Measurement of stress hormones is a common objective method for assessment of mental stress. However, the stress of blood sampling alone may also increase stress hormone levels. In the present study, we sampled salivary biomarkers from healthy volunteers under noninvasive conditions and determined their efficacy to assess mental stress. Specifically, we examined the relationship between State Anxiety Inventory score (STAI-s) in subjects exposed to arithmetic stress and salivary chromogranin-A, alpha-amylase, or cortisol. The STAI-s was significantly correlated to salivary alpha-amylase (r = 0.589; P < 0.01) but not to salivary chromogranin-A or cortisol. Therefore, salivary alpha-amylase is a useful indicator of psychosocial stress.

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This study quantitatively assessed injection pressure, pain, and anxiety at the start of injection of a local anesthetic into the oral mucosa, and confirmed the relationship between injection pressure and pain, as well as between injection pressure and anxiety. Twenty-eight healthy men were selected as subjects and a 0.5-inch (12 mm) 30-gauge disposable needle attached to a computer-controlled local anesthetic delivery system (the Wand) was used. A 0.5 mL volume of local anesthetic solution was injected submucosally at a speed of either 30 or 160 s/mL. Three seconds after the start of local anesthetic injection, injection pressure was measured and pain and anxiety were assessed. Injection pressure was measured continuously in real time by using an invasive sphygmomanometer and analytical software, and pain was assessed on the Visual Analogue Scale and anxiety on the Faces Anxiety Scale. A significant correlation was evident between injection pressure and pain (rs = .579, P = .00124) and between intensity of injection pressure and state anxiety (rs = .479, P = .00979). It is therefore recommended that local anesthetic be injected under low pressure (less than 306 mm Hg) to minimize pain and anxiety among dental patients.

1 Orexin A and B, recently identi®ed in the rat hypothalamus are endogenous neuropeptide agonists for the G-protein coupled orexin-1 (OX1) and orexin-2 (OX2) receptors. 2 In the present study, we have examined the eects of orexin A, B and raised extracellular K + on noradrenaline release from the rat cerebrocortical slice. We have compared this with other sleep ± wake-related (excitatory) neurotransmitters; dopamine, glutamate, serotonin and histamine. 3 Neurotransmitter release studies were performed in rat cerebrocortical slices incubated in modi®ed Krebs buer (with and without Ca 2+ +EGTA 1 mM) with various concentrations of orexin A, B and K + for various times. 4 Orexin A and B-evoked (10 77 M) noradrenaline release was time-dependent reaching a maximum some 10 min after stimulation. K + (40 mM) evoked release was also time dependent but reached a maximum after 6 min. Orexin A, B and K + stimulation of release was concentration dependent with pEC 50 and E max (% of basal) values of 8.74+0.32 (1.8 nM) and 263+14% and 8.61+0.38 (2.4 nM) and 173+7% and 1.43+0.02 (37 mM) and 1430+70%, respectively. Orexin-evoked release was partially extracellular Ca 2+ dependent. 5 Of the other transmitters studied there was a weak orexin A and B stimulation of glutamate release. In contrast K + evoked dopamine, glutamate, histamine and serotonin release with pEC 50 and E max (% of basal) values of 1.47+0.05 (34 mM) and 3430+410%, 1.38+0.04 (42 mM) and 1240+50%, 1.47+0.02 (34 mM) and 480+10% and 1.40+0.05 (40 mM) and 560+60% respectively. 6 We conclude that the neuropeptides orexin A and B evoke noradrenaline release from rat cerebrocortical slices.

The present data indicate that coerulean noradrenergic neurones may be responsible for both GABA- and NMDA-mediated anaesthetic actions.