Sodium and chloride movement into the central canal of cat spinal cord.
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Biomedical subjects
Publications and source records attributed to D T Frazier.
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Experiments utilizing internally perfused squid giant axons have been carried out to determine the mode of action of tricaine (MS-222) in producing its anesthetic effects. Tricaine, in concentrations of 1 and 3 mM, was applied to the internal surface of the membrane via the perfusion system. Peak sodium current and steady-state potassium current were measured by the axial-wire voltage clamp technique. Tricaine suppressed both of these membrane ionic currents with the major effect being on the peak sodium current. Its action on nerve membrane appeared quite similar to other local anesthetics. One major difference was noted in that tricaine shifts sodium conductance curves in the direction of depolarization along the potential axis, an effect quite similar to that observed with increasing external Ca2+ concentration and with application of pentobarbital.
Inhalation of cigarette smoke has been shown to induce bronchoconstriction which should stimulate slowly adapting pulmonary stretch receptors (PSRs). To test this possibility, the activity of PSRs was recorded from fine afferent filaments of the vagus nerve before and after 120 ml of smoke generated from high-nicotine cigarettes was delivered into the lungs in a single breath in anesthetized, open-chest and artificially ventilated dogs. The base-line activity of PSRs did not change during the first two breaths following smoke delivery. However, PSR activity started to increase by the third breath (post-smoke), concomitant with an increase in tracheal (transpulmonary) pressure. Both the smoke-induced increase in tracheal pressure and the delayed effect on PSRs were prevented by a pretreatment with aerosolized isoproterenol, a bronchodilator, suggesting that the delayed response of PSRs to smoke was elicited by the change in bronchomotor tone. Although smoke evoked a delayed stimulation in the majority (61%) of the PSRs studied, it caused a mild delayed inhibition (24%) or had no effect (15%) in some of the receptors. The variable responses to smoke among PSRs are probably related to the smoke-induced heterogeneous changes of mechanical properties in the lungs and their different anatomic locations.