Age-related decrease of cholinergic parasympathetic reflex vasodilation in the rat masseter muscle.

Skeletal muscle hemodynamics, including that in jaw muscles, is an important in their functions and is modulated by aging. Marked blood flow increases mediated by parasympathetic vasodilation may be important for blood flow in the masseter muscle (MBF); however, the relationship between parasympathetic vasodilation and aging is unclear. We examined the effect of aging on parasympathetic vasodilation evoked by trigeminal afferent inputs and their mechanisms by investigating the MBF during stimulation of the lingual nerve (LN) in young and old urethane-anesthetized and vago-sympathectomized rats. Electrical stimulation of the central cut end of the LN elicited intensity- and frequency-dependent increases in MBF in young rats, while these increases were significantly reduced in old rats. Increases in the MBF evoked by LN stimulation in the young rats were greatly reduced by hexamethonium and atropine administration. Increases in MBF in young rats were produced by exogenous acetylcholine in a dose-dependent manner, whereas acetylcholine did not influence the MBF in old rats. Significant levels of muscarinic acetylcholine receptor type 1 (MR1) and type 3 (MR3) mRNA were observed in the masseter muscle in young rats, but not in old rats. Our results indicate that cholinergic parasympathetic reflex vasodilation evoked by trigeminal afferent inputs to the masseter muscle is reduced by aging and that this reduction may be mediated by suppression of the expression of MR1 and MR3 in the masseter muscle with age.

Case report of unique anastomosis between facial and inferior alveolar arteries.

PURPOSE: Understanding anatomical variations of the facial artery and its branches is important for dental and medical practitioners. METHODS: Routine cadaveric dissection of the head and neck was performed to demonstrate the origin and branches of the facial artery. RESULTS: Facial artery emerged from a common linguofacial trunk off the external carotid artery. On the face, the facial artery first gave off a pre-masseteric branch. Immediately after, an aberrant artery emerged from the facial artery that coursed along the ramus of the mandible, which upon further dissection and examination was found to anastomose with inferior alveolar artery within the ramus of the mandible. CONCLUSIONS: We report a unique anastomosis between facial and inferior alveolar arteries, vessels that have not been previously shown to communicate. This case report may provide useful information for oral and maxillofacial surgeons as well as dentists performing inferior alveolar nerve blocks.

Minimally Invasive Approach for Resection of Masseteric Vascular Malformations.

OBJECTIVE: Vascular malformations (VMs) in the head and neck region often cause esthetic as well as functional problems for patients. Intramuscular VMs (IVM), such as those in the masseter, can cause severe facial asymmetry and typically are excised transcutaneously to facilitate wide exposure and safe dissection from the facial nerve. This requires extensive dissection, prolonged healing, and can lead to suboptimal facial scarring. METHODS: We describe the technique of resecting large IVMs of the masseter muscle in 3 patients using an entirely intraoral approach with continuous nerve monitoring and without visible facial scarring or secondary deformity. Preoperative injection of sclerotherapy was performed to reduce intra-operative bleeding and optimize resection. RESULTS: Successful excision was performed without complication in 3 patients to date. Total average operating room time was 120 minutes (range 95-145 minutes). Estimated blood loss was 213 mL (range 180-240 mL). The patients were discharged home either post-operative day (POD) 1 or 2, with 1 returning to work POD 4. Facial nerve function was normal postoperatively and no hematomas developed. Subjective masticatory function was equivalent to preoperative levels in all patients. CONCLUSIONS: Intraoral excision of VMs of the masseter muscle can be safely performed without added risk or complication. Continuous facial nerve monitoring allows minimally invasive approaches to be considered with less risk of iatrogenic facial nerve injury. We purport that this is a safe and effective method with substantially better esthetic outcomes compared with traditional transcutaneous approaches.

Blood oxygenation of masseter muscle during sustained elevated muscle activity in healthy participants.

Myofascial pain associated with temporomandibular disorders has often been linked to pathological muscle hyperactivity. As a result, localised disturbances of intramuscular blood flow could lead to a lower level of oxygen distribution, hypoxia and microcirculatory changes. To assess haemodynamic changes in the masseter muscle during sustained elevated muscle activity (SEMA). Sixteen healthy participants performed thirty 1-min bouts of SEMA with intervals of 1-min 'rest' periods between the bouts on a bite force transducer device. The participants completed three sessions with different percentage of their maximal voluntary occlusal bite force (MVOBF): 0% (no task), 10% or 40% MVOBF tasks. The order of the sessions was randomised with 1- to 2-week intervals. Haemodynamic characteristics of the masseter muscle were estimated with use of a laser blood oxygenation monitor. Tissue blood oxygen saturation (StO2 ) during SEMA was lower than during rest (P < 0·001). The relative changes in total haemoglobin (Total-Hb) and StO2 were influenced by condition (SEMA and rest) and with interactions between condition and session (0%, 10% and 40% MVOBF tasks). These results suggest that SEMA may lead to hypoxia in the masseter muscle and that the haemodynamic characteristics and muscle symptoms depend on the magnitude of muscle contractions. Overall, the present findings may help to provide better insights into relationships between jaw muscle activity, haemodynamic changes and symptom developments with implications for clinical conditions such as bruxism characterised by different levels of tooth-grinding and tooth-clenching muscle activity.

Effect of changes in end-tidal carbon dioxide tension on oral tissue blood flow during dexmedetomidine infusion in rabbits.

A decrease in arterial carbon dioxide tension induces an increase in masseter muscle blood flow and a decrease in mandibular bone marrow blood flow during general anesthesia. In addition, dexmedetomidine infusion reduces oral tissue blood flow. In this study we investigated how end-tidal carbon dioxide tension (ET-CO2 ) changes influence on oral tissue blood flow during continuous dexmedetomidine infusion in rabbits. Eleven male Japan White rabbits were anesthetized with sevoflurane. Then, ET-CO2 was set at 30 mmHg and adjusted to 40 and 60 mmHg, and heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure, common carotid artery blood flow, mandibular bone marrow blood flow, masseter muscle blood flow, and blood flow in other oral tissues were measured. Following this, the ET-CO2 was returned to 30 mmHg and dexmedetomidine was infused over 60 min. The measurements were repeated. Most parameters increased, regardless of whether or not dexmedetomidine was present, and heart rate and masseter muscle blood flow decreased in an ET-CO2 -dependent manner. Dexmedetomidine infusion suppressed ET-CO2 -dependent masseter muscle blood flow change. Masseter muscle blood flow during ET-CO2 at 30 mmHg with dexmedetomidine was the same as that during ET-CO2 at 40 mmHg without dexmedetomidine. Our findings suggest that dexmedetomidine infusion and slight hypocapnia under general anesthesia suppress an increase in masseter muscle blood flow as well as reducing mandibular bone marrow blood flow. These results may be of significance for decreasing bleeding during oral and maxillofacial surgery.

Tissue Blood Flow During Remifentanil Infusion With Carbon Dioxide Loading.

The aim of this study was to investigate the effect of changes in end-tidal carbon dioxide tension (ETCO2) during remifentanil (Remi) infusion on oral tissue blood flow in rabbits. Eight male tracheotomized Japan White rabbits were anesthetized with sevoflurane under mechanical ventilation. The infusion rate of Remi was 0.4 µg/kg/min. Carbon dioxide was added to the inspired gas to change the inspired CO2 tension to prevent changes in the ventilating condition. Observed variables were systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), heart rate (HR), common carotid artery blood flow (CCBF), tongue mucosal blood flow (TBF), mandibular bone marrow tissue blood flow (BBF), masseter muscle tissue blood flow (MBF), upper alveolar tissue blood flow (UBF), and lower alveolar tissue blood flow (LBF). The CCBF, TBF, BBF, UBF, and LBF values were increased, while MBF was decreased, under hypercapnia, and vice versa. The BBF, UBF, and LBF values were increased, while the MBF value was decreased, under hypercapnia during Remi infusion, and vice versa. The BBF, MBF, UBF, and LBF values, but not the CCBF and TBF values, changed along with ETCO2 changes during Remi infusion.

Surgical treatment of masseteric venous malformations and outcomes.

Intramuscular venous malformations are often misdiagnosed as other types of tumors with similar presentations. We describe here the typical presentation of a venous malformation within the masseter muscle, including the physical findings and imaging, and present our experience with the surgical excision of these lesions. This is a review of 10 patients with venous malformations localized to the masseter muscle who presented to our institution between 2008 and 2011. The patients included 6 females and 4 males. Of these venous malformations, 80% were noted in childhood, and the remainder manifested later in adolescence. Pain, swelling, and facial asymmetry were the presenting complaints. Magnetic resonance imaging, Doppler ultrasonography, and whole-body blood scintigraphy were used to characterize the lesions. All patients were treated by total resection of the lesion while preserving the marginal mandibular branch of the facial nerve. Magnetic resonance imaging showed the lesions to be isointense with surrounding muscle on T1-weighted images and hyperintense on T2-weighted images. Gross examination of the resected specimens revealed multicolored tissue with dilated vascular channels, frequently containing phleboliths. After the operation, all patients showed improvement in both symptoms and appearance. This improvement was sustained at a mean follow-up of 21 months. Masseteric venous malformations typically present with a pattern of clinical and imaging findings that should allow surgeons to distinguish them from other diseases in the cheek area. Complete surgical excision is a treatment option for these patients and can be performed without facial nerve injury or excessive bleeding. This procedure can result in excellent outcomes for localized intramasseteric venous malformation.

Segmental masseteric flap for dynamic reanimation of facial palsy.

The masseter muscle is one of the major chewing muscles and contributes to define facial contour. It is an important landmark for aesthetic and functional surgery and has been used for facial palsy reanimation or as source of donor motor nerve. We present an anatomic study to evaluate the possibility of using a muscle subunit for dynamic eye reanimation. Sixteen head halves were dissected under magnification to study the neurovascular distribution and determine safe muscle subunits; areas of safe/dangerous dissection were investigated. Once isolated, the arc of rotation of the muscular subunit was measured on fresh body to verify the reach to the lateral canthus. The patterns of neurovascular distribution and areas of safe dissection were identified; the anterior third of the muscle represents an ideal subunit with constant nerve and artery distribution. The muscle is too short to reach the lateral canthus; a fascia graft extension is needed. The information provided identified the main neurovascular branches and confirms the feasibility of a dynamic segmental flap. The need of efficient motor units for facial reanimation demands for different surgical options. A detailed anatomic description of the neurovascular bundle is mandatory to safely raise a functional motor subunit.

The soft tissue landmarks to avoid injury to the facial artery during filler and neurotoxin injection at the nasolabial region.

The aim of this study was to locate the course of the facial artery and to propose "the danger line" vulnerable to vascular complications following filler injection. The entire facial soft tissues were harvested from 14 Thai soft embalmed cadavers as a facial flap specimen. Measurements of the distance, the depth, and the diameter of the facial artery were done at level of the oral commissure and the nasal ala. The distance between the facial artery and the oral commissure was 15.3 ± 3.7 mm and the depth from the skin was 11.1 ± 3.1 mm. The distance between the facial artery and the nasal ala was 6.7 ± 4.4 mm and the depth was 11.6 ± 3.7 mm. The diameters of the facial artery at level of the oral commissure and the nasal ala were 2.6 ± 0.8 and 1.9 ± 0.5 mm, respectively. Maximum risk of arterial complication from dermal filler injection lateral to the oral commissure is located approximately 15 mm at the depth of 11 mm. High risk of arterial injury at the lateral nasal ala is located at 7 mm with the depth of 12 mm.

Management of intramuscular venous malformations of the masseter muscle.

Less than 1% of vasoformative tumours throughout the body occur in skeletal muscle and 15% of them arise in head and neck musculature. The masseter muscle is the most frequent site and accounts for approximately 5% of all intramuscular vascular malformations in the head and neck region. Masseteric venous malformations have a typical clinical presentation and imaging characteristics that should allow clinicians to distinguish them from other abnormalities presenting in this area. We present seven cases of these unusual intramasseteric venous malformations and the diagnosis and management of these lesions is discussed. The diagnosis was made on clinical grounds and was confirmed on MRI. All underwent surgical excision through a facelift approach and were successfully removed from within the substance of the masseter muscle with preservation of the facial nerve. Venous malformations within the masseter are rare but are easy to diagnose and can be reliably surgically excised without complications.

Roles played by histamine in strenuous or prolonged masseter muscle activity in mice.

Bruxism and/or clenching, resulting in fatigue or dysfunction of masseter muscles (MM), may cause temporomandibular disorders. Functional support of the microcirculation is critical for prolonged muscle activity. Histamine is a regulator of the microcirculation and is supplied by release from its stores and/or by de novo production via the induction of histidine decarboxylase (HDC). Interleukin (IL)-1, a cytokine involved in temporomandibular disorders, is an inducer of HDC. In the present study, we examined the roles of histamine, HDC and IL-1 in MM activity. Experiments were conducted using our R+G+ model. A mouse restrained (R+) inside a narrow cylinder (front end blocked with a thin plastic strip) gnaws away (G+) the strip to escape, with the weight reduction in the strip serving as an index of MM activity. Fexofenadine (a peripherally acting histamine H1 receptor antagonist) reduced MM activity in normal mice. Both H1 receptor-deficient and HDC-deficient mice exhibited low MM activity. Prolonged R+G+ induced HDC activity in MM. Mast cell-deficient mice exhibited strikingly low HDC induction in MM (and also in the quadriceps femoris muscle) in response to muscle activity or IL-1ß. Mast cells were present around blood vessels and nerves in the epimysium and perimysium of MM. These results, together with others reported previously, suggest that: (i) peripheral histamine supports strenuous MM activity; (ii) strenuous MM activity stimulates mast cells to release histamine and to induce HDC (which replenishes the histamine pool in mast cells, possibly mediated by IL-1); and (iii) peripheral histamine H1 receptor antagonists may be effective in treating temporomandibular disorders or preventing prolonged clenching and/or bruxism.

Experimental tooth clenching. A model for studying mechanisms of muscle pain.

The overall goal of this thesis was to broaden knowledge of pain mechanisms in myofascial temporomandibular disorders (M-TMD). The specific aims were to: Develop a quality assessment tool for experimental bruxism studies (study I). Investigate proprioceptive allodynia after experimental tooth clenching exercises (study II). Evaluate the release of serotonin (5-HT), glutamate, pyruvate, and lactate in healthy subjects (study III) and in patients with M-TMD (study IV), after experimental tooth clenching exercises. In (I), tool development comprised 5 steps: (i) preliminary decisions, (ii) item generation, (iii) face-validity assessment, (iv) reliability and discriminative validity testing, and (v) instrument refinement. After preliminary decisions and a literature review, a list of 52 items to be considered for inclusion in the tool was generated. Eleven experts were invited to participate on the Delphi panel, of which 10 agreed. After four Delphi rounds, 8 items remained and were included in the Quality Assessment Tool for Experimental Bruxism Studies (Qu-ATEBS). Inter-observer reliability was acceptable (k = 0.77), and discriminative validity high (phi coefficient 0.79; P < 0.01). During refinement, 1 item was removed; the final tool comprised 7 items. In (II), 16 healthy females participated in three 60-min sessions, each with 24- and 48-h follow-ups. Participants were randomly assigned to a repetitive experimental tooth clenching task with a clenching level of 10%, 20%, or 40% of maximal voluntary clenching force (MVCF). Pain intensity, fatigue, perceived intensity of vibration (PIV), perceived discomfort (PD), and pressure pain threshold (PPT) were measured throughout. A significant increase in pain intensity and fatigue but not in PD was observed over time. A significant increase in PIV was only observed at 40 min, and PPT decreased significantly over time at 50 and 60 min compared to baseline. In (III), 30 healthy subjects (16 females, and 14 males) participated in two sessions at a minimum interval of 1 wk. Microdialysis was done to collect 5-HT, glutamate, pyruvate, and lactate and to measure masseter muscle blood flow. Two hours after the start of microdialysis, participants were randomized to a 20-min repetitive experimental tooth clenching task (50% of MVCF) or a control session (no clenching). Pain intensity was measured throughout the experiment. Substance levels and blood flow were unaltered at all time points between sessions, and between genders in each session. Pain intensity was significantly higher after clenching in the clenching session compared to the same time point in the control session. In (IV), 15 patients with M-TMD and 15 healthy controls participated in one session and the methodology described above was used. M-TMD patients had significantly higher levels of 5-HT and significantly lower blood flows than healthy controls. No significant differences for any substance at any time point were observed between groups. Time and group had significant main effects on pain intensity. Qu-ATEBS, the 7-item evidence-based quality assessment tool, is reliable, exhibits face-validity, and has excellent discriminative validity. Tooth clenching was associated with pain, fatigue, and short-lasting mechanical hyperalgesia, but not with proprioceptive allodynia. It seems that tooth clenching is not directly related to delayed onset muscle soreness. In healthy subjects and in patients with M-TMD, levels of 5-HT, glutamate, pyruvate, and lactate were unaltered after tooth clenching. But 5-HT levels were significantly higher and blood flows significantly lower in M-TMD patients than in healthy controls at all time points. These two factors may facilitate the release, and enhance the effects, of other algesic substances that may cause pain.

Masseter tissue oxygen saturation predicts normal central venous oxygen saturation during early goal-directed therapy and predicts mortality in patients with severe sepsis.

OBJECTIVE: This study aimed to investigate, in patients with severe sepsis, the correlation between central venous oxygen saturation and tissue oxygen saturation at different levels. DESIGN: Prospective observational study. SETTING: General intensive care unit at an academic medical center in France. PATIENTS: Thirty-eight patients with underresuscitated severe sepsis and septic shock on intensive care unit admission. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: During early resuscitation according to the 6-hr bundles of the Surviving Sepsis Campaign guidelines, tissue oxygen saturation was recorded every other hour at the level of the thenar, masseter, and deltoid muscles along with central hemodynamics, arterial lactate concentrations, and central venous oxygen saturation. Over the 6-hr resuscitation period, thenar tissue oxygen saturation was consistently higher than masseter tissue oxygen saturation (p = .04) and deltoid tissue oxygen saturation (p = .002), and masseter tissue oxygen saturation was consistently higher than deltoid tissue oxygen saturation (p = .04). Receiver operating characteristic curves analyses showed that masseter tissue oxygen saturation was better predictor of central venous oxygen saturation >70% than thenar tissue oxygen saturation (area under the curve, 0.80; 95% confidence interval 0.71-0.89 vs. 0.67; 95% confidence interval 0.56-0.77; p = .02). The crude 28-day mortality was 36.8%. Receiver operating characteristic curve analysis showed that masseter tissue oxygen saturation (area under the curve 0.87; 0.75-0.98) and deltoid tissue oxygen saturation (area under the curve 0.88; 0.77-0.98) but not thenar tissue oxygen saturation (area under the curve 0.66; 0.46-0.86) or central venous oxygen saturation (area under the curve 0.56; 0.38-0.80) were strong predictors of 28-day mortality. CONCLUSIONS: This study suggested that in the early 6-hr resuscitation period, masseter tissue oxygen saturation accurately identified patients with severe sepsis and central venous oxygen saturation >70%. Both masseter tissue oxygen saturation and deltoid tissue oxygen saturation but not central venous oxygen saturation or thenar tissue oxygen saturation are strong predictors of 28-day mortality.

GABAB receptors in the NTS mediate the inhibitory effect of trigeminal nociceptive inputs on parasympathetic reflex vasodilation in the rat masseter muscle.

The present study was designed to examine whether trigeminal nociceptive inputs are involved in the modulation of parasympathetic reflex vasodilation in the jaw muscles. This was accomplished by investigating the effects of noxious stimulation to the orofacial area with capsaicin, and by microinjecting GABA(A) and GABA(B) receptor agonists or antagonists into the nucleus of the solitary tract (NTS), on masseter hemodynamics in urethane-anesthetized rats. Electrical stimulation of the central cut end of the cervical vagus nerve (cVN) in sympathectomized animals bilaterally increased blood flow in the masseter muscle (MBF). Increases in MBF evoked by cVN stimulation were markedly reduced following injection of capsaicin into the anterior tongue in the distribution of the lingual nerve or lower lip, but not when injected into the skin of the dorsum of the foot. Intravenous administration of either phentolamine or propranolol had no effect on the inhibitory effects of capsaicin injection on the increases of MBF evoked by cVN stimulation, which were largely abolished by microinjecting the GABA(B) receptor agonist baclofen into the NTS. Microinjection of the GABA(B) receptor antagonist CGP-35348 into the NTS markedly attenuated the capsaicin-induced inhibition of MBF increase evoked by cVN stimulation, while microinjection of the GABA(A) receptor antagonist bicuculline did not. Our results indicate that trigeminal nociceptive inputs inhibit vagal-parasympathetic reflex vasodilation in the masseter muscle and suggest that the activation of GABA(B) rather than GABA(A) receptors underlies the observed inhibition in the NTS.

Vascular Lesions: GLUT-1 expression as a diagnostic tool to discriminate tumors from malformations.

Vascular lesions constitute a widely heterogeneous group of tumors and malformations. For head and neck vascular anomalies, most studies have not attempted to make the differential diagnosis between true hemangiomas and vascular malformations, because an accurate diagnosis remains a challenge for physicians. The successful treatment of vascular anomalies depends on a profound knowledge of their biologic behavior and correct classification. Recently, specific immunohistochemical markers such as erythrocyte-type glucose transporter protein 1 have been described to differentiate hemangiomas from vascular malformations. This report describes 2 cases of intramuscular vascular anomalies involving the masseter muscle histologically diagnosed primarily as cavernous hemangiomas and presents the imaging and pathologic findings. Ample surgical excision was performed through an intraoral approach. Immunohistochemistry showed no uptake of glucose transporter protein 1. The literature was reviewed and the designation intramasseteric vascular malformation for this entity is proposed.

Tissue blood flow reductions induced by remifentanil in rabbits and the effect of naloxone and phentolamine on these changes.

OBJECTIVES: The purpose of this study was to investigate the effects of naloxone and phentolamine on the blood flow changes in rabbit oral tissue induced by remifentanil during sevoflurane anesthesia. MATERIALS AND METHODS: Male Japan White rabbits were anesthetized with sevoflurane under mechanical ventilation. Remifentanil was continuously infused at a rate of 0.4 µg/kg/min. Naloxone 0.01 mg/kg or phentolamine 0.01 mg/kg was administered during remifentanil infusion. Observed variables were systolic and diastolic blood pressures, mean arterial pressure, heart rate, common carotid artery blood flow, tongue mucosal blood flow, mandibular bone marrow blood flow, masseter muscle blood flow, and upper and lower alveolar tissue blood flows. The common carotid artery blood flow was monitored continuously using an ultrasonic blood flowmeter. Tongue mucosal blood flow was monitored continuously using a laser Doppler blood flowmeter. Mandibular bone marrow blood flow, masseter muscle blood flow, and upper and lower alveolar tissue blood flows were measured using a hydrogen clearance tissue blood flowmeter. One-way analysis of variance for repeated measurements followed by the Student-Newman-Keuls test was used. RESULTS: Remifentanil produced decreases in the heart rate, systolic blood pressure, and common carotid artery blood flow by about 15% and mandibular bone marrow blood flow, masseter muscle blood flow, and upper and lower alveolar tissue blood flows by about 30%. In the naloxone group, all variables recovered after naloxone administration. In contrast, in the phentolamine group, tissue blood flow recovered, whereas heart rate, systolic blood pressure, and common carotid artery blood flow did not recover after phentolamine administration. CONCLUSIONS: Remifentanil deceased oral tissue blood flow and systemic hemodynamic variables. Naloxone and phentolamine produced a recovery of oral tissue blood flow with and without systemic hemodynamic recovery, respectively.

Dexmedetomidine dose dependently decreases oral tissue blood flow during sevoflurane and propofol anesthesia in rabbits.

PURPOSE: The aim of the present study was to investigate the effect of dexmedetomidine (DEX) continuous infusion on blood flow in rabbit oral tissues during sevoflurane or propofol anesthesia. METHODS: A total of 24 male tracheotomized Japanese white rabbits were anesthetized with sevoflurane or propofol under mechanical ventilation. An initial loading dose of 6.0 µg/kg/hr DEX was administered for 10 minutes. DEX was then maintained at 0.2, 0.4, and 0.6 µg/kg/hr for 1 hour, respectively. The observed variables were systolic blood pressure, diastolic blood pressure, mean arterial pressure, heart rate, common carotid artery blood flow, tongue mucosal blood flow (TBF), mandibular bone marrow blood flow (BBF), masseter muscle blood flow (MBF), upper alveolar tissue blood flow (UBF), lower alveolar tissue blood flow (LBF), and vascular resistance for each tissue (tongue mucosal vascular resistance, mandibular bone marrow vascular resistance, masseter muscle vascular resistance, upper alveolar tissue vascular resistance, and lower alveolar tissue vascular resistance). RESULTS: The heart rate, systolic blood pressure, mean arterial pressure, common carotid artery blood flow, TBF, BBF, MBF, UBF, and LBF showed dose-dependent decreases during DEX infusion during both sevoflurane and propofol anesthesia. The decreasing ratios in TBF, BBF, MBF, UBF, and LBF were greater than those in heart rate, systolic blood pressure, mean arterial pressure, and common carotid artery blood flow. The vascular resistance of the oral tissues was increased in a dose-dependent manner during DEX infusion in both sevoflurane and propofol anesthesia. CONCLUSION: Our findings suggest that infusion of DEX decreases TBF, BBF, MBF, UBF, and LBF in a dose-dependent manner without significant changes in systemic hemodynamic variables during sevoflurane or propofol anesthesia.

Transposition of the hemimasseteric muscle for dynamic rehabilitation of facial paralysis.

BACKGROUND: The masseter muscle is one of the muscles involved in mastication. Transposition of this muscle has been used for dynamic reanimation of facial palsy since the early years of the 20th century. We present an anatomic study of the masseter muscle and its neurovascular bundle to determine the possibility of using hemimasseteric transposition of the muscle for the rehabilitation of facial paralysis. METHODS: Six white fresh cadavers were used to study the masseter nerve and the vascular supply to the masseteric muscle. Dissection was performed in each hemiface of each specimen. All the masseter nerve bundles were dissected to study their distribution. ANATOMIC STUDY: A constant anatomy was examined in all the specimens dissected. Dissection was performed inside the muscle body to expose the whole masseter nerve and its branches. A tree-like design of the nerve branches was observed. Each nerve branch was accompanied by its corresponding vascular pedicle, which guaranteed the vascular supply to the muscle divisions. CONCLUSIONS: The knowledge of the anatomy of the masseter nerve and its vascular supply is the key to preventing nerve damage when the muscle is split for facial reanimation. The possibility of selecting the bundle included in the transposed section of the muscle could be used for dynamic reanimation of the paralyzed face.

Topography of the arteries supplying the masseter muscle: Using dissection and Sihler's method.

Various surgical procedures require surgeons to have detailed knowledge of the course of blood vessels in the masseter muscle, such as masseter muscle flap formation, mandibular angle resection, parotidectomy, and mandibular ramus osteotomy. Without this knowledge serious complications can occur, endangering the lives of patients. Occasionally, during routine dissections we sometimes encounter an additional branch. The purpose of this study was to provide a comprehensive detailed anatomic description of the blood supply of the masseter muscle. This will provide critical information for various surgical procedures. Twenty-five Korean cadavers were dissected and subjected to modified Sihler's method to reveal the branching patterns of the arteries surrounding the masseter muscle, and its intramuscular blood supply. The masseter can be supplied by seven branches from the external carotid artery. Among these, the masseteric branch from the deep temporal artery has not been described previously. This previously undescribed branch enters the medial surface of the masseter, turning medially around the anterior border of the ramus immediately after the branching point of the deep temporal artery. The branch originating from the transverse facial artery was the largest, and the branches originating from the external carotid artery and deep temporal artery were the smallest. Examination of intramuscular patterns revealed that the branches of the transverse facial artery were the most widely distributed. When considering arterial diameters and distribution areas, the branches of the transverse facial artery can be considered the main components of the seven branches supplying the masseter muscle.

Large-dose epinephrine reduces skeletal muscle blood flow under general anesthesia in rabbits.

The goal of this study was to investigate the effect of an epinephrine continuous infusion on muscle blood flow in rabbits. Sixteen male Japan White rabbits were randomly allocated to 1 of 2 groups: epinephrine continuous infusion at 0.01 µg/kg/min (Ep-0.01 group, n = 8) and at 0.1 µg/kg/ min (Ep-0.1 group, n = 8). The observed variables were heart rate, femoral artery blood pressure, common carotid artery blood flow (CCBF), masseter muscle blood flow (MBF), and quadriceps muscle blood flow (QBF). In the Ep-0.01 group, CCBF, MBF, and QBF were increased by 14, 22, and 21% from respective control values. In contrast, in the Ep-0.1 group, CCBF, MBF and QBF were decreased by 10, 30, and 27% from respective control values. There were no differences in the percentage change between MBF and QBF during epinephrine continuous infusion. Positive correlations were observed between CCBF and MBF and between CCBF and QBF. In conclusion, skeletal muscle blood flow was increased during the small-dose epinephrine infusion, whereas it was decreased during large-dose infusion.