Abstract
In this study, we investigated whether increases in hippocampal blood flow (HBF) by tooth pulp stimulation (TPS) are mediated via the activation of cyclooxygenase-2 (COX-2). We measured mean arterial blood pressure (MABP) and HBF in urethane-anesthetized rats using laser Doppler flowmetry and examined the effects of etodolac, a specific COX-2 inhibitor, on TPS-induced MABP and HBF responses. The MABP response was not attenuated by the intraperitoneal (i.p.) administration of etodolac (10 mg/kg); however, the HBF response was significantly attenuated by etodolac administration. These results suggest that COX-2 may be involved in the mechanisms regulating TPS-induced HBF responses.
Highlights
A positive relationship between anxiety and pain is a common experience in the dental clinic [1,2]
analysis of variance (ANOVA) computed according to changes in mean arterial blood pressure (MABP) responses induced by tooth pulp stimulation (TPS) revealed that the main effects of group and time and the interaction between group and time were not significant (F(1/17) = 1.314, p = 0.268; F(1/17) = 0.053, p = 0.949; F(1/17) = 1.287, p = 0.290, respectively) (Figure 2)
The mean value of TPS-induced hippocampal blood flow (HBF) responses measured before methylcellulose or etodolac administration was 7.9 ± 0.9 laser Doppler unit (n = 18)
Summary
A positive relationship between anxiety and pain is a common experience in the dental clinic [1,2]. Okawa et al [2] discussed the effects of level of anxiety about dental treatment on pain during treatment. Regarding their discussion, Ploghous et al [1] showed that anxietyinduced hyperalgesia is associated with activation of entorhinal cortex of the hippocampal formation and suggested that accurate dental preparation alleviated pain by disenganging the hippocampal formation. We previously showed that TPS increases hippocampal blood flow (HBF) in rats, and that the nonselective adenosine receptor antagonist, theophylline, attenuates TPS-induced HBF responses [4]. We suggested that TPS-induced HBF responses may be, at least in part, mediated through adenosine receptors. We measured HBF and mean arterial blood pressure (MABP) in rats and examined the effects of a selective COX-2 inhibitor, etodolac, on TPSinduced HBF responses
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