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Hyperglycemia does not modify the pupillary effects of mu and kappa opiate agonists in mice.

The effects of mu and kappa opiate agonists were assessed on the pupillary size in normoglycemic and hyperglycemic conditions in mice. The mu agonists used were, morphine (10, 30 and 100 mg/kg), fentanyl (50, 100 and 150 micrograms/kg) and sufentanil (5, 10 and 20 micrograms/kg). The highly selective kappa opiate agonists used were, U-50488H and U-69593 (30 mg/kg). Chronic hyperglycemia was induced by streptozotocin injection (200 mg/kg i.p) 7-8 days before the experiment. Acute hyperglycemia was induced by intraperitoneal glucose (5 g/kg i.p) injection at the time of subcutaneous injection of opiates. In the normoglycemic mice, the mu agonists produced significant mydriasis (P less than 0.05), while kappa agonists had no effect on the pupil. However, both acute and chronic hyperglycemic condition did not affect the mydriatic ratio of the mu opiate agonists. These results indicate that mu opiate receptors induce mydriasis in mice and suggest that the hyperglycemia is not the mechanism involved in the opiate induced mydriasis in mice. With the dose of kappa agonists used, the involvement of kappa receptors in the pupillary effects in mice were not clear. These results support the hypothesis that hyperglycemia is not the primary mechanism for the altered sensitivity of opiates in the animal models of diabetes.