts peripherally to allay pain.3 In fact, these experiments were undertaken at his sug3gestion and with the thought in minid that aspirin antipyresis might conceivably be due in part to peripheral action, and that the present experimental approach might reveal such action. The dosage (intravenous) of sodiunm acetylsalicylate emnployed approxirnated that found by Dr. Lim to block bradykinin-induiced pain responses, to wit, 100 mg/kg.

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