THE EFFECTS OF RESERPINE ON THE RESPONSES OF THE NICTITATING MEMBRANE IN THE CAT

摘要

References(27) Cited-By(6) Bein (1) was the first to describe that the administration of reserpine potentia!ed the pressor responses of the experimental animals to adrenaline and noradrenaline. The discharge of the catecholamines from the adrenal glands and from the other sympathetic structures such as the heart, liver, spleen and hypothalamus have been shown by Holzbauer and Vogt (2), Carlsson and Hillarp (3), Shore et al. (4) and others (5-8). Although the animals which have received reserpine, did not exhibit very obvious signs of an increased sympathetic activity such as would be expected during a discharge of adrenal medullary amines, Everett et al. (9) showed that the mice revealed a transient phase of piloerection, Kuschke and Franz (10) demonstrated a hyperglycemic effect in the rabbi. Rises of blood pressure in the rat and the spinal dog, the contraction of the denervated nicti!ating membrane in the cat have been reported following the injection of reserpine by de Jongh and van Proosdij-Hartzema (11) and Maxwell et al. (12). Torii (13) also showed that the carotid injection of reserpine (0.1 mg/kg) to intact rabbit or the intravenous injection of reserpine (1 to 3 mg/kg) to the iproniazid-trested rabbit induced increased spontaneous movements and the signs of the increased sympathetic ac!ivi'y. Within 30 minutes after the intravenous injection of reserpine the pressor responses of the animal to stimulation of the thalamic and hypothalamic nuclei had been rather potentiated. Burn et al. (14, 15) confirmed that the contract ive response of the spiral strips of the thoracic aor, a of the reserpinized rabbit to adrenaline and -noradrenaline was much sensitive than that of the normal one and that the contractive responses of the nictitating membrane of the cat to the same amines were also potentiated by the successive dose of reserpine. Burn and Rand (14) discussed the mechanism of the supersensitivity of these structures by reserpine concluding that the depletion of the catecholaminestin the tissues by reserpine might be responsible. It would be expected to elucidate the mechanism of reserpine hypersensitivity to catecholamines by studying the effect of reserpine on the responses of the normal and denervated nictiating membranes to sympathomimetic stimuli. The effect of reserpine on the membranes was also, compared with those of the denervation, cocainization, ephedrinization, iproniazidizatitn and noradrenaline infusion.