The Role of Spinal NO on the Mechanical Allodynia in the Inflammation Model by Freund's Complete Adjuvant / 대한마취과학회지

ABSTRACT

BACKGROUND: The effect of spinal nitric oxide (NO) on mechanical allodynia brought about by Freund's complete adjuvant (FCA)-induced inflammation is not known. From our previous experiment nitric oxide synthase (NOS) inhibitor nitroG-L-arginine methyl ester (L-NAME) given intraplantarly during the induction period decreased a mechanical hyperalgesia occurring because of FCA-induced inflammation. Therefore, we investigated the spinal effect of NO on mechanical allodynia after the development of allodynia produced by FCA-induced inflammation in rats. METHODS: Male Sprague Dawley rats were prepared with lumbar intrathecal catheter implantation. Inflammation was induced in the rats by injecting 0.1 ml of FCA under halothane anesthesia. Behavioral tests were done 1, 3, 6, 24, and 48 hours after injection of FCA. In the other group, intrathecal L-NAME (10 microgram) was given prior to FCA injection to examine the effect of pretreatment. On postinjection day 2, either L-NAME (10 microgram) or methylene blue (10 and 30 microgram) was administered intrathecally after the baseline measurement. The withdrawal response on mechanical allodynia was assessed by applying von Frey filaments to the right lesioned hindpaw and contralateral paw (as control) at 15, 30, 45, 60, 90, and 120 minutes. Sodium nitroprusside was administered intrathecally to determine the reversal effect of increased threshold in the L-NAME group. RESULTS: Injection of FCA produced a significant mechanical allodynia over time. Pretreatment with L-NAME did not prevent such a mechanical allodynia. Intrathecal L-NAME, but not methylene blue, reduced the mechanical allodynia, which was reversed by sodium nitroprusside. CONCLUSIONS: Spinal NO is likely invloved in the mechanism of the development and maintenance of mechanical allodynia in a state of FCA-induced inflammation.