[Drug Therapy for Shock-Resistant Ventricular Fibrillation: Comparison of Nifekalant and Amiodarone].

Early direct current (DC) shock is the most important therapy for ventricular fibrillation. Following the increased availability of automated external defibrillators (AED), the survival rate of cardiopulmonary arrest patients with ventricular fibrillation has improved. Although patients with shock-resistant ventricular fibrillation require additional antiarrhythmic drug therapy, the optimal protocol has not been established. Nifekalant is a pure potassium channel blocker with a pyrimidinedione structure. Nifekalant was approved in Japan for the treatment of life-threatening ventricular tachyarrhythmias in 1999, and is widely used as a class III antiarrhythmic intravenous drug. Intravenous amiodarone was approved in Japan in 2007, and exhibits various effects on ion channels, receptors, sympathetic activity, and thyroid function. Nifekalant and amiodarone also exhibit many pharmacological and pharmacodynamic differences. As nifekalant has no negative inotropic effect and a rapid action and clearance with a short half-life, it has some advantages over amiodarone for use in cardiopulmonary resuscitation. Indeed, data from clinical and animal studies suggest that nifekalant is superior to amiodarone for resuscitation of cardiopulmonary arrest resulting from shock-resistant ventricular fibrillation. A 300-mg bolus intravenous injection of amiodarone is considered an overdose for resuscitation of shock-resistant ventricular fibrillation. Further clinical studies are required to evaluate the effects of nifekalant compared with amiodarone, and to determine the optimal dose of amiodaone, for resuscitation of shock-resistant ventricular fibrillation.

[A Case of Hypoglossal Nerve Palsy after Cervical Spine Surgery].

A 46-year-old woman with cervical disc herniation underwent C4-6 laminoplasty and C4-5 foraminotomy under general anesthesia. The patient complained of the tongue deviation toward the right after surgery. She underwent several examinations and was diag- nosed as right hypoglossal nerve palsy caused by peripheral nerve disorder. It was considered that the main damage was the external branch of hypoglossal nerve which was likely to occur as a complication of compression because of the location. The cause of hypoglossal nerve palsy was assumed to be possibly direct compression of the hypoglossal nerve by the tracheal tube. In prone position surgery, it is important to take care of pressure to the tongue because the intraoral space tends to be reduced by edema of the face and neck.

Lidocaine preferentially inhibits the function of purinergic P2X7 receptors expressed in Xenopus oocytes.

BACKGROUND: Lidocaine has been widely used to relieve acute pain and chronic refractory pain effectively by both systemic and local administration. Numerous studies reported that lidocaine affects several pain signaling pathways as well as voltage-gated sodium channels, suggesting the existence of multiple mechanisms underlying pain relief by lidocaine. Some extracellular adenosine triphosphate (ATP) receptor subunits are thought to play a role in chronic pain mechanisms, but there have been few studies on the effects of lidocaine on ATP receptors. We studied the effects of lidocaine on purinergic P2X3, P2X4, and P2X7 receptors to explore the mechanisms underlying pain-relieving effects of lidocaine. METHODS: We investigated the effects of lidocaine on ATP-induced currents in ATP receptor subunits, P2X3, P2X4, and P2X7 expressed in Xenopus oocytes, by using whole-cell, two-electrode, voltage-clamp techniques. RESULTS: Lidocaine inhibited ATP-induced currents in P2X7, but not in P2X3 or P2X4 subunits, in a concentration-dependent manner. The half maximal inhibitory concentration for lidocaine inhibition was 282 ± 45 µmol/L. By contrast, mepivacaine, ropivacaine, and bupivacaine exerted only limited effects on the P2X7 receptor. Lidocaine inhibited the ATP concentration-response curve for the P2X7 receptor via noncompetitive inhibition. Intracellular and extracellular N-(2,6-dimethylphenylcarbamoylmethyl) triethylammonium bromide (QX-314) and benzocaine suppressed ATP-induced currents in the P2X7 receptor in a concentration-dependent manner. In addition, repetitive ATP treatments at 5-minute intervals in the continuous presence of lidocaine revealed that lidocaine inhibition was use-dependent. Finally, the selective P2X7 receptor antagonists Brilliant Blue G and AZ11645373 did not affect the inhibitory actions of lidocaine on the P2X7 receptor. CONCLUSIONS: Lidocaine selectively inhibited the function of the P2X7 receptor expressed in Xenopus oocytes. This effect may be caused by acting on sites in the ion channel pore both extracellularly and intracellularly. These results help to understand the mechanisms underlying the analgesic effects of lidocaine when it is administered locally at least.

Depressed production of beta-defensins from mouse splenic dendritic cells following thermal injury and its influence on susceptibility to infection.

PURPOSE: Beta-defensins (BDs) and dendritic cells (DC) have been described as major effectors on host antimicrobial innate immunities. In the present study, the ability of DC to produce BDs was explored using DC from normal mice and full-thickness (FT)-burned mice. METHODS: DCs were isolated from spleens of mice, and 1 × 10(6) cells/ml of them were cultured with LPS or SAC. Culture fluids harvested 24 h after cultivation were assayed for BD1 and BD3 and antibacterial activity (colony-counting, Pseudomonas aeruginosa). Also, DCs were tested for BD mRNAs by RT-PCR. RESULTS: Sixty-five percent of the bacterial killing activity was shown by the culture fluids of splenic DC from normal mice, while only 15 % killing activity was shown by the culture fluids of splenic DC from FT-burned mice. X-irradiated NOD SCID IL-2rγ(null) mice inoculated with splenic DC from FT-burned mice showed increased susceptibility to P. aeruginosa infection compared to those from normal mice. Mice splenic DC expressed BD1 mRNA constitutively and expressed BD3 mRNA after stimulation. These BDs were produced by mice splenic DC. As compared with DC from normal mice, DC from FT-burned mice produced decreased amounts of BD1 and BD3 in their culture fluids. CONCLUSIONS: These results indicate that (1) DC from spleens of mice have an ability to produce BDs, and (2) the production of BDs by DC is influenced strongly by thermally injured stress. Since FT-burned mice are susceptible to P. aeruginosa infection, BDs produced by DC may play an important role on the host's antibacterial resistance.

[Anesthetic management of a Dialysis Patient with Chronic Inflammatory Demyelinating Polyneuropathy].

We report the successful management of anesthesia in a 46-year-old male dialysis patient with chronic inflammatory demyelinating polyneuropathy (CIDP). He underwent an osteosynthesis of the ankle joint using general anesthesia combined with epidural anesthesia. The anesthetic concerns in patients with CIDP are the possibility of postoperative respiratory dysfunction due to anesthetics or muscle relaxants and that of postoperative neurological deterioration due to spinal or epidural anesthesia. In this case, sevoflurane (1.5-2%) did not cause respiratory dysfunction postoperatively and muscle relaxant effect of rocuronium was effectively reversed by sugammadex. Epidural anesthesia using ropivacaine (0.2-0.375%) and fentanyl did not worsen the neurological symptoms of CIDP post-operatively.

[Measurement of the Minimum Pressure in the Bronchial Cuff during One-lung Ventilation Using a Capnometer].

BACKGROUND: It is recommended to avoid overinflation of the bronchial cuff, leading to ischemic pressure damages to the respiratory mucosa and bronchial rupture. We investigated the minimum bronchial cuff pressure of 35 Fr double lumen tubes (DLTs) during one lung ventilation using a capnometer. METHODS: We studied 50 patients who were scheduled to undergo thoracic surgery. General anesthesia was induced and the patients were intubated with 35 Fr left DLT. With a fiberoptic bronchoscope, the DLT was positioned appropriately. The bronchial cuff was inflated first with air 3-3.5 ml. Lung isolation was confirmed by auscultation. Measurements were performed with the patient in the lateral position. Ventilating one lung isolatedly for 5 minutes, we confirmed non ventilated condition with a capnometer displaying flat line. The bronchial cuff was deflated 0.5-ml steps just before displaying the respiratory pattern by the capnogram. The bronchial cuff pressure and volume were recorded at this point RESULTS: The minimum pressures of bronchial cuff (volume) for one lung ventilation are for male 5.46 ± 0.6 cmH2O (2.33?0.1 ml) and for female 1.5?0.5 cmH20 (1.09 ± 0.3 ml). These values are smaller than the recommended value (< 25 cmH2O). There was no case in which the collapse of the operated lung was insufficient. CONCLUSIONS: In this study, the bronchial pressure higher than 12 cmH2O was not necessary for one lung ventilation. If high intracuff pressure is necessary to seal the bronchus, there are possibilities of the incompatibility of the size of DLT and the herniation of the bronchial cuff to the proximal side. The method of confirmation of OLV using a capnometer can display the non ventilated condition on the monitor objectively. We can thus decrease troubles during operations.

[A Case of General Anesthesia in a Patient with Spinal and Bulbar Muscular Atrophy].

We report a successful management of anesthesia in a 55-year-old male patient with spinal and bulbar muscular atrophy (SBMA). His respiratory and swallowing functions were preserved preoperatively. He underwent an osteosynthesis for a femoral neck fracture under general anesthesia using nondepolarizing muscle relaxant. The anesthetic concerns in patients with SBMA are the possibility of postoperative respiratory dysfunction due to anesthetics or muscle relaxants and that of postoperative neurological deterioration due to spinal or epidural anesthesia. In this case, the effect of an intubating dose of rocuronium (0.5 mg · kg(-1)) was markedly prolonged, but it was completely reversed by sugammadex (2 mg · kg(-1)). Postoperative course was uneventful and clinical symptoms of SBMA did not become exacerbated.

Neurosteroids allopregnanolone sulfate and pregnanolone sulfate have diverse effect on the α subunit of the neuronal voltage-gated sodium channels Nav1.2, Nav1.6, Nav1.7, and Nav1.8 expressed in xenopus oocytes.

BACKGROUND: The neurosteroids allopregnanolone and pregnanolone are potent positive modulators of γ-aminobutyric acid type A receptors. Antinociceptive effects of allopregnanolone have attracted much attention because recent reports have indicated the potential of allopregnanolone as a therapeutic agent for refractory pain. However, the analgesic mechanisms of allopregnanolone are still unclear. Voltage-gated sodium channels (Nav) are thought to play important roles in inflammatory and neuropathic pain, but there have been few investigations on the effects of allopregnanolone on sodium channels. METHODS: Using voltage-clamp techniques, the effects of allopregnanolone sulfate (APAS) and pregnanolone sulfate (PAS) on sodium current were examined in Xenopus oocytes expressing Nav1.2, Nav1.6, Nav1.7, and Nav1.8 α subunits. RESULTS: APAS suppressed sodium currents of Nav1.2, Nav1.6, and Nav1.7 at a holding potential causing half-maximal current in a concentration-dependent manner, whereas it markedly enhanced sodium current of Nav1.8 at a holding potential causing maximal current. Half-maximal inhibitory concentration values for Nav1.2, Nav1.6, and Nav1.7 were 12 ± 4 (n = 6), 41 ± 2 (n = 7), and 131 ± 15 (n = 5) µmol/l (mean ± SEM), respectively. The effects of PAS were lower than those of APAS. From gating analysis, two compounds increased inactivation of all α subunits, while they showed different actions on activation of each α subunit. Moreover, two compounds showed a use-dependent block on Nav1.2, Nav1.6, and Nav1.7. CONCLUSION: APAS and PAS have diverse effects on sodium currents in oocytes expressing four α subunits. APAS inhibited the sodium currents of Nav1.2 most strongly.

Thrombomodulin improved liver injury, coagulopathy, and mortality in an experimental heatstroke model in mice.

BACKGROUND: Heatstroke is a life-threatening illness and causes high mortality due to multiple organ injuries. Thrombomodulin (TM) is an endothelial anticoagulant cofactor that plays an important role in the regulation of intravascular coagulation. In this study, we investigated the effect of TM on the inflammatory process, liver function, coagulation status, and mortality in experimental heatstroke. METHODS: Male C3H/HeN (8-10 weeks) mice were randomly assigned to the TM-treated group (TG-Pre) or nontreated heatstroke group (HS). In group TG-Pre, mice were treated with recombinant soluble TM (1 mg/kg, intraperitoneally) before heat exposure. In some experiments, recombinant soluble TM was administrated during heat exposure (TG-Delay). Heatstroke was induced by exposure to ambient temperature of 38°C for 4 hours. After heat exposure, the levels of tumor necrosis factor-α, interleukin-6, and plasma high-mobility group box 1 (HMGB1), liver function, plasma aspartate aminotransferase and alanine aminotransferase concentrations, and immunohistochemical and histopathological characteristics of the livers were determined. The coagulation status, plasma protein C levels, and thrombin-antithrombin complex levels were also measured. RESULTS: In group HS, plasma cytokines and HMGB1 concentrations increased after heat exposure. Plasma aspartate aminotransferase and alanine aminotransferase concentrations increased after heat exposure. In group HS livers, strong and extensive immunostaining for HMGB1 was observed. In addition, there was extensive hepatocellular necrosis and collapse of nuclei observed. In group HS, plasma protein C levels were suppressed and plasma thrombin-antithrombin complex levels increased. In group TG-Pre, plasma cytokines and HMGB1 concentrations were suppressed after heat exposure compared with group HS. Liver injury, coagulopathy, and mortality also improved in group TG-Pre. Furthermore, recombinant soluble TM treatment decreased mortality even with delayed treatment. CONCLUSIONS: This study demonstrated that recombinant soluble TM suppressed plasma cytokines and HMGB1 concentrations after heat exposure. Recombinant soluble TM also improved liver injury and coagulopathy. Recombinant soluble TM treatment improved mortality even with delayed treatment. Recombinant soluble TM may be a beneficial treatment for heatstroke patients.

The endocannabinoid anandamide inhibits voltage-gated sodium channels Nav1.2, Nav1.6, Nav1.7, and Nav1.8 in Xenopus oocytes.

BACKGROUND: Anandamide is an endocannabinoid that regulates multiple physiological functions by pharmacological actions, in a manner similar to marijuana. Recently, much attention has been paid to the analgesic effect of endocannabinoids in terms of identifying new pharmacotherapies for refractory pain management, but the mechanisms of the analgesic effects of anandamide are still obscure. Voltage-gated sodium channels are believed to play important roles in inflammatory and neuropathic pain. We investigated the effects of anandamide on 4 neuronal sodium channel α subunits, Nav1.2, Nav1.6, Nav1.7, and Nav1.8, to explore the mechanisms underlying the antinociceptive effects of anandamide. METHODS: We studied the effects of anandamide on Nav1.2, Nav1.6, Nav1.7, and Nav1.8 α subunits with ß1 subunits by using whole-cell, 2-electrode, voltage-clamp techniques in Xenopus oocytes. RESULTS: Anandamide inhibited sodium currents of all subunits at a holding potential causing half-maximal current (V1/2) in a concentration-dependent manner. The half-maximal inhibitory concentration values for Nav1.2, Nav1.6, Nav1.7, and Nav1.8 were 17, 12, 27, and 40 µmol/L, respectively, indicating an inhibitory effect on Nav1.6, which showed the highest potency. Anandamide raised the depolarizing shift of the activation curve as well as the hyperpolarizing shift of the inactivation curve in all α subunits, suggesting that sodium current inhibition was due to decreased activation and increased inactivation. Moreover, anandamide showed a use-dependent block in Nav1.2, Nav1.6, and Nav1.7 but not Nav1.8. CONCLUSION: Anandamide inhibited the function of α subunits in neuronal sodium channels Nav1.2, Nav1.6, Nav1.7, and Nav1.8. These results help clarify the mechanisms of the analgesic effects of anandamide.

Comparison of nifekalant and amiodarone for resuscitation of out-of-hospital cardiopulmonary arrest resulting from shock-resistant ventricular fibrillation.

PURPOSE: Nifekalant is a pure potassium channel blocker that has been used to treat ventricular tachyarrhythmias since 1999 in Japan. Intravenous amiodarone was approved later than nifekalant in Japan, and it is still unclear which of the two agents is superior. The aim of this study was to compare the efficacy of nifekalant and amiodarone for resuscitation of out-of-hospital cardiopulmonary arrest caused by shock-resistant ventricular fibrillation. METHODS: From December 2005 to January 2011, ambulance services transported 283 out-of-hospital cardiopulmonary arrest patients to our hospital. Of these, 25 patients were treated with nifekalant or amiodarone in response to ventricular fibrillation that was resistant to two or more shocks. We undertook a retrospective analysis of these 25 patients. RESULTS: We enrolled 20 men and 5 women with a mean age (± standard deviation) of 61.1 ± 16.4 years. All 25 patients were treated with tracheal intubation and intravenous epinephrine. Fourteen patients received nifekalant and 11 patients received amiodarone. The rates of return of spontaneous circulation (ROSC) (nifekalant, 5/14, versus amiodarone, 4/11; P = 0.97) and survival to discharge (nifekalant, 4/14, versus amiodarone, 2/11; P = 0.89) were not significantly different between the two groups. The time from nifekalant or amiodarone administration to ROSC was 6.0 ± 6.6 and 20.3 ± 10.0 min, respectively, which was significantly different (P < 0.05). CONCLUSION: In this small sample size study, nifekalant, compared with amiodarone, is equally effective for ROSC and survival to discharge after shock-resistant ventricular fibrillation and can achieve ROSC more quickly. Further prospective studies are needed to confirm our results.

[A case of prolongation of rocuronium neuromuscular blockade in a pregnant patient receiving magnesium].

A 35-year-old pregnant female with systemic lupus erythematosus and lupus nephritis underwent emergency cesarean section at 24 weeks of gestation under general anesthesia. The patient had received magnesium sulfate with a diagnosis of pregnancy-induced hypertension since 20 weeks of gestation. Anesthesia was induced with thiopental 3.5 mg x kg(-1) and tracheal intubation was facilitated by administration of rocuronium 1.0 mg x kg(-1). No additional rocuronium was needed during operation. After operation, no twitch was noted on the ulnar nerve TOF monitor. The TOF returned to 4/4 at postoperative 11 hours and the patient was extubated uneventfully. When rocuronium is used to facilitate general endotracheal anesthesia in a patient for emergency cesarean delivery, it is important to recognize that magnesium may prolong neuromuscular block significantly.

[Case of sudden asystole during direct laryngoscopy].

A 78-year-old man, weighing 74 kg and 172 cm in height suddenly developed asystole during direct laryngoscopy. His heart started beating soon after chest compressions. Direct larygoscopy can stimulate the vagal nerve of the larynx. Although a gradual decrease in heart rate ordinarily occurs prior to asystole, few reports describe the sudden asystole during direct laryngoscopy. Intravenous injection of atropine could avoid the adverse event. Anesthesiologists should pay attention to the occurence of asystole and prepare for resuscitation.

Pentazocine inhibits norepinephrine transporter function by reducing its surface expression in bovine adrenal medullary cells.

(±)-Pentazocine (PTZ), a non-narcotic analgesic, is used for the clinical management of moderate to severe pain. To study the effect of PTZ on the descending noradrenergic inhibitory system, in the present study we examined the effect of [(3)H]norepinephrine (NE) uptake by cultured bovine adrenal medullary cells and human neuroblastoma SK-N-SH cells. (-)-PTZ and (+)-PTZ inhibited [(3)H]NE uptake by adrenal medullary cells in a concentration-dependent (3-100 µM) manner. Eadie-Hofstee analysis of [(3)H]NE uptake showed that both PTZs caused a significant decrease in the V(max) with little change in the apparent K(m), suggesting non-competitive inhibition. Nor-Binaltorphimine and BD-1047, κ-opioid and σ-receptor antagonists, respectively, did not affect the inhibition of [(3)H]NE uptake induced by (-)-PTZ and (+)-PTZ, respectively. PTZs suppressed specific [(3)H]nisoxetine binding to intact SK-N-SH cells, but not directly to the plasma membranes isolated from the bovine adrenal medulla. Scatchard analysis of [(3)H]nisoxetine binding to SK-N-SH cells revealed that PTZs reduced the B(max) without changing the apparent K(d). Western blot analysis showed a decrease in biotinylated cell-surface NE transporter (NET) expression after the treatment with (-)-PTZ. These findings suggest that PTZ inhibits the NET function by reducing the amount of NET in the cell surface membranes through an opioid and σ-receptor-independent pathway.

The antinociceptive effect of SNAP5114, a gamma-aminobutyric acid transporter-3 inhibitor, in rat experimental pain models.

BACKGROUND: Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the mammalian central nervous system. GABAergic transmission has an important role in regulating nociception at the spinal dorsal horn. It is terminated by rapid uptake of the neurotransmitter from the synaptic cleft into neurons and glial cells, via specific GABA transporters (GATs). Among the 4 GATs, GAT-3 has the greatest expression in central nervous system regions closely associated with nociceptive transmission, including the spinal cord. In this study, we examined the antinociceptive effect of intrathecal administration of a selective GAT-3 inhibitor, SNAP5114, on acute, inflammatory, and neuropathic pain in experimental models. METHODS: Male Sprague-Dawley rats were used to assess thermal, mechanical, and chemical nociception in the tail flick and hotplate tests, the paw pressure test, and the formalin test. A rotarod test was performed to assess motor function. Chronic constriction injury to the sciatic nerve was induced in the rats. The electronic von Frey test and the plantar test were then performed to assess mechanical allodynia and thermal hyperalgesia. SNAP5114 (10, 50, 100, or 200 µg) was administered intrathecally to examine antinociceptive activity. To confirm whether the action of SNAP5114 was mediated by GABAergic transmission, the GABAA receptor antagonist bicuculline (0.3 µg) or the GABAB receptor antagonist CGP35348 (30 µg) was administered intrathecally before 200 µg of SNAP5114 in the tail flick test, the formalin test, and the electronic von Frey test. RESULTS: Spinally applied SNAP5114 in normal rats dose-dependently prolonged withdrawal latencies in the tail flick test and suppressed the late-phase response in the formalin test. SNAP5114 did not affect motor performance. In the chronic constriction injury rats, SNAP5114 inhibited mechanical allodynia dose-dependently. The antinociceptive action of SNAP5114 was partially reversed by bicuculline or CGP35348 at doses at which the antagonist alone did not affect baseline behavioral responses. CONCLUSIONS: These results suggest that SNAP5114 exerts antinociceptive effects by activating GABAA and GABAB receptors in the spinal cord. The GAT-3 inhibitor may prove useful in treatment of various painful conditions.

[Postoperative palsies of the common peroneal nerve and the tibial nerve associated with lateral position].

A 36-year-old woman with systemic lupus erythematous secondary to diabetes underwent right total hip arthroplasty in the left lateral position. An epidural catheter was inserted at the L1-2 interspace and placed cephalad prior to induction of general anesthesia. After the operation, she complained of numbness on the dorsum and plantar of the left foot and was unable to dorsiflex and plantarflex the ankle. The symptoms persisted after discontinuation of the epidural infusion of a local anesthetic, and they became exacerbated after the second operation in the left lateral position. Electromyography and nerve conduction study revealed palsies of the left common peroneal nerve and the tibial nerve due to local compression and also showed mononeuritis multiplex. Fortunately, the symptoms disappeared completely eight months post-operation. It should be noted that lateral positioning may be at a substantial risk of perioperative peripheral neuropathy in patients with diseases causing neural disorder.

[Anesthetic management of a child with fibrodysplasia ossificans progressiva (FOP)].

General anesthesia was successfully performed in a 9-year-old boy with FOP. FOP is a very rare inherited disease of the connective tissue, characterized by progressive heterotopic ossification of skeletal muscles, tendons, and ligaments. Trauma and invasive medical procedures can induce heterotopic ossification. Anesthetic concerns for FOP patients include particular attention to airway management and susceptibility to respiratory complications. Regarding the airway management in general anesthesia, excessive stretching of the jaw and extension of the head may lead to the ankylosis of the temporo-mandibular joint and the neck stiffness. Ankylosis of the costvertebral joints induces restrictive ventilatory impairment, which causes atelectasis and lung infection in the perioperative period. Relating to anesthetic management for a child with FOP, anesthesiologists should keep in mind the prevention of exacerbation of the symptoms and subsequent impairment of activities of daily living postoperatively.

[A case of prolonged reduction in arterial oxygen saturation measured by pulse oxymetry after administering patent blue in an elderly patient].

A 93-year-old woman with a vulvar cancer was scheduled for resection of the tumor and sentinel lymph node biopsy under general anesthesia. At the beginning of the operation, a total of 20 ml of 2.5% patent blue was injected into the tumor and the surroundings to identify sentinel lymph node. After the injection, arterial oxygen saturation measured by pulse oximetry gradually dropped to 80%. The oxygen saturation recovered to the original level at 300 min post-injection, but blue pigmentation distributed throughout her body persisted until the following day. Her perioperative course was uneventful. In case of desaturation after dye injection, it is important to rule out true hypoxemia immediately by performing arterial blood gas analysis. Conversely, CO-oximetry is not necessarily useful for accurate diagnosis.

[A report of 6 cases with facial flushing, decreased arterial blood pressure and increased heart rate during thoracic surgery].

We report 6 cases with facial flushing, decreased arterial blood pressure and increased heart rate during thoracic surgery. These symptoms appeared 28 +/- 9 minutes (mean +/- SD) after the beginning of the surgery. Arterial blood pressure decreased significantly from 92/48 mmHg to 72/40 mmHg. While heart rate increased significantly from 66 to 83 beats x min(-1). Arterial blood pressure returned to the original values 22 +/- 9 minutes from the appearance of the symptoms. When facial flushing concomitant with circulatory instability occurs during lung surgery, it is important to rule out immediately anaphylactic reaction to the drugs administered and to maintain circulation appropriately.

[A case of myocardial ischemia induced by oxytocin during cesarean section].

A 38-year-old pregnant woman underwent cesarean section with combined spinal epidural anesthesia. Immediately after intravenous administration of oxytocin, she developed chest and bilateral shoulder pain. Simultaneously, face flushing and ST segment depression on electrocardiogram were observed. Her blood pressure decreased and heart rate increased. She was treated with bolus injection of phenylephrine and continuous infusion of nicorandil and noradrenaline. At the end of surgery, all the symptoms disappeared. Because oxytocin may induce myocardial ischemia probably due to coronary vasoconstriction and peripheral vasodilation, it is important for anesthesiologists to note that oxytocin should be given to patients as slowly as possible. Alternative agents such as mythylergometrine may be used safely for an individual who is susceptive to oxytocin.