Differences in control of parasympathetic vasodilation between submandibular and sublingual glands in the rat.

We examined blood flow in the submandibular gland (SMGBF) and sublingual gland (SLGBF) during electrical stimulation of the central cut end of the lingual nerve (LN) in the urethane-anesthetized rats using a laser speckle imaging flow meter. LN stimulation elicited intensity- and frequency-dependent SMGBF and SLGBF increases, and the magnitude of the SMGBF increase was higher than that of the SLGBF increase. The increase in both glands was significantly inhibited by intravenous administration of the autonomic cholinergic ganglion blocker hexamethonium. The antimuscarinic agent atropine markedly inhibited the SMGBF increase and partly inhibited the SLGBF increase. The atropine-resistant SLGBF increase was significantly inhibited by infusion of vasoactive intestinal peptide (VIP) receptor antagonist, although administration of VIP receptor antagonist alone had no effect. The recovery time to the basal blood flow level was shorter after LN stimulation than after administration of VIP. However, the recovery time after LN stimulation was significantly delayed by administration of atropine in a dose-dependent manner to the same level as after administration of VIP. Our results indicate that 1) LN stimulation elicits both a parasympathetic SMGBF increase mainly evoked by cholinergic fibers and a parasympathetic SLGBF increase evoked by cholinergic and noncholinergic fibers, and 2) VIP-ergic mechanisms are involved in the noncholinergic SLGBF increase and are activated when muscarinic mechanisms are deactivated.

Distribution and absorption of local anesthetics in inferior alveolar nerve block: evaluation by magnetic resonance imaging.

PURPOSE: The aim of this study was to evaluate the distribution and absorption of local anesthetic solutions in inferior alveolar nerve block using magnetic resonance imaging. MATERIALS AND METHODS: Forty healthy volunteers were divided into 4 groups and injected with 1.5 mL for inferior alveolar nerve block and 0.3 mL for lingual nerve block. The solutions used for the different groups were 2% lidocaine, 2% lidocaine with 0.125 mg/mL epinephrine, 4% articaine with 0.006 mg/mL epinephrine, and 4% articaine with 0.012 mg/mL epinephrine. All subjects had axial T2-weighted and fat-suppressed images at 0, 60, and 120 minutes after injection. The localization, area, and intensity (signal characteristics) of the solutions were analyzed and onset and duration times of the anesthesia were recorded. RESULTS: There were no significant differences between groups with regard to the intensity and area of the solutions at 0, 60, and 120 minutes after injection, but differences were found within each group. CONCLUSIONS: No between-group differences were found on magnetic resonance imaging in the distribution and absorption of lidocaine with or without epinephrine and articaine with 0.006 and 0.012 mg/mL epinephrine. All solutions were noticeably absorbed at 120 minutes after injection.

Ultrasound-Guided Inferior Alveolar Nerve Block in the Horse: Assessment of the Extraoral Approach in Cadavers.

Blinded techniques to desensitize the inferior alveolar nerve (IAN) include intraoral, angled, and vertical extraoral approaches with reported success rates of 100%, 73%, and 59%, respectively. It has not been determined whether an ultrasound-guided extraoral approach is feasible. Further, the fascicular nature of the inferior alveolar and lingual nerves of the horse has not been described. The objectives of this study were to describe a low-volume ultrasound-guided vertical extraoral inferior alveolar nerve block technique and to describe the fascicular nature of these nerves. An ultrasound-guided approach to the IAN was conducted with a microconvex transducer and an 18-G, 15-cm spinal needle using a solution containing iodinated-contrast and methylene blue dye. Accuracy was assessed by contrast visualized at the mandibular foramen on computed tomography (CT) and methylene blue dye staining of the nerves on gross dissection. Sections of inferior alveolar and lingual nerves were submitted for histological analysis. Assessment by CT and dissection determined success rates of 81.3% and 68.8%, respectively; 68.8% of injections had inadvertent methylene blue dye staining of the lingual nerve. Nerve histology revealed both the inferior alveolar and lingual nerves to be multifascicular in nature. Mean fascicle counts for the inferior alveolar and lingual nerves were 29 and 30.8, respectively. The technique is challenging and no more accurate than previously published blinded techniques. Any extraoral approach to the IAN is likely to also desensitize the lingual nerve.

Effect of SB-750364, a specific TRPV1 receptor antagonist, on injury-induced ectopic discharge in the lingual nerve.

Abnormal neural activity generated at a site of nerve injury is thought to contribute to the development of dysaesthesia. Vanilloid receptor 1 (TRPV1), a transducer of noxious stimuli, may be involved in the initiation of this abnormal activity and could provide a useful therapeutic target. We investigated the effect of a specific TRPV1 antagonist (SB-750364) on injury-induced discharge in the lingual nerve. In 12 anaesthetised adult ferrets the left lingual nerve was sectioned and animals were allowed to recover for 3-7 days. In terminal experiments under general anaesthesia, the nerve was re-exposed and electrophysiological recordings made from spontaneously active axons in fine filaments dissected from the nerve central to both the injury site and the junction with the chorda tympani. SB-750364 was infused via the cephalic vein in order to achieve three increasing but stable systemic blood levels of the compound (0.3, 1.0 and 3.0 microM). Twenty-eight spontaneously active units were studied, with discharge frequencies ranging from 0.02 to 4.9 Hz. There was a significant reduction in spontaneous activity in 17 units (61%) at 1.0 microM or less of SB-750364 (p<0.01; Friedman test with Dunn's multiple comparisons). A further 4 units (14%) showed a significant reduction in activity at 3.0 microM (p<0.01). In the remaining 7 units (25%) the discharge was unaffected (p>0.05). These data show that the TRPV1 antagonist SB-750364 can reduce the level of spontaneous activity initiated in some axons following lingual nerve injury.

Gow-Gates technique: a pilot study for extraction procedures with clinical evaluation and review.

The aim of this study was to compare the effectiveness of 2 different volumes of anesthetic solution for a premolar-molar extraction, and to determine the onset of complete mandibular conduction anesthesia via a Gow-Gates mandibular block. One operator performed 32 blocks with a 27-gauge needle on patients who required a dental extraction: 16 blocks using 1.8 mL of anesthetic solution, and 16 blocks using 3.6 mL of anesthetic solution. The parameters evaluated were frequency of successful anesthesia and onset of complete anesthesia. Significant differences (P < .005) were observed in the evaluation of volume: the 3.6 mL group yielded a higher success rate (82.5%) than the 1.8 mL group (17.5%). The onset of complete conduction anesthesia was achieved in 8 minutes by 56% of the subjects (9 of 16) with 3.6 mL and only one subject in 16 (6%) with 1.8 mL. A larger volume of anesthetic solution (3.6 mL) is required to achieve a higher success rate and a faster onset of action for a dental extraction without the use of reinforcement anesthesia. The volume of anesthetic solution is indirectly proportional to the onset of complete anesthesia. A premolar-molar extraction can be done, with 3.6 mL of anesthetic solution, in more than 50% of the patients 8 minutes after injection.

Effects of isoflurane on parasympathetic vasodilatation in the rat submandibular gland.

Volatile anesthetics have been known to suppress parasympathetic reflex vasodilatation in the lower lip and palate. However, in the submandibular gland, little is known about the effects of these anesthetics on the parasympathetic vasodilatation elicited by reflex and direct (i.e., non-reflex) activation of the parasympathetic vasodilator mechanisms. Although both parasympathetic vasodilatations were inhibited by isoflurane in a concentration- and time-dependent manner, the effects of continuous administration of the alpha(1)-adrenoceptor agonist methoxamine were markedly different: The reflex vasodilatation was not affected by methoxamine, while the direct vasodilatation was significantly reduced. Picrotoxin (GABA(A) receptor antagonist) attenuated the inhibitory effect of isoflurane on direct vasodilatation and the systemic arterial blood pressure. These findings suggest that the isoflurane-induced inhibitory effects on direct vasodilatation are produced by a decrease of peripheral vascular tone by GABAergic mechanisms, whereas those on the reflex vasodilatation are produced exclusively by the inhibition of the reflex center.

Effects of transitory lingual nerve impairment on speech: an acoustic study of sibilant sound /s/.

By measuring spectral characteristics of the sibilant /s/ this study investigated whether the reduced orosensory feedback caused by lingual nerve impairment affects the acoustics and articulation of sibilants. A further goal was to examine speakers' capability to compensate for the deviant control of the delicate movements required for the proper production of /s/ by experimentally modifying the function of the tongue in a way that reduces the necessary somatosensory information in articulation. Five healthy men with no speech, language or hearing abnormalities were enrolled. They produced the sibilant /s/ in a variety of phonetic contexts in two sessions: first in normal conditions and then with local anaesthesia of the right lingual nerve. From the speech samples, the spectral characteristics of the sibilant sound (i.e. the centre of gravity, standard deviation, skewness and kurtosis) were analysed acoustically. The results showed that the reduced tactile sensation has effects on the tongue function resulting in individual and variable spectral alterations. The variation between different speakers indicates individual ability to compensate for the effects caused by the sensory dysfunction of the tongue. It seems, therefore, that the compensatory mechanisms for speech production are highly speaker-dependent.

Nerve injury caused by mandibular block analgesia.

Fifty-four injection injuries in 52 patients were caused by mandibular block analgesia affecting the lingual nerve (n=42) and/or the inferior alveolar nerve (n=12). All patients were examined with a standardized test of neurosensory functions. The perception of the following stimuli was assessed: feather light touch, pinprick, sharp/dull discrimination, warm, cold, point location, brush stroke direction, 2-point discrimination and pain perception. Gustation was tested for recognition of sweet, salt, sour and bitter. Mandibular block analgesia causes lingual nerve injury more frequently than inferior alveolar nerve injury. All grades of loss of neurosensory and gustatory functions were found, and a range of persisting neurogenic malfunctions was reported. Subjective complaints and neurosensory function tests indicate that lingual nerve lesions are more incapacitating than inferior alveolar nerve lesions. Unlike most mechanical injuries after surgery, injection injuries were not followed by a course of spontaneous improvement of neurosensory and/or gustatory function. This may indicate neurotoxicity as a central aetiological factor. Fifty-four percent of the nerve injuries were associated with Articaine 4%, and a substantial increase in the number of injection injuries followed its introduction to the Danish market.

Failure to obtain adequate anaesthesia associated with a bifid mandibular canal: a case report.

The inferior alveolar nerve (IAN) block is the most common method for obtaining mandibular anaesthesia in dental practice but it is estimated to have a success rate of only 80 to 85 per cent. Causes of failure include problems with operator technique and anatomical variation between individuals. This case report involves a patient who received IAN blocks on two separate occasions that resulted in only partial anaesthesia of the ipsilateral side of the mandible. Radiographic assessment disclosed the presence of bifid mandibular canals that were present bilaterally and that may have affected the outcomes of the local anaesthetic procedures. Previous studies of bifid mandibular canals are reviewed and suggestions provided that should enable clinicians to differentially diagnose, and then manage, cases where IAN blocks result in inadequate mandibular anaesthesia.

Bupivacaine as pre-emptive analgesia in third molar surgery: Randomised controlled trial.

We conducted a prospective, randomised study on the use of pre-emptive analgesia in 45 patients who had bilateral impacted third molars removed. Bupivacaine 0.5% with adrenaline 1:200,000 was injected on one side, the other side acting as control. A visual analogue scale was used to measure the extent of postoperative pain. There was a significant reduction (p = 0.05) in postoperative pain on the injected side at 6, 12, and 72 h and an overall reduction in pain up to 7 days.

The effect of carbamazepine on injury-induced ectopic discharge in the lingual nerve.

Previous studies have shown that the development of ectopic activity from damaged axons following nerve injury may contribute to the aetiology of sensory disturbances, including dysaesthesia. Pharmacological manipulation of this activity could provide a method of treatment for this intractable condition. In this study we have investigated the effect of carbamazepine, an anti-convulsant, as it is known to have membrane stabilising properties. In eight anaesthetised adult ferrets the left lingual nerve was sectioned and the animals allowed to recover for 3 days. Then, in terminal experiments under general anaesthesia, the nerve was re-exposed and electrophysiological recordings were made from spontaneously active units in fine filaments dissected from the nerve proximal to the injury site. Carbamazepine in a modified cyclodextrin (hydroxypropyl-beta-cyclodextrin) was administered intravenously in increments, in order to achieve a progressively increasing systemic concentration, and serum levels were determined at the point that activity ceased. Twenty-one spontaneously active units were studied, with conduction velocities of 2.1-28.9 m s(-1) and discharge frequencies of 0.25-15.3 Hz. Spontaneous activity ceased in 13 units with a serum concentration of carbamazepine ranging from 3.5 to 8.4 mg/l, which was within the normal therapeutic range (4-12 mg/l). Four units ceased activity with carbamazepine levels above the therapeutic range (15.4-17.2 mg/ml), but the remaining four continued to discharge throughout the recording period. These data suggest that systemic carbamazepine can reduce the level of spontaneous activity initiated in some axons following lingual nerve injury.

The effect of bilateral lingual nerve anesthesia and increased occlusal vertical dimension on the onset of swallowing in adult males.

The present study attempts to determine whether the onset of swallowing is affected by bilateral lingual and inferior alveolar nerve anesthesia and by raising the occlusal vertical dimension by wearing an occlusal bite plate. Twenty young male volunteers were selected and asked to chew and swallow corned beef and a corned beef and liquid mixture in their usual manner before and after modifications were made. Oral and pharyngeal swallowing was investigated using videofluoroscopic examination in the lateral plane. Eight objective indicators, including oral containment time, swallowing threshold, and pharynx-to-swallow intervals were estimated. Oral containment time, total sequence duration, total number of chews, and total number of swallows of the two test foods were significantly different before and after the modifications. Individual pharynx-to-swallow intervals also varied. The results indicate that modification of the masticatory condition affects the onset of swallowing and that changes in the onset varied among the participants.

The effect of triamcinolone hexacetonide on the spontaneous and mechanically-induced ectopic discharge following lingual nerve injury in the ferret.

Investigations into the aetiology of nerve injury-induced dysaesthesia have revealed the development of spontaneous and mechanically-induced activity from damaged axons. Pharmacological manipulation of this activity could provide a method of treatment for this intractable condition. This study has investigated the effect of a corticosteroid applied to the injury site, as these agents are known to reduce inflammation and scarring. In 24 anaesthetised adult ferrets the left lingual nerve was sectioned and the animals allowed to recover. In eight of these animals the nerve was re-exposed under anaesthesia after 1 month and 100 microl of corticosteroid (triamcinolone hexacetonide, 20 mg/ml) was injected into and around the injury site. In eight others, 100 microl of the steroid carrier was injected, and the eight remaining animals were used as controls. In terminal experiments under general anaesthesia, 3 months after the initial injury, electrophysiological recordings were made from axons in fine filaments dissected from the nerve central to both the injury site and junction with the chorda tympani nerve. Spontaneous activity (SA) was found in approximately 13% of units in control animals, 12% following the application of steroid, and 14% in the carrier group. Mechanically-induced activity at the injury site was found in approximately 13% of units in controls, significantly fewer after the application of steroid 4% (P<0.001) and 12% in the carrier group. These data suggest that local application of the corticosteroid triamcinolone hexacetonide could reduce the level of mechanically-induced, but not spontaneous, dysaesthesia following lingual nerve injury.

Corticofugal inhibitory effects on lingually induced postsynaptic potentials in cat hypoglossal motoneurons.

The suppression of lingually or cortically induced postsynaptic potentials produced by conditioning stimulation of the cerebral cortex or the lingual nerve was studied in cat hypoglossal motoneurons. We have demonstrated that lingually or cortically induced inhibitory postsynaptic potentials were effectively suppressed by a conditioning stimulus of the cerebral cortex or the lingual nerve. In hypoglossal motoneurons after blocking inhibitory postsynaptic potentials by the administration of strychnine, lingually induced excitatory postsynaptic potentials and spikes were effectively suppressed by cortical stimulation. Whereas, a conditioning stimulus of the lingual nerve suppressed only a long-latency excitatory postsynaptic potential evoked by a test stimulus of the cerebral cortex, while a short-latency excitatory postsynaptic potential was unaffected. Picrotoxin and bicuculline appeared to act by reducing the suppression of lingually induced excitatory postsynaptic potentials produced by cortical conditioning stimulation.

Acetylcholine-sensitive cells in the caudal medulla of the rat: distribution, pharmacology and effects of pentobarbitone.

1. The distribution of cholinoceptive and non-cholinoceptive cells in various nuclei of the caudal medulla of the rat is described. 2. The nature of the responses of cells of the paramedian reticular nucleus and of the perihypoglossal nuclei to electrophoretically applied acetylcholine (ACh) was investigated. 3. In unanaesthetized decerebrate preparations ACh responses were usually of a "fast onset-fast offset" nature. Dihydro-beta-erythroidine was a more effective antagonist than atropine. 4. In rats anaesthetized with barbiturate nearly all the tach responses showed a slower onset and prolonged action. Atropine was the more effective antagonist. 5. The synaptic responses of cells of the paramedian reticular and perihypoglossal nuclei to stimulation of glossopharyngeal, superior laryngeal, lingual and hypoglossal nerves were investigated. It is concluded that ACh does not mediate the responses at the level of these nuclei.

Tongue adaptation temperature influences lingual nerve responses to thermal and menthol stimulation.

Menthol, a tangible substance present in many orally administered products, can produce a powerful influence on the perceived intensity of subsequent thermal stimulation in humans as well as the response magnitudes of thermally sensitive neurons in rats. However, there are no prior studies examining the influence of adaptation temperature on perceived intensity and/or response magnitudes of thermally sensitive neurons to subsequent menthol stimulation. We identified 32 thermally sensitive neurons that increased their discharge rate to a gradual temperature decrement beginning from 35 degrees C and dropping to 10 degrees C at 1 degree C/s. Based on their response threshold, time-to-peak, and range of sensitivity, these thermally sensitive lingual neurons were found to be divisible into two distinct groups. Group 1 neurons (n = 21) responded best to the upper cool range (34-15 degrees C) of the temperature decrement, whereas Group 2 neurons (n = 11) responded to the lower cold range (32-10 degrees C) of the temperature decrement. Our Group 1 and Group 2 neurons may be analogous to low threshold and high threshold cold receptors identified previously in primates. We also examined the responses of lingual neurons to 0%, 25%, 50% and 75% dilution's of a stock menthol concentration (1.28 mM) at 25 and 35 degrees C adaptation temperatures. Menthol responses across all concentrations were far larger after adaptation to 35 degrees C compared to 25 degrees C. Furthermore, only during 35 degrees C adaptation did responses to menthol stimulation persist during the ensuing 20 s after menthol off-set and water on-set.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of menthol on peripheral nerve and cortical unit responses to thermal stimulation of the oral cavity in the rat.

Neurophysiological responses were recorded in individual fibers of the lingual and chorda tympani nerves and in single cortical neurons in the rat in response to a battery of tactile, thermal and chemical stimuli applied to the oral cavity. Two categories of thermally sensitive units were identified. Chorda tympani fibers and one type of cortical unit ('Type I') were activated by cold water stimulation but were unaffected by warm water or menthol. In contrast, lingual fibers and a different category of cortical units ('Type II') were extremely sensitive to menthol exposure. These units were cold water sensitive, however, this sensitivity was suppressed following menthol presentation.

Pharmacological studies of facial motoneurones in the rat.

Experiments were performed on 39 male albino rats anaesthetized with pentobarbitone sodium and paralyzed with gallamine triethiodide. Facial motoneurones consistently showed a progressive alteration of spike shape and decrease in spike firing frequency during the continuous microelectrophoretic application of the excitant amino acids D,L-homocysteate, L-glutamate, L-aspartate, and kainate, but infrequently during that of N-methyl-D-aspartate. The relative potencies of these excitants on facial motoneurones are reported. The potential usefulness of N-methyl-D-aspartate to produce amino acid-evoked motoneurone action potentials is discussed. The microelectrophoretically-applied depressant amino acid antagonist strychnine selectively and reversibly blocked the depressant effects of glycine on facial motoneurones. The depression of amino acid-induced firing of facial motoneurones by stimuli to the lingual or glossopharyngeal nerves were reversibly antagonized by microelectrophoretically applied strychnine but not by bicuculline.

Characteristics of mucosal nociceptors in the rat oral cavity: an in vitro study.

Characteristics of mucosal nociceptors were investigated by recording activities from single fibers in the lingual nerve in an in vitro jaw-nerve preparation of rats. We found four subtypes of nociceptors in the medial side gingival area of the oral mucosa in the lower jaw: 11 A delta-high threshold mechanonociceptors (A delta-HTMs), 7 A delta-mechanoheat nociceptors (A delta-MHs), 21 A delta-polymodal nociceptors (A delta-POLYs) and 28 C-polymodal nociceptors (C-POLYs). Thus the majority of the nociceptors was polymodal type (ca. 73% of the recorded fibers), ca. 43% of which consisted of A delta-POLYs scarcely found in the skin but commonly found in the deep tissue, muscle or colon. In contrast to the skin, the size of the receptive field of both A delta and C polymodal types was larger than that of either A delta-HTM or A delta-MH type. The von Frey threshold of all types of mucosal nociceptor was higher than that of the skin, though their heat threshold was almost the same as that of the skin nociceptors. These results show that the mucosal nociceptors are different from the skin nociceptors in the frequency distribution of their types and certain physiological properties.

Taste prestimulation increases the chorda tympani nerve response to menthol.

Electrophysiological recordings of the summated response of the chorda tympani nerve to menthol stimulation of the tongue were obtained from 15 adult Sprague-Dawley rats. The chorda tympani nerve response to menthol was of short duration, ending within 2.5 s after stimulus onset, leaving the receptors in a state of insensitivity to subsequent menthol stimulation. Rinse durations with deionized-distilled water up to 10 min failed to bring the receptors back to their original prestimulus state. Although stimulation with menthol prevented taste receptors from responding to subsequent presentations of menthol, the chorda tympani nerve would respond normally to NaCl, NH4Cl, KCl, sodium acetate, glucose, citric acid, and quinine-HCl solutions. Prior stimulation with one of these taste solutions resulted in the recovery of the menthol response. The magnitude of the recovered menthol response depended on the magnitude of the phasic response elicited by the preceding taste stimulus. A general explanation involving possible reception and transduction mechanisms was offered to account for menthol's unexpected stimulatory effects on the chorda tympani nerve.