[Case of bronchial obstruction by thrombosis after cardiopulmonary bypass].

A 78-year-old man underwent total arch replacement for an aortic arch aneurysm under cardiopulmonary bypass. After protamine sulfate administration, his peak inspiratory pressure suddenly rose, and his arterial oxygen saturation dropped. We checked his bronchus with a bronchoscope and found that his left main bronchus was blocked by a large thrombus. We tried to remove the thromus with suction via the bronchoscope channel, but it was too large to pick out. We had no way to perform this removal, and we called a respiratory specialist who performed the removal. The size, shape and time of onset suggested that the thrombus had been formed by residual blood left after administration of protamine. This case indicated that residual blood in the bronchus should be cheeked carefully after cardiopulmonary bypass.

Direct negative chronotropic action of desflurane on sinoatrial node pacemaker activity in the guinea pig heart.

BACKGROUND: Desflurane inhalation is associated with sympathetic activation and concomitant increase in heart rate in humans and experimental animals. There is, however, little information concerning the direct effects of desflurane on electrical activity of sinoatrial node pacemaker cells that determines the intrinsic heart rate. METHODS: Whole-cell patch-clamp experiments were conducted on guinea pig sinoatrial node pacemaker cells to record spontaneous action potentials and ionic currents contributing to sinoatrial node automaticity, namely, hyperpolarization-activated cation current (If), T-type and L-type Ca currents (ICa,T and ICa,L, respectively), Na/Ca exchange current (INCX), and rapidly and slowly activating delayed rectifier K currents (IKr and IKs, respectively). Electrocardiograms were recorded from ex vivo Langendorff-perfused hearts and in vivo hearts. RESULTS: Desflurane at 6 and 12% decreased spontaneous firing rate of sinoatrial node action potentials by 15.9% (n = 11) and 27.6% (n = 10), respectively, which was associated with 20.4% and 42.5% reductions in diastolic depolarization rate, respectively. Desflurane inhibited If, ICa,T, ICa,L, INCX, and IKs but had little effect on IKr. The negative chronotropic action of desflurane was reasonably well reproduced in sinoatrial node computer model. Desflurane reduced the heart rate in Langendorff-perfused hearts. High concentration (12%) of desflurane inhalation was associated with transient tachycardia, which was totally abolished by pretreatment with the ß-adrenergic blocker propranolol. CONCLUSIONS: Desflurane has a direct negative chronotropic action on sinoatrial node pacemaking activity, which is mediated by its inhibitory action on multiple ionic currents. This direct inhibitory action of desflurane on sinoatrial node automaticity seems to be counteracted by sympathetic activation associated with desflurane inhalation in vivo.

Remifentanil has a minimal direct effect on sinoatrial node pacemaker activity in the Guinea pig heart.

BACKGROUND: Whereas remifentanil administration is associated with severe bradycardia, it has yet to be fully investigated whether the negative chronotropic action of remifentanil is mediated by its direct action on sinoatrial (SA) node pacemaker activity in the heart versus indirect results of enhanced vagal activity. METHODS: We examined the effects of remifentanil and fentanyl on the spontaneous action potentials of guinea pig SA node cells at concentrations of 5, 10, 100, and 1000 nM using the amphotericin B-perforated whole-cell patch-clamp technique. Isolated guinea pig hearts were perfused in a Langendorff mode with 5, 10, 100, and 1000 nM remifentanil. RESULTS: The spontaneous firing rate and diastolic depolarization rate (DDR) of the SA node action potentials were 189.1 ± 14.8 /min and 74.1 ± 2.9 mV/s (n = 8), respectively, under control conditions, and were not significantly affected by exposure to 5 nM (P = 1.0 for both spontaneous firing rate and DDR; n = 6), 10 nM (P = 0.62 for spontaneous firing rate, P = 0.99 for DDR; n = 6), or 100 nM (P = 0.23 for spontaneous firing rate, P = 0.38 for DDR; n = 6) remifentanil. However, 1000 nM remifentanil modestly but significantly decreased the spontaneous firing rate (P = 0.0087) and DDR (P = 0.0072, n = 6). Remifentanil did not affect the heart rate of isolated Langendorff-perfused guinea pig hearts at concentrations of 5 nM (P = 0.98), 10 nM (P = 0.35), or 100 nM (P = 0.24) but significantly reduced the heart rate at 1000 nM (P < 0.0001). Fentanyl did not affect the spontaneous firing rate and DDR at concentrations of 5 nM (P = 1.0 for both spontaneous firing rate and DDR) and 10 nM (P = 0.62 for spontaneous firing rate, P = 0.79 for DDR), but it significantly reduced both at 100 nM (P = 0.00038 for spontaneous firing rate, P = 0.0080 for DDR) and 1000 nM (P < 0.0001 for both spontaneous firing rate and DDR). CONCLUSIONS: Clinically relevant concentrations (nanomolar order concentrations) of remifentanil do not produce significant direct effects on intrinsic cardiac automaticity; thus, suggesting that remifentanil-induced bradycardia in the clinical setting is independent of its direct cardiac effects.

Intradiscal pulsed radiofrequency for chronic lumbar discogenic low back pain: a one year prospective outcome study using discoblock for diagnosis.

BACKGROUND: Discogenic pain is an important cause of low back pain (LBP). We have developed a pulsed radiofrequency (PRF) technique, using Diskit II needles (NeuroTherm, Middleton, MA, USA) placed centrally in the disk, for applying radiofrequency current in the disc (Intradiscal PRF method). OBJECTIVE: The purpose of this study was to investigate the effect of this intradiscal pulsed radiofrequency method in patients with chronic discogenic LBP diagnosed by discoblock, in terms of pain relief and reduction of disability. STUDY DESIGN: Prospective case series clinical outcome study. METHODS: The participants consisted of 23 patients with a mean age of 35.3 ± 9.86 years with chronic discogenic LBP that was not responsive to aggressive nonoperative care. A Diskit II needle (15-cm length, 20G needle with a 20-mm active tip) was placed centrally in the disc. PRF was applied for 15 minutes at a setting 5x5 ms/s and 60 V. Outcome measures included the pain intensity score on a 0-10 numeric rating scale (NRS) and the Roland-Morris Disability Questionnaire (RMDQ) at pre-treatment, one, 3, 6, and 12 months post-treatment. RESULTS: The mean pain severity scores (NRS) improved significantly from 7.47 ± 0.85 pre-treatment to 3.13 ± 2.58 at the 12 month follow-up (P < 0.01). The RMDQ showed significant (P < 0.01) improvement from 11.4 ± 1.57 pre-treatment to 2.90 ± 2.97 at the 12 month follow-up (P < 0.01). Nineteen of 23 (82.6%) of the patients demonstrated NRS improvements of greater than 2, and 15 of 23 (65.2%) had > 50% pain reduction, 12 months after treatment. LIMITATIONS: The number of patients was relatively low and secondary outcomes such as medication requirement or psychological effects were not addressed. CONCLUSIONS: This intradiscal PRF method with consecutive PRF 5/5/60V, 15 min (with Diskit needle) appears to be a safe, minimally invasive treatment option for patients with chronic discogenic LBP.

Sevoflurane protects ventricular myocytes against oxidative stress-induced cellular Ca2+ overload and hypercontracture.

BACKGROUND: Oxidative stress is implicated in pathogenesis of cardiac reperfusion injury, characterized by cellular Ca overload and hypercontracture. Volatile anesthetics protect the heart against reperfusion injury primarily by attenuating Ca overload. This study investigated electrophysiological mechanisms underlying cardioprotective effects of sevoflurane against oxidative stress-induced cellular injury. METHODS: The cytosolic Ca levels and cell morphology were assessed in mouse ventricular myocytes, using confocal fluo-3 fluorescence imaging, whereas membrane potentials and L-type Ca current (ICa,L) were recorded using whole-cell patch-clamp techniques. Phosphorylation of Ca/calmodulin-dependent protein kinase II was examined by Western blotting. RESULTS: Exposure to H2O2 (100 µM) for 15 min evoked cytosolic Ca elevation and hypercontracture in 56.8% of ventricular myocytes in 11 experiments, which was partly but significantly reduced by nifedipine, tetracaine, or SEA0400. Sevoflurane prevented H2O2-induced cellular Ca overload in a concentration-dependent way (IC50 = 1.35%). Isoflurane (2%) and desflurane (10%) also protected ventricular myocytes by a degree similar to sevoflurane (3%). Sevoflurane suppressed H2O2-induced electrophysiological disturbances, including early afterdepolarizations, voltage fluctuations in resting potential, and abnormal automaticities. H2O2 significantly enhanced ICa,L by activating Ca/calmodulin-dependent protein kinase II, and subsequent addition of sevoflurane, isoflurane, or desflurane similarly reduced ICa,L to below baseline levels. Phosphorylated Ca/calmodulin-dependent protein kinase II increased after 10-min incubation with H2O2, which was significantly prevented by concomitant administration of sevoflurane. CONCLUSIONS: Sevoflurane protected ventricular myocytes against H2O2-induced Ca overload and hypercontracture, presumably by affecting multiple Ca transport pathways, including ICa,L, Na/Ca exchanger and ryanodine receptor. These actions appear to mediate cardioprotection against reperfusion injury associated with oxidative stress.

Involvement of peripheral NMDA receptor in melittin-induced thermographic flare.

Intradermal injection of an active compound of European honeybee toxin, melittin, into the forearm in humans produces temporary pain and evokes sustained increase of local skin temperature. This increase of skin temperature is suppressed by the pretreatment of a voltage gated sodium channel blocker, lidocaine, suggesting that neurogenic inflammation is involved in the skin temperature increase after the melittin treatment. In this study, we tested a hypothesis that the melittin-induced skin temperature increase is augmented by an N-methyl-D-aspartate (NMDA) glutamate receptor that is present on the peripheral terminals of cutaneous primary afferents. Skin temperature was examined after the local application of incremental doses of melittin by a computer-assisted-thermography in pentobarbital-anesthetized rats. Local subcutaneous glutamate was collected through a microdialysis probe and glutamate levels were measured by a high pressure liquid chromatography with electrochemical detection method. Intraplantar injection of melittin resulted in the increase of subcutaneous glutamate levels and the increase of local skin temperature, which was partially attenuated by co-injection of an NMDA receptor antagonist, MK-801. In addition, intraplantar injection of NMDA itself increased the local skin temperature. Our data suggest that melittin-induced increase of skin temperature is enhanced through the activation of peripheral NMDA receptors by locally released glutamate. We suggest that topical administration of NMDA receptor antagonists could be an effective treatment of neuro-inflammatory pain.

Results of intradiscal pulsed radiofrequency for lumbar discogenic pain: comparison with intradiscal electrothermal therapy.

BACKGROUND: We have developed an intradiscal pulsed radiofrequency (Disc PRF) technique, using Diskit II® needles (NeuroTherm, Wilmington, MA, USA), as a minimally invasive treatment option for chronic discogenic low back pain (LBP). The purpose of this study was to compare the representative outcomes of Disc PRF and Intradiscal Electrothermal Therapy (IDET) in terms of pain relief and reduction of disability. METHODS: Thirty-one patients with chronic discogenic LBP who underwent either Disc PRF (n = 15) or IDET (n = 16) were enrolled in the study. A Diskit II® needle (15-cm length, 20-gauge needle with a 20-mm active tip) was placed centrally in the disc. PRF was applied for 15 min at a setting of 5 × 50 ms/s and 60 V. The pain intensity score on a 0-10 numeric rating scale (NRS) and the Roland-Morris Disability Questionnaire (RMDQ) were assessed pretreatment and at 1, 3, and 6 months post-treatment. RESULTS: The mean NRS was significantly improved from 7.2 ± 0.6 pretreatment to 2.5 ± 0.9 in the Disc PRF group, and from 7.5 ± 1.0 to 1.7 ± 1.5 in the IDET group, at the 6-month follow-up. The mean RMDQ also showed significant improvement in both the Disc PRF group and the IDET group at the 6-month follow-up. There were no significant differences in the pretreatment NRS and RMDQ scores between the groups. CONCLUSIONS: Disc PRF appears to be an alternative to IDET as a safe, minimally invasive treatment option for patients with chronic discogenic LBP.

Percutaneous intradiscal high-pressure injection of saline and lidocaine in patients with lumbar intervertebral disc extrusion.

The intradiscal high-pressure injection of saline and lidocaine (IDHP) is a minimally invasive percutaneous procedure for a lumbar intervertebral disc extrusion. The purpose of this study was to investigate the clinical outcomes of IDHP in terms of pain relief, reduction of disability, and risk of complications. Thirty patients with primarily radicular pain due to an extrusion-type disc herniation who underwent IDHP were enrolled in the study. A visual analogue pain scale (VAS) and the Japanese Orthopedic Association (JOA) scoring system for the treatment of low back disorders were used at pre-treatment, 2 weeks post-treatment, and 3 months post-treatment. The mean VAS decreased significantly (p < 0.01) from 64.3 mm at pre-treatment to 26.3 mm at 2 weeks post-treatment and 15.5 at 3 months post-treatment. The mean JOA score improved significantly (p < 0.01) from 14.7 to 21.3 at 2 weeks post-treatment and 24.6 at 3 months post-treatment. IDHP appeared to produce significant effects in patients with radicular pain, leading to the improvement of VAS and JOA scores. IDHP appears to be a safe, minimally invasive treatment option for a lumbar intervertebral disc extrusion.

The results of percutaneous intradiscal high-pressure injection of saline in patients with extruded lumbar herniated disc: comparison with microendoscopic discectomy.

OBJECTIVES: Intradiscal high-pressure injection of saline (IDHP) is a noninvasive procedure for a lumbar intervertebral disc extrusion and an alternative treatment to surgery, such as microendoscopic discectomy (MED). The purpose of this study was to compare the representative outcomes of IDHP with MED in terms of pain relief, reduction of disability, and risk of complications. METHODS: Forty-five patients with primarily radicular pain due to an extrusion type disc herniation who underwent either IDHP (N = 24) or MED (N = 21) were enrolled in the study. The visual analog pain scale (VAS) and the Japanese Orthopedic Association (JOA) scoring system for the treatment of low-back disorders were assessed at pretreatment, 2 weeks posttreatment, and JOA was again taken 3 months posttreatment. Patients were asked to choose their satisfaction from four alternatives, "excellent,""good,""fair," and "poor," 3 months after treatment. RESULTS: Mean VAS decreased from 65.1 to 18.8 mm in the IDHP group, and from 80.6 to 16.5 in the MED group. Mean JOA recovery rates at 3 months posttreatment were 67.2 and 75.2, and patients with "excellent" or "good" results were 73.7% and 78.6% in the IDHP and in MED, respectively. CONCLUSIONS: IDHP produced significant effects on patients with radicular pain, leading to the improvement of VAS and JOA. Although IDHP displayed slightly less efficacy than MED, IDHP appears to be an alternative as a nonoperative treatment for a lumbar intervertebral disc extrusion.

[Left ventricular migrating thrombus detected by intraoperative transesophageal echocardiography].

Transesophageal echocardiography (TEE) helps detecting intra-cavity thrombus size, mobility and fragility, which are of great importance in surgical removal of the thrombus. Thrombus characteristics may render surgical thrombectomy incomplete, raising the risk of catastrophic embolization. A 50-year-old man, suffering from congestive heart failure, developed a mobile thrombus in the left ventricle (LV). He was scheduled for a LV thrombectomy. TEE showed two thrombi on the apical side of the left ventricle, measuring 2.1 x 1.3 cm and 2.1 x 1.0 cm each. A surgical removal of these thrombi was performed under cardiopulmonary bypass (CPB). Just before separation from CPB, TEE detected a high echogenic mass in the LV Surgical re-explorations found residual thrombi, whose size, figure and echo signal strength resembled papillary muscles. This experience leads us to advocate repeated search for thrombi using TEE scans, in order to facilitate complete removal of thrombi prior to closing the ventriculotomy, and prior to weaning from CPB.

Inhibitory effects of sevoflurane on pacemaking activity of sinoatrial node cells in guinea-pig heart.

BACKGROUND AND PURPOSE: The volatile anaesthetic sevoflurane affects heart rate in clinical settings. The present study investigated the effect of sevoflurane on sinoatrial (SA) node automaticity and its underlying ionic mechanisms. EXPERIMENTAL APPROACH: Spontaneous action potentials and four ionic currents fundamental for pacemaking, namely, the hyperpolarization-activated cation current (I(f) ), T-type and L-type Ca²âº currents (I(Ca,T) and I(Ca,L) , respectively), and slowly activating delayed rectifier K⁺ current (I(Ks) ), were recorded in isolated guinea-pig SA node cells using perforated and conventional whole-cell patch-clamp techniques. Heart rate in guinea-pigs was recorded ex vivo in Langendorff mode and in vivo during sevoflurane inhalation. KEY RESULTS: In isolated SA node cells, sevoflurane (0.12-0.71 mM) reduced the firing rate of spontaneous action potentials and its electrical basis, diastolic depolarization rate, in a qualitatively similar concentration-dependent manner. Sevoflurane (0.44 mM) reduced spontaneous firing rate by approximately 25% and decreased I(f) , I(Ca,T) , I(Ca,L) and I(Ks) by 14.4, 31.3, 30.3 and 37.1%, respectively, without significantly affecting voltage dependence of current activation. The negative chronotropic effect of sevoflurane was partly reproduced by a computer simulation of SA node cell electrophysiology. Sevoflurane reduced heart rate in Langendorff-perfused hearts, but not in vivo during sevoflurane inhalation in guinea-pigs. CONCLUSIONS AND IMPLICATIONS: Sevoflurane at clinically relevant concentrations slowed diastolic depolarization and thereby reduced pacemaking activity in SA node cells, at least partly due to its inhibitory effect on I(f) , I(Ca,T) and I(Ca,L) . These findings provide an important electrophysiological basis of alterations in heart rate during sevoflurane anaesthesia in clinical settings.

[Evaluation of the side effects of intravenous patient controlled analgesia after spine surgery].

BACKGROUND: We have adopted intrravenous patient controlled analgesia (IV-PCA) for spine surgery. We could not find reports about detailed examinations of the side effects of IV-PCA using morphine after spine surgery, so we investigated retrospectively side effects in cases using morphine IV-PCA. METHODS: Eighty-five patients underwent IV-PCA after spine surgery. The contents of PCA pump were morphine 20 mg (= 2 ml), droperidol 2 mg (= 0.8 ml), and saline 77 ml. We fixed continuous infusion at 2 ml x hr(-1), bolus infusion at 2 ml x hr(-1), and lockout time at 15 minutes. Respiration time, SpO2, blood pressure, pulse rate, nausea and vomiting, and VAS were monitored while IV-PCA was in use. When severe side effects were noticed, IV-PCA was discontinued by physician in charge. We judged discontinuation of IV-PCA as occurrence of severe side effects. RESULTS: IV-PCA was discontinued in seven patients. The causes of discontinuation were nausea and vomiting, hypotension, and bradycardia. Nausea and vomiting was the most common cause and found mostly in women. CONCLUSIONS: Because IV-PCA was discontinuated in 8.2% of patients, it was thought that its management depending on patients' personal state was necessary to utilize IV-PCA as a method of postoperative analgesia.

Sevoflurane protects ventricular myocytes from Ca2+ paradox-mediated Ca2+ overload by blocking the activation of transient receptor potential canonical channels.

BACKGROUND: Volatile anesthetics produce cardioprotective action by attenuating cellular Ca2+ overload. The Ca2+ paradox is an important model for studying the mechanisms associated with Ca2+ overload-mediated myocardial injury, and was recently found to be mediated by Ca2+ entry through the transient receptor potential canonical channels upon Ca2+ repletion. This study investigated the effect of sevoflurane on cellular mechanisms underlying the Ca2+ paradox. METHODS: The Ca2+ paradox was examined in fluo-3 or mag-fluo-4-loaded mouse ventricular myocytes using confocal laser scanning microscope, upon Ca2+ repletion after 15 min of Ca2+ depletion in the absence and presence of sevoflurane. RESULTS: The Ca2+ paradox was evoked in approximately 65% of myocytes upon Ca2+ repletion, as determined by an abrupt elevation of cytosolic Ca2+ accompanied by hypercontracture. The Ca2+ paradox was significantly suppressed by sevoflurane administered for 3 min before and during Ca2+ repletion (Post) or during Ca2+ depletion and repletion (Postlong), and Postlong was more beneficial than Post application. The sarcoplasmic reticulum Ca2+ levels gradually decreased during Ca2+ depletion, and the Ca2+ paradox was readily evoked in myocytes with reduced sarcoplasmic reticulum Ca2+ levels. Postlong but not Post application of sevoflurane prevented decrease in sarcoplasmic reticulum Ca2+ levels by blocking Ca2+ leak through ryanodine receptors. Whole cell patch-clamp recordings revealed that sevoflurane rapidly blocked thapsigargin-induced transient receptor potential canonical currents. CONCLUSIONS: Sevoflurane protects ventricular myocytes from Ca2+ paradox-mediated Ca2+ overload by blocking transient receptor potential canonical channels and by preventing the decrease in sarcoplasmic reticulum Ca2+ levels, which is associated with less activation of transient receptor potential canonical channels.

[Antihypertensive drugs].

Lately, treatment for hypertension has changed in Japan, according to Japanese Society of Hypertension Guideline 2000 (JSH 2000). We present the characteristics of antihypertensive drugs, and directions for their preoperative use.

[Steroids].

We sometimes encounter preoperative patients with steroid treatment. These patients require steroid cover around the operative period because their adrenal cortical function is suppressed. Steroid supplementing therapy has changed since a generation ago. Therefore, steroid treatment is one of the items that anesthegiologists must study immediately.

Ca2+ paradox injury mediated through TRPC channels in mouse ventricular myocytes.

BACKGROUND AND PURPOSE The Ca(2+) paradox is an important phenomenon associated with Ca(2+) overload-mediated cellular injury in myocardium. The present study was undertaken to elucidate molecular and cellular mechanisms for the development of the Ca(2+) paradox. EXPERIMENTAL APPROACH Fluorescence imaging was performed on fluo-3 loaded quiescent mouse ventricular myocytes using confocal laser scanning microscope. KEY RESULTS The Ca(2+) paradox was readily evoked by restoration of the extracellular Ca(2+) following 10-20 min of nominally Ca(2+)-free superfusion. The Ca(2+) paradox was significantly reduced by blockers of transient receptor potential canonical (TRPC) channels (2-aminoethoxydiphenyl borate, Gd(3+), La(3+)) and anti-TRPC1 antibody. The sarcoplasmic reticulum (SR) Ca(2+) content, assessed by caffeine application, gradually declined during Ca(2+)-free superfusion, which was further accelerated by metabolic inhibition. Block of SR Ca(2+) leak by tetracaine prevented Ca(2+) paradox. The Na(+) /Ca(2+) exchange (NCX) blocker KB-R7943 significantly inhibited Ca(2+) paradox when applied throughout superfusion period, but had little effect when added for a period of 3 min before and during Ca(2+) restoration. The SR Ca(2+) content was better preserved during Ca(2+) depletion by KB-R7943. Immunocytochemistry confirmed the expression of TRPC1, in addition to TRPC3 and TRPC4, in mouse ventricular myocytes. CONCLUSIONS AND IMPLICATIONS These results provide evidence that (i) the Ca(2+) paradox is primarily mediated by Ca(2+) entry through TRPC (probably TRPC1) channels that are presumably activated by SR Ca(2+) depletion; and (ii) reverse mode NCX contributes little to the Ca(2+) paradox, whereas inhibition of NCX during Ca(2+) depletion improves SR Ca(2+) loading, and is associated with reduced incidence of Ca(2+) paradox in mouse ventricular myocytes.

[Anesthetic management for laparoscopic resection of adrenal pheochromocytoma in a woman with chronic renal failure].

A 52-year-old woman, undergoing hemodialysis for chronic renal failure over thirty years, developed pheochromocytoma. Her serum concentrations of noradrenaline (NA) and adrenaline were 5,330 pg x ml(-1) and 212 pg x ml(-1), respectively. She had often developed hypertensive crisis and also hypotensive crisis during hemodialysis, and quite often she had to give up continuing hemodialysis before its end. Anesthesia was induced by propofol, remifentanil and maintained with oxygen, air, propofol and remifentanil. Before starting operation, continuous hemodiafiltration (CHDF) was performed without any water removal. Although hypotension occurred temporarily after CHDF, severe hemodynamic changes were not observed during operation owing to NA substitution and infusion of 5% plasma protein fraction, and the operation was finished uneventfully. The molecular weight of NA is 169.18, and it can be filtered by CHDF. Because of removal of excessive NA by CHDF, we can avoid severe hemodynamic changes often observed in other case reports. CHDF was useful for anesthetic management of a patient with adrenal pheochromocytoma.

[Significance of computer crossmatching in anesthesiology].

We introduced a computer crossmatching system into our institution in June 2002. This method gives a great advantage for anesthesiologists by being able to provide adequate blood within five minutes after ordering using this system. We have adapted all cases for transfusion (around 97% of all transfusions), including not only scheduled but also emergent cases to the system in our institution. We have experienced no clinical problems by the introduction of the system from 2002 to 2007. Because the system provides many advantages for various related aspects, for example, decreasing blood disposal and labor saving for laboratory technicians, we expect that the system will be used widely.

Noble gas binding to human serum albumin using docking simulation: nonimmobilizers and anesthetics bind to different sites.

BACKGROUND: Nonimmobilizers are structurally similar to anesthetics, but do not produce anesthesia at clinically relevant concentrations. Xenon, krypton, and argon are anesthetics, whereas neon and helium are nonimmobilizers. The structures of noble gases with anesthetics or nonimmobilizers are similar and their interactions are simple. Whether the binding site of anesthetics differs from that of nonimmobilizers has long been a question in molecular anesthesiology. METHODS: We investigated the binding sites and energies of anesthetic and nonimmobilizer noble gases in human serum albumin (HSA) because the 3D structure of HSA is well known and it has an anesthetic binding site. The computational docking simulation we used searches for binding sites and calculates the binding energy for small molecules and a template molecule. RESULTS: Xenon, krypton, and argon were found to bind to the enflurane binding site of HSA, whereas neon and helium were found to bind to sites different from the xenon binding site. Rare gas anesthetic binding was dominated by van der Waals energy, while nonimmobilizer binding was dominated by solvent-effect energy. Binding site preference was determined by the ratios of local binding energy (van der Waals energy) and nonspecific binding energy (solvent-effect energy) to the total binding energy. van der Waals energy dominance is necessary for anesthetic binding. CONCLUSIONS: This analysis of binding energy components provides a rationale for the binding site difference of anesthetics and nonimmobilizers, reveals the differences between the binding interactions of anesthetics and nonimmobilizers, may explain pharmacological differences between anesthetics and nonimmobilizers, and provide an understanding of anesthetic action at the atomic level.

[Anesthetic management for electroconvulsive therapy using target-controlled infusion of propofol].

A 66-year-old man received medical treatment of depression for several years. He had a suspected malignant syndrome and in addition the symptom had deteriorated, and the electroconvulsive therapy (ECT) was administered. Though suxamethonium chloride is usually used as a muscular relaxant in the electroconvulsive therapy, we used vecuronium bromide (VCB) considering malignant syndrome. Maintenance of anesthesia was necessary because of the long effect of VCB. Anesthesia was induced and maintained by target controlled infusion (TCI) of propofol. Because propofol suppresses the convulsion, it is necessary to adjust the depth of anesthesia by propofol, and we used TCI of propofol. When the predicted blood propofol concentrations were 1.5 microg x ml(-1) and 2.0 microg x ml(-1), electric stimulation was given to the patient and enough seizure duration was obtained. TCI of propofol is useful for ECT to patients for whom suxamethonium chloride can not be used.