PHARMACOLOGICAL STUDIES ON PUPILLARY REFLEX DILATATION

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Abstract
The physiological role of the sympathetic and parasympathetic nervous systems in pupillary reflex dilatation was analyzed in unanesthetized cats and dogs which were immobilized with decamethonium. Furthermore, the responses of the pupil, nictitating membrane and systemic blood pressure to sciatic stimulation were investigated as well as the influence of some drugs upon these responses. In both species pupillary reflex dilatation was always markedly diminished but not abolished by cervical sympathectomy. The sympathetic nervous system, therefore, plays a much more important role in pupillary reflex dilatation than does inhibition of the parasympathetic innervation. Pupillary reflex dilatation elicited by sciatic stimulation is abolished after high cervical transection. This fact proves that the response is not mediated directly to the peripheral sympathetic chain via Budge''s ciliospinal center, but must ascend to higher brain structures before it is mediated to efferent sympathetic pathways. In cats, barbiturates caused pupillary dilatation, followed by subsequent contraction, both in intact and in sympathectomized pupils of cats. Therefore, the pupillary effects of barbiturates are considered to be mostly due to the parasympathetic mechanism. The reflex dilatation via the sympathetic nerve (active sympathetic reflex dilatation) was always decreased by barbiturates, while that elicited by inhibition of the parasympathetic oculomotor nucleus was increased by smaller doses and decreased by large doses of the drug. The cat''s pupil dilated after injections of Metrazol [pentylenetetrazole] and showed marked oscillations in size during the initial period. The dilatation is dependent on both sympathetic excitation and parasympathetic inhibition. In larger doses than 10 mg/kg, Metrazol excites the sympathetic nervous system first and then depresses it. Therefore, sympathetic reflex dilatation is increased first and decreased afterwards. The responses of the nictitating membrane and blood pressure to sciatic stimulation generally were also reduced after an initial increase. On the other hand, pupillary dilatation due to parasympathetic inhibition was never depressed. As the dose of Metrazol was increased, it was enhanced. In cats, chlorpromazine injections produced mydriasis, both in the normal and in the sympathectomized pupil. This mydriasis is, therefore, due to parasympathetic inhibition. Furthermore, parasympathetic-inhibitory reflex dilatation appeared to be unaffected by chlorpromazine. The sympathetic part of pupillary reflex dilatation, contraction of the nictitating membrane and elevation of blood pressure resulting from sciatic stimuli were depressed after chlorpromazine. Morphine dilated the cat''s pupil and contracted the pupil of the dog. In cats, morphine mydriasis in the sympathectomized pupil was generally weaker than in the normal pupil. This mydriasis is accomplished by both the sympathetic-excitatory and parasympathetic-inhibitory mechanisms. The reflex dilatation elicited by sciatic stimuli was increased after morphine. Both the sympathetic and parasympathetic mechanisms participate in this increase, but the latter appears to play a dominant role. In dogs, morphine miosis seems to depend on excitation of the midbrain.