Trigeminal neuralgia increases cerebral blood flow in a focal cerebral ischemic model in rats

To investigate the influences of trigeminal neuropathic pain on the cerebral blood flow in a ET-1 focal cerebral ischemia model.

Male Sprague-Dawley (SD) rats (220-260 g) were randomly divided into a model group (trigeminal neuralgia, TN group) and a sham operation group (sham group). The TN group received bilateral infraorbital nerve chronic constriction surgery, and the sham group only underwent exposure of the infraorbital nerve. The mechanical pain threshold of the rats was continuously monitored for 30 days post surgery. On postoperative day 30, the animals were anesthetized, and 3 μL (120 pM/μL) ET-1 was injected into the surroundings of the middle cerebral artery (MCA) to establish a cerebral focal ischemia-reperfusion injury model in rats. The changes in cerebral blood flow of these two groups were monitored 30 min after the injection of ET-1.

The mechanic pain threshold values between rats in the two groups were not significantly different (P>0.05). The threshold value in the TN group on postoperative day 9 significantly decreased compared with that before surgery (P<0.01). Between postoperative days 9 and 30, the pain threshold values in the TN group were significantly lower than those in the sham group (P<0.01). From postoperative day 10, the mean arterial pressure in the TN group significantly increased compared with that before surgery (P<0.05), and the blood pressure (BP) in the TN group was higher than that in the sham group between postoperative days 10 and 30 (P<0.05). After 75 min of ET-1 microinjection, the cerebral blood flow in the rat frontal cortex exhibited reperfusion, and the cerebral blood flow in the TN group was significantly higher than that in the sham group (P<0.05). In addition, the content of calcitonin gene-related peptide (CGRP) in the blood of rats in the TN group was significantly higher than that in the sham group (P<0.05).

Trigeminal neuropathic pain may increase the mean arterial pressure and the content of CGRP in the plasma of rats, thus increasing the cerebral blood flow in the frontal cortex of the ET-1 ischemia-reperfusion model.