Types of cell culture inserts affect cell crosstalk between co-cultured macrophages and adipocytes.

Cell culture inserts offer an in vivo-like microenvironment to investigate cell-cell interactions between co-cultivated cells. However, it is unclear if types of inserts affect cell crosstalk. Here, we developed an environment-friendly cell culture insert, XL-insert, which can reduce plastic waste with lower cost. We compared XL insert with two types of commercial disposable culture inserts, Koken® insert with atelocollagen membrane (Col-inserts) and Falcon® inserts with plastic membrane (PET-inserts) on cell-cell interactions in co-cultivated THP-1 macrophages and OP9 adipocytes. Scanning electron microscope, immunoassay and imaging analysis showed that among three types of inserts, XL-inserts allowed cytokines from co-cultivated macrophages and adipocytes to diffuse freely and offered preferable in vivo-like microenvironment for cell-cell interactions. PET-inserts showed limitations for intercellular communication due to some pores being blocked by somas on the membrane that caused much lower permeability for cytokines passing through. Col-inserts blocked large sized cytokines but allowed small sized molecules to permeate resulting in improved lipid accumulation and adiponectin secretion in OP9 adipocytes. Taken together, our data demonstrated that membrane type and pore size on the membrane affect the cross-talk between co-cultivated cells very differently. Some previous co-culture studies might have different results if the inserts were changed.

Buccal Nerve Trunk Block Anesthetizes the Buccal Mucosa Beyond the Papilla of the Parotid Duct.

PURPOSE: The limited area of anesthesia of the buccal mucosa with concomitant conventional buccal nerve block (conventional BNB) may be involved in failed inferior alveolar nerve block (IANB). The aims of this study were to examine the extent of anesthesia by buccal nerve trunk block (BNTB) and compare the success rates of IANB with BNB. METHODS: This prospective parallel-group randomized single-blinded clinical trial included patients scheduled for removal of a mandibular third molar at the Nippon Dental University Hospital between September 2021 and March 2022. The primary predictor variable was the approach for BNB (BNTB vs conventional BNB). The primary outcome was the extent of tactile sensory loss and anesthesia of the buccal mucosa. The secondary outcomes included onset time and duration of BNBs and the success rate of the IANB with concomitant BNB for third molar extraction, assessed by the proportions of intraoperative pain perception and supplemental infiltration anesthesia. The other study variables were sex, age, and injection side. Comparisons were analyzed by Fisher's exact test or the Mann-Whitney U test. The P value was set to .05. RESULTS: A total of 38 patients (14 male, 24 female) with a mean age of 28.9 years (range, 18 to 67 years) were enrolled, with 19 patients each in the BNTB group and conventional BNB group. The effective tactile sensory loss rates at ∼5 mm above the height of the papilla of the parotid duct of the premolar and molar regions were greater following BNTB (71 and 95%, respectively) than following conventional BNB (37%; P < .01 and 58%; P < .01, respectively). The proportions of intraoperative pain perception of the BNTB group and the conventional BNB group were 10 and 42% (P = .06), respectively, and those of supplemental infiltration anesthesia were 5 and 26% (P = .18), respectively. CONCLUSIONS: BNTB provided a wider extent of anesthesia of the buccal mucosa than conventional BNB and may improve the anesthesia success of IANB for removal of mandibular third molars.

Usefulness of preoperative computed tomography findings for airway management in patients with acute odontogenic infection: a retrospective study.

Odontogenic infection is more likely to affect the airway and interfere with intubation than non-odontogenic causes. Although anesthesiologists predict the difficulty of intubation and determine the method, they may encounter unexpected cases of difficult intubation. An inappropriate intubation can cause airway obstruction due to bleeding and edema by damaging the pharynx and larynx. This study was performed to determine the most important imaging findings indicating preoperative selection of an appropriate intubation method. This retrospective study included 113 patients who underwent anti-inflammatory treatment for odontogenic infection. The patients were divided into two groups according to the intubation method: a Macintosh laryngoscope (45 patients) and others (video laryngoscope and fiberscope) (68 patients). The extent of inflammation in each causative tooth, the severity of inflammation (S1-4), and their influence on the airway were evaluated by computed tomography. The causative teeth were mandibular molars in more than 90%. As the severity of inflammation increased, anesthesiologists tended to choose intubation methods other than Macintosh laryngoscopy. In the most severe cases (S4), anesthesiologists significantly preferred other intubation methods (33 cases) over Macintosh laryngoscopy (9 cases). All patients with S4 showed inflammation in the parapharyngeal space, and the airway was affected in 41 patients. The mandibular molars were the causative teeth most likely to affect the airway and surrounding region. In addition to clinical findings, the presence or absence of inflammation that has spread to the parapharyngeal space on preoperative computed tomography was considered an important indicator of the difficulty of intubation.

Effects of vasopressin on anesthetic response time and circulatory dynamics of lidocaine.

This study aimed to investigate the hypothesis that vasopressin extends the anesthetic response time of lidocaine and does not affect the circulatory dynamics. Rats were sedated with isoflurane; subsequently, breathing was maintained through mechanical ventilation. We infiltrated the first molar area of the upper left jaw with saline (NS, test solution), 2% lidocaine (L), 0.025 IU vasopressin-supplemented 2% lidocaine, 0.05 IU vasopressin-supplemented 2% lidocaine, 0.1 IU vasopressin-supplemented 2% lidocaine, and 0.2 IU vasopressin-supplemented 2% lidocaine (VL4). Further, anesthetic response times were measured up to 30 min using electric pulp testing methods (n = 4). The anesthetic response times of NS, L, and VL4 were measured up to 45 min with the aforementioned results as reference values (n = 7). The circulatory dynamics of NS, L, VL4, and 0.2 IU vasopressin (V) were measured up to 45 min using a non-invasive blood pressure measuring device. VL4 extended the anesthetic response times of lidocaine compared to L (p < 0.05). Further, V and VL4 significantly increased the systolic and diastolic blood pressure and significantly decreased the pulse rate (p < 0.05). VL4 is not a suitable addition to the local anesthetic solution used in dentistry. Further study is needed to determine vasopressin concentration that extends the anesthetic effect without affecting the circulatory dynamics.

Effect of epinephrine on the distribution of ropivacaine and lidocaine using radioactive isotopes in rat maxilla and pulp.

We compared the effect of epinephrine on the distribution of ropivacaine and lidocaine by using radioactive isotopes in rat maxilla and pulp. Twenty microliters of 3H-labeled 0.5% ropivacaine, 14C-labeled 2.0% lidocaine, or epinephrine-supplemented isotopes were injected into the maxilla. The radioactivity was measured and autoradiography was obtained. Epinephrine led to increase in amounts of both anesthetics in the maxilla and pulp; however, each anesthetic did so in a different manner. Addition of epinephrine to lidocaine decreased radioactivity in maxilla and pulp with time. Conversely, when ropivacaine with epinephrine was administered, radioactivity did not change until 20 min in the maxilla and reached its peak at 20 min in the pulp. Autoradiography of lidocaine faded with time even with epinephrine use; however, with ropivacaine, higher accumulation image was observed after 20 min compared to that after 2 min. When epinephrine was combined with lidocaine, the amount of lidocaine in maxilla and pulp decreased with time, similar to when lidocaine was used alone. Conversely, when ropivacaine-epinephrine combination was administered, the amount of ropivacaine remained unchanged for 20 min in the maxilla and reached its peak at 20 min in the dental pulp.

Effect of epinephrine on the absorption of lidocaine following application to the oral mucosa in rats.

BACKGROUND: We investigated the role of epinephrine in prolonging the localization of lidocaine on the oral mucosa and inhibiting its absorption in the blood of rats. METHODS: We used 7-8-week-old pathogen-free Wistar male rats (n = 128) for our study. We divided them into the control group administered with 14C-labeled lidocaine hydrochloride gel only and the study group administered with 14C-labeled lidocaine hydrochloride gel with epinephrine. The medications were administered in the palatal mucosa of the rats. The amount of mucosa, palatine bone, and serum lidocaine was measured by radioactivity using a liquid scintillation counter and was observed using autoradiograms. RESULTS: Initially, there was no significant difference in the lidocaine levels between the lidocaine and lidocaine with epinephrine groups in the palatal mucosa (751.9 ± 133.8 vs. 669.8 ± 101.6 ng/mg [2 min]). After 4 min, the values were significantly lower in the lidocaine with epinephrine group (1040.0 ± 142.8 vs. 701.2 ± 109.0 ng/mg [20 min]). After 40 min, the lidocaine level became significantly higher in the lidocaine with epinephrine group (586.8 ± 112.4 vs. 1131.3 ± 155.2 ng/mg [40 min]). Similar results were observed in the palatine bone and serum. CONCLUSION: Epinephrine prolonged the localization of lidocaine applied to the mucosa and inhibited its absorption into the bloodstream of rats. Clinical studies are required to evaluate the use of epinephrine-containing topical anesthetics on the oral mucosa.

Effect of adding vasopressin on the distribution of lidocaine in tissues, anesthetic action, and circulatory dynamics.

We examined whether vasopressin affects the distribution, anesthesia duration, and circulatory dynamics of lidocaine. Blood flow was measured after injecting 0.003, 0.03, or 0.3 U/mL vasopressin and 2% lidocaine (L) to the upper lip of rats. Radioactivity and distribution of 14C-labeled L (CL) in the palate, palatal mucosa, maxilla bone, and blood was measured by autoradiography after injecting CL and CL + 0.03 U/mL vasopressin. To evaluate anesthesia duration, somatosensory-evoked potentials, blood pressure, and pulse rate were measured after L, 0.03 U/mL vasopressin, and L + 0.03 U/mL vasopressin injection to the palatal mucosa. Blood flow from 10 to 60 min was significantly lower with 0.03 U/mL vasopressin and L + 0.03 U/mL vasopressin than with L. Radioactivity in the palatal mucosa and maxilla bone was significantly higher at 5-60 min and 2-60 min with CL + 0.03 U/mL vasopressin than with CL. Blood radioactivity reached the maximum at 0.5 and 50 min with CL and CL + 0.03 U/mL vasopressin, respectively. Autoradiogram showed higher distribution with CL + 0.03 U/mL vasopressin than CL. Peak-to-peak amplitude 30-60 min was significantly lower with L + 0.03 U/mL vasopressin than with L. Lidocaine did not affect blood pressure and pulse rate with 0.03 U/mL vasopressin-only or combined with 2%-lidocaine. Topical 0.03 U/mL vasopressin injection reduced the tissue blood flow, promoted the localization and retention, and extended the anesthesia duration of lidocaine, leaving circulatory dynamics unaffected.

Impact of dexmedetomidine on the tissue distribution, anesthetic action, and hemodynamic effects of mepivacaine.

The present study investigated the regional blood flow, tissue distribution, local anesthetic action, and hemodynamic effects of mepivacaine containing dexmedetomidine hydrochloride (DEX) in rats. Blood flow was measured after injection of 0.5% mepivacaine (M group), 12.5 µg/ml DEX (D group), or 0.5% mepivacaine containing 12.5 µg/ml DEX (DM group) into the upper lip. Mepivacaine distribution was autoradiographically observed in maxillary bone resected after injection of 0.5% 3H-mepivacaine (HM group) or 0.5% 3H-mepivacaine containing 12.5 µg/ml DEX (DHM group) into the palatal mucosa adjacent to the right maxillary first molar. Radioactivity was also measured using a liquid scintillation counter. SEP were measured to analyze anesthetic action. Blood pressure and heart rate were measured to compare hemodynamic effect. The addition of DEX significantly decreased blood flow compared to M group from 10 to 60 min after injection. The addition of DEX significantly increased the amount of radioactivity compared to HM group in the palatal mucosa from 5 to 60 min after injection and in the body of the maxilla from 2 to 60 min after injection. Maximum blood radioactivity was measured at 5 min after injection in HM group and 50 min after injection in DHM group. The addition of DEX significantly decreased peak-to-peak amplitudes compared to M group until 60 min after injection. No significant hemodynamic differences were observed. DEX enhances the action of mepivacaine in reducing regional blood flow prolongs its tissue retention, and increases the local anesthetic action without affecting hemodynamics on local administration.

Respiratory rate is an inadequate parameter of ventilation in non-intubated sedation.

We compared the respiratory rate (RR) and transcutaneous carbon dioxide pressure ([Formula: see text]) during intravenous sedation (IVS), to determine whether RR is a useful parameter for monitoring ventilation. This was a prospective cohort study. The study sample comprised dental patients who received IVS via propofol or midazolam administration at Nippon Dental University Hospital. We simultaneously measured RR (through capnography), [Formula: see text] (using the [Formula: see text] monitor), and percutaneous oxygen saturation (SpO2). RR was the predictor and the outcome variable was [Formula: see text]. Data were analyzed by Dunnett's test and Pearson's correlation coefficient. P < 0.05 was considered statistically significant. The study sample consisted of 15 patients. No significant changes were identified in the RR and SpO2 measurements over time. However, [Formula: see text] values obtained from 20 to 40 min after induction of sedation were significantly higher than baseline values (P < 0.05). A correlation was found between RR and [Formula: see text] (P < 0.05), but the correlation coefficient was low (r = 0.22), indicating a weak correlation between these two factors. The results of this study suggest that RR is an inadequate parameter for monitoring ventilation during IVS; however, [Formula: see text] may be useful for monitoring.

Imidazoline 1 receptor activation preserves respiratory drive in spontaneously breathing newborn rats during dexmedetomidine administration.

BACKGROUND: Dexmedetomidine is an alpha-2 (α2 ) adrenoceptor and imidazoline 1 (I1 ) receptor agonist that provides sedation without loss of respiratory drive. AIMS: The aim of this study was to elucidate the involvement of α2 -adrenoceptor and I1 receptor in the cardiorespiratory changes induced by dexmedetomidine in spontaneously breathing newborn rats. METHODS: An abdominal catheter to administer drugs and three subcutaneous electrodes to record electrocardiographic data were inserted into 2- to 5-day-old Wistar rats under isoflurane anesthesia. In individual chambers, each rat was intraperitoneally administered dexmedetomidine (50 µg·kg-1 ) followed 5 min later by normal saline or 1, 5, or 10 mg·kg-1 atipamezole (selective α2 -adrenoceptor antagonist) or efaroxan (α2 -adrenoceptor/I1 receptor antagonist). Cardiorespiratory indices were recorded before and after drug administration. RESULTS: The administration of dexmedetomidine alone resulted in significant changes to most of the cardiorespiratory indices examined. The addition of 5 or 10 mg·kg-1 atipamezole or 1 mg·kg-1 efaroxan completely ameliorated the dexmedetomidine-associated reduction in heart rate (HR). The addition of 1 mg·kg-1 atipamezole or 1 or 5 mg·kg-1 efaroxan completely ameliorated the dexmedetomidine-associated reduction in respiratory frequency. Mean inspiratory flow (VT /TI ; VT is tidal volume and TI is inspiratory time), which is an index of respiratory drive, was not significantly affected by the administration of dexmedetomidine alone (P = 0.273) or dexmedetomidine + atipamezole (P = 0.605, 0.153, 0.138 for 1, 5, 10 mg·kg-1 atipamezole, respectively); however, it was significantly decreased after the administration of dexmedetomidine + efaroxan (P = 0.029, <0.001, <0.001 for 1, 5, 10 mg·kg-1 efaroxan, respectively). CONCLUSIONS: Our results suggest that in newborn rats undergoing dexmedetomidine sedation, the α2 -adrenoceptor, but not I1 receptor, is involved in the regulation of HR and respiratory frequency, and that activation of the I1 receptor plays a major role in the maintenance of respiratory drive.

Effects of adrenaline on circulatory dynamics and cardiac function in rats administered chlorpromazine.

We aimed to elucidate changes in circulatory dynamics and cardiac function during concomitant use of chlorpromazine (CPZ) and adrenaline (AD). An arterial line and left intraventricular pressure-volume measurement catheter were inserted in rats. CPZ 10 mg/kg was administered to the left great adductor muscle, followed by normal saline (NS) or AD 50 µg/kg through the tongue 20 min later. End-diastolic volume (V ed), end-systolic pressure (P es), stroke volume (SV), stroke work (SW), end-systolic volume elastance (E es), systolic blood pressure (SBP), diastolic blood pressure (DBP), and pulse rate (PR) were measured. Following AD administration, V ed significantly decreased at 2-4 and 10 min than that in control rats; P es significantly decreased at 1 min; E es significantly increased from 2 to 10 min; SV did not change significantly, and SW significantly reduced at 1 and 2 min; SBP and DBP were lower at 1-3 min than in the control; and PR increased at 10 min. These findings suggest that when AD-containing local anesthetics are administered during dental treatment of patients taking CPZ, there is a risk of a temporary drop in blood pressure. However, the blood pressure is recovered a few minutes later by the increase in afterload and the myocardial contractile force.

Dexmedetomidine (12.5 µg/mL) improves tissue distribution, anesthetic action, and hemodynamic effects of lidocaine after palatal infiltration in rats.

Dexmedetomidine hydrochloride (DEX) is a α2-adrenergic receptor agonist that causes vasoconstriction by acting on α2B-adrenergic receptors in peripheral blood vessels. The authors aimed to determine the influence of DEX on tissue distribution, anesthetic action, and hemodynamic effects of lidocaine in rats. The investigators injected indigo carmine-containing (14)C-labeled lidocaine hydrochloride (2 %) without and with 3.1, 12.5, or 50 µg/mL DEX or 10 µg/mL epinephrine into the right palatal mucosa mesial to the maxillary first molar of specific pathogen-free male Wistar rats. Autoradiography and liquid scintillation counting were performed to evaluate (14)C-labeled lidocaine concentrations in the palatal mucosa, maxillary bone, maxillary nerve, and peripheral blood. Somatosensory-evoked potentials were measured to analyze anesthetic action, and blood pressure and pulse rate were measured to compare hemodynamic effects. DEX extended the tissue distribution of lidocaine in a concentration-dependent manner. Lidocaine with 12.5 µg/mL DEX had similar blood peak arrival time and peak-to-peak amplitude as lidocaine with 10 µg/mL epinephrine, but it reduced pulse rate. The results of this study suggest that 12.5 µg/mL DEX improves tissue distribution, anesthetic action, and hemodynamic effects of lidocaine in rats. Therefore, 12.5 µg/mL DEX may be a suitable alternative to epinephrine in lidocaine formulations, especially for patients with ischemic heart disease and hypertension.

The effect of superior cervical ganglion resection on peripheral facial palsy in rats.

PURPOSE: Stellate ganglion block is performed to treat peripheral facial palsy because it increases blood flow and promotes nerve regeneration. Although stellate ganglion block increases blood flow around the facial nerve that runs outside the temporal bone, it may not affect blood flow inside the bone. Therefore, although stellate ganglion block is an effective procedure when the facial nerve is damaged outside the temporal bone, no studies have investigated the relationship between the site of nerve damage and the therapeutic effect of stellate ganglion block. Here, we investigated the efficacy of stellate ganglion block for facial palsy caused by facial nerve damage both inside and outside the temporal bone in rats. METHODS: A rat facial palsy model was created with nerve cooling that damaged the facial nerve inside or outside the temporal bone. A rat facial palsy stellate ganglion block model was also created by performing superior cervical ganglion resection on facial palsy model rats, and the duration of paralysis was examined. RESULTS: Facial nerve cooling inside and outside the temporal bone resulted in a mean duration of paralysis of 13.8 ± 1.6 days and 18.3 ± 2.2 days, respectively. Superior cervical ganglion resection in which the facial nerve had been cooled inside and outside the temporal bone reduced the mean duration of paralysis by 2.4 ± 1.3 days and 5.4 ± 1.3 days, respectively. CONCLUSION: Stellate ganglion block was more effective in facial palsy caused by damage to the facial nerve outside, rather than inside, the temporal bone.

Epinephrine Affects Pharmacokinetics of Ropivacaine Infiltrated Into Palate.

Pulpal anesthesia success rates for ropivacaine following maxillary infiltration anesthesia seem to be low. We investigated the hypothesis that the addition of epinephrine would affect the pharmacokinetics of ropivacaine by retaining ropivacaine in the mucosa of the injected area through the time-dependent distribution of ropivacaine in the rat maxilla and serum following maxillary infiltration anesthesia using (3)H-labeled ropivacaine. We then examined the vasoactivity of ropivacaine with or without epinephrine on local peripheral blood flow. The addition of epinephrine to ropivacaine increased ropivacaine concentrations in the palatal mucosa and adjacent maxilla by more than 3 times that of plain ropivacaine at 20 minutes. By observing the autoradiogram of (3)H-ropivacaine, plain ropivacaine in the maxilla was remarkably reduced 20 minutes after injection. However, it was definitely retained in the palatal mucosa, hard palate, adjacent maxilla, and maxillary nerve after the administration with epinephrine. Ropivacaine with epinephrine significantly decreased labial blood flow. This study suggests that 10 µg/mL epinephrine added to 0.5% ropivacaine could improve anesthetic efficacy and duration for maxillary infiltration anesthesia over plain ropivacaine.

Are muscle relaxants needed for nasal intubation in propofol and remifentanil anesthesia?

PURPOSE: The authors hypothesized that a muscle relaxant would have no meaningful difference in intubation conditions during nasal intubation under remifentanil and propofol anesthesia. MATERIALS AND METHODS: This parallel-group, double-blinded, randomized controlled trial included 44 patients who received saline (S group; n = 22) or rocuronium (R group; n = 22). In addition to remifentanil 0.5 µg/kg per minute and propofol 5 mg/kg per hour, propofol 0.5 mg/kg was administered until loss of consciousness. Nasal intubation was performed 10 minutes after administration of R or S 0.6 mg/kg. Significant differences in intubation conditions and salivary amylase levels before and after intubation were tested (P < .05). RESULTS: Vocal cord status (P = .003) and response to intubation or cuff filling (P = .008) were significantly different, but intubation conditions were not. Salivary amylase level was significantly lower with R administration (P = .022). No patient complained of postoperative throat pain and hoarseness. CONCLUSION: Muscle relaxants during nasal intubation performed after bolus administration of propofol 0.9 mg/kg in addition to 10 minutes of remifentanil 0.5 µg/kg per minute plus propofol 5 mg/kg per hour are unnecessary.

Enzyme-Digested Edible Bird's Nest (EBND) Prevents UV and Arid Environment-Induced Cellular Oxidative Stress, Cell Death and DNA Damage in Human Skin Keratinocytes and Three-Dimensional Epithelium Equivalents.

The aim of this study is to investigate the repressive effects of enzyme-digested edible bird's nest (EBND) on the combination of arid environment and UV-induced intracellular oxidative stress, cell death, DNA double-strand breaks (DSBs) and inflammatory responses in human HaCaT keratinocytes and three-dimensional (3D) epithelium equivalents. An oxygen radical antioxidant capacity assay showed that EBND exhibited excellent peroxyl radical scavenging activity and significantly increased cellular antioxidant capacity in HaCaT cells. When EBND was administered to HaCaT cells and 3D epitheliums, it exhibited significant preventive effects on air-drying and UVA (Dry-UVA)-induced cell death and apoptosis. Dry-UVA markedly induced intracellular reactive oxygen species (ROS) generation in HaCaT cells and 3D epitheliums as quantified by CellROX® Green/Orange reagents. Once HaCaT cells and 3D epitheliums were pretreated with EBND, Dry-UVA-induced intracellular ROS were significantly reduced. The results from anti-γ-H2A.X antibody-based immunostaining showed that EBND significantly inhibited Dry-UVA-induced DSBs in HaCaT keratinocytes. Compared with sialic acid, EBND showed significantly better protection for both keratinocytes and 3D epitheliums against Dry-UVA-induced injuries. ELISA showed that EBND significantly suppressed UVB-induced IL-6 and TNF-α secretion. In conclusion, EBND could decrease arid environments and UV-induced harmful effects and inflammatory responses in human keratinocytes and 3D epithelium equivalents partially through its antioxidant capacity.

Effects of vasopressin administration in the oral cavity on cardiac function and hemodynamics in rats.

BACKGROUND: The vasoconstrictive effect of epinephrine in local anesthetics affects the heart, which leads to hesitation among dentists in injecting local anesthetics into patients with cardiovascular disease. Due to its vasoconstrictive effects, the present study investigated the effects of vasopressin administration on cardiac function in rats. METHODS: Experiment 1 aimed to determine the vasopressin concentration that could affect cardiac function. An arterial catheter was inserted into the male Wistar rats. Next, 0.03, 0.3, and 3.0 U/mL arginine vasopressin (AVP) (0.03V, 0.3V, and 3.0V) was injected into the tongue, and the blood pressure was measured. The control group received normal saline only. In Experiment 2, following anesthesia infiltration, a pressure-volume catheter was placed in the left ventricle. Baseline values of end-systolic elastance, end-diastolic volume, end-systolic pressure, stroke work, stroke volume, and end-systolic elastance were recorded. Next, normal saline and 3.0V AVP were injected into the tongue to measure their effect on hemodynamic and cardiac function. RESULTS: After 3.0V administration, systolic blood pressures at 10 and 15 min were higher than those of the control group; they increased at 10 min compared with those at baseline. The diastolic blood pressures at 5-15 min were higher than those of the control group; they increased at 5 and 10 min compared with those at baseline. The preload decreased at 5 and 10 min compared to that at baseline. However, the afterload increased from 5 to 15 min compared with that of the control group; it increased at 10 min compared with that at baseline. Stroke volume decreased at 10 and 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. Stroke work decreased from 5 to 15 min compared with that of the control group; it decreased from 5 to 15 min compared with that at baseline. CONCLUSION: Our results showed that 3.0 U/mL concentration of vasopressin resulted in increased blood pressure, decreased stroke volume and stoke work, decreased preload and increased afterload, without any effect on myocardial contractility.

Anesthetic Management of a Patient With Catecholaminergic Polymorphic Ventricular Tachycardia.

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare inherited arrhythmogenic disorder induced by adrenergic stress. Electrophysiologically, it is characterized by emotional stress- or exercise-induced bidirectional ventricular tachycardia that may result in cardiac arrest. Minimizing perioperative stress is critical as it can reduce fatal arrhythmias in patients with CPVT. Dexmedetomidine (DEX), a centrally acting sympatholytic anesthetic agent, was used in the successful intravenous (IV) moderate sedation of a 27-year-old female patient with CPVT, a history of cardiac events, and significant dental fear and anxiety scheduled to undergo mandibular left third molar extraction. Oral surgery was successfully performed under DEX-based IV sedation to reduce stress, and no arrhythmias were observed. IV sedation with DEX provided a sympatholytic effect with respiratory and cardiovascular stability in this patient with CPVT who underwent oral surgery.

Hemodynamic Impact of Drug Interactions With Epinephrine and Antipsychotics Under General Anesthesia With Propofol.

OBJECTIVE: Antipsychotic drugs exhibit α-1 adrenergic receptor-blocking activity. When epinephrine and antipsychotic drugs are administered in combination, ß-2 adrenergic effects are thought to predominate and induce hypotension. This study aimed to assess hemodynamic parameters in patients regularly taking antipsychotics who were administered epinephrine-containing lidocaine under general anesthesia in a dental setting. METHODS: Thirty patients taking typical and/or atypical antipsychotics and scheduled for dental procedures under general anesthesia were enrolled. Five minutes after tracheal intubation, baseline systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and percutaneous oxygen saturation (SpO2) measurements were taken. The SBP, DBP, HR, and SpO2 measurements were repeated 2, 4, 6, 8, and 10 minutes after the injection of 1.8 mL of 2% lidocaine (36 mg) with 1:80,000 epinephrine (22.5 mcg) via buccal infiltration. RESULTS: Differences between the baseline measurements and those of each time point were analyzed using Dunnett test, and no statistically significant changes were observed. CONCLUSIONS: Our findings demonstrate that the use of epinephrine at a clinically relevant dose of 22.5 mcg for dental treatment under general anesthesia is unlikely to affect the hemodynamic parameters of patients taking antipsychotic medications.