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Owing to recent advances in surgical technology, substantial time is required for preparing surgical equipment before incision. The purpose of this study was to demonstrate the time progression from a patient's operating room entrance to incision and to evaluate the duration of each anesthetic procedure and surgical preparation.We marked the following seven points on the anesthetic chart: (1) entrance; (2) i.v. line placement; (3) preoxygenation; (4) intubation; (5) completion of patient positioning (Anesth-Set); (6) applying antiseptic solution; and (7) incision. Afterward, we analyzed the event time periods according to anesthetic procedure, patient position, surgical service, and surgical procedure (such as the utilization of endoscopy, navigation systems, and sentinel lymph node biopsy).On average, it took approximately 3 min to start i.v. placement, 7 min until preoxygenation, 15 min until intubation, and 30 min until Anesth-Set. Epidural, arterial, and central venous catheterization required 15, 9, and 13 min, respectively. It took 20 min from Anesth-Set to incision, on average; 22, 4, and 5 min were required to prepare the navigation system, endoscope, and sentinel lymph node biopsy, respectively. In total, it took an average of 49.8 +/- 17.1 min from entrance to incision, which was significantly longer (30.4 +/- 8.8 min) than it took in 1985-1986.The mean time taken from the patient's operating room entrance to incision is now significantly longer than before. This may be attributed, at least in part, to the preparation of equipment associated with new surgical technologies.

The water channel protein aquaporin (AQP) may play roles in the homeostasis of water content in the brain and brain edema. One possible mechanism of brain edema is glial swelling due to lactic acidosis associated with ischemia. Here, we investigated the effect of lactic acid on the expression and cellular distribution of AQP 4 in cultured rat astrocytes. After 24 h of incubation, the AQP4 expression level increased maximally with 35 mM lactic acid. The AQP4 expression levels also increased with hydrochloric acid or acetic acid. In contrast, with sodium lactate, the AQP4 levels did not increase. The increase in AQP4 expression level occurred without a significant increase in AQP4 mRNA expression level by lactic acid. Under the conditions of de novo protein synthesis inhibition with cycloheximide, lactic acid increased the AQP4 expression level. Furthermore, lactic acid increased the AQP4 expression level on the cell surface of the astrocytes, as determined by a cell surface biotinylation assay and immunocytochemical examination. The increase in AQP4 expression level on the cell membrane of astrocytes induced by lactic acid may be a new regulation mechanism of AQP4 in the brain.

We developed a novel "skin-traction method" in which the puncture point of the skin over the internal jugular vein (IJV) is stretched upward with several pieces of surgical tape in the cephalad and caudad directions to facilitate cannulation of the IJV. We investigated whether this method increases the cross-sectional area of the IJV.In 11 healthy volunteers, the cross-sectional area, anteroposterior diameter, and transverse diameter of the right IJV (RIJV) were recorded by ultrasound echo at head tilts of +10 degrees , +5 degrees , 0 degrees , -5 degrees , and -10 degrees with and without the skin-traction method.The skin-traction method significantly increased the cross-sectional areas of the RIJV at head tilts of +10 degrees , +5 degrees , and 0 degrees . In the flat position, the skin-traction method increased the cross-sectional area of the RIJV from 1.21 +/- 0.44 cm(2) to 1.75 +/- 0.60 cm(2) (44.6% increase), which is almost the same as that in the Trendelenburg position without this method (1.60 +/- 0.54 cm(2) at -5 degrees and 1.83 +/- 0.56 cm(2) at -10 degrees ). The anteroposterior diameter of the RIJV was significantly increased in all positions with this method, although the transverse diameter was not.This method significantly increased the cross-sectional area of the RIJV by increasing the anteroposterior diameter of the RIJV. Even in the flat position, this method was almost as efficacious as the Trendelenburg position. This method thus appears to facilitate IJV cannulation.

We report a case of hypermagnesemia in a hospitalized patient after prolonged laxative use; due to preexisting impaired consciousness and digestive problems, the hypermagnesemia was difficult to detect until it almost became fatal. A 64-year-old man who was a patient at another hospital for treatment of head injury and gastric ulcer had developed circulatory collapse and was transferred to our hospital. Hypermagnesemia (serum magnesium concentration 11.0 mg.dl(-1)) was thought to be the cause of the circulatory collapse and treatments were successful. A magnesium laxative had been administered for more than a month at the previous hospital, but the patient's serum magnesium level was never measured. Care should be taken when a magnesium laxative is administered to patients who already have impaired consciousness and digestive problems that are early symptoms of hypermagnesemia.

The very high solubility of carbon monoxide (CO) in blood suggests that its elimination depends predominantly on ventilation and not perfusion. Nevertheless, hyperventilation is not used for CO elimination because of the adverse effects of hypocapnia. With isocapnic hyperpnea (IH), ventilation can be increased considerably without hypocapnia. This raises the issue of whether CO elimination is limited by perfusion during IH. We studied the effect of increasing cardiac output on t1/2, the half-time of decline of blood carboxyhemoglobin concentration ([COHb]), during normal ventilation (NV) and during IH.After ethics approval was received, 13 pentobarbital-anesthetized ventilated dogs were exposed to CO to increase their [COHb]. They were then ventilated with NV or IH. At each level of ventilation, dogs were randomly assigned to treatment with dobutamine (to increase cardiac output) or to no dobutamine treatment. After the return of [COHb] to control levels, each dog was re-exposed to CO and treated with the same ventilatory mode, but the alternative inotropic treatment.Gas exchange, [COHb], and hemodynamic measures were recorded during the study. Cardiac index values in the IH group were 4.1 +/- 0.5 and 8.2 +/- 1.2 l.min(-1).m(-2) without and with dobutamine infusion, respectively. Dobutamine infusion was associated with a reduction in t1/2 from 20.3 +/- 3.6 to 16.9 +/- 2.4 min (P = 0.005) in the IH group, but no change in the NV group.These findings suggest that CO elimination during IH treatment is limited at least partly by pulmonary blood flow and may therefore be further augmented by increasing cardiac output.

Tumor necrosis factor (TNF) and tissue factor (TF) produced by monocytes and macrophages have been shown to be among the aggravating factors for chronic heart failure (CHF), because they induce cardiac dysfunction and thrombotic complications, respectively. Carvedilol, a nonselective beta-adrenoceptor antagonist with alpha(1)- adrenoceptor blockade action, has been demonstrated to improve the outcome of patients with severe CHF, suggesting that carvedilol might inhibit the production of TNF and TF. In this study, this possibility is examined using isolated human monocytes stimulated with lipopolysaccharide (LPS) in vitro. Carvedilol (10 muM) significantly inhibited LPS-induced production of TNF and TF by monocytes, whereas prazosin (a selective alpha(1)-adrenoceptor antagonist), bisoprolol (a selective beta(1)-adrenoceptor antagonist), ICI-118,551 (a selective beta(2)-adrenoceptor antagonist), and arotinolol (a nonselective beta-adrenoceptor antagonist with alpha(1)-adrenoceptor blockade action) did not. Carvedilol inhibited both expression of early growth response factor-1 (Egr-1) and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, but it did not inhibit activation of either nuclear factor-kappaB or activator protein-1 in monocytes stimulated with LPS. These results suggest that carvedilol inhibits LPS-induced production of TNF and TF by inhibiting activation of the ERK1/2-Egr-1 pathway independent of its adrenoceptor inhibitory activities in monocytes.

Orotracheal intubation is the standard technique for airway management, but several untoward airway complications are possible with this method. To avoid airway trauma caused by the tube tip during intubation, the Parker Flex-Tip tube (PFT), which has a flexible, tapered tip, was developed. It has been reported that the PFT facilitates fiberoptic orotracheal intubation and introducer-guided tracheal intubation. In this study, we compared the PFT to a standard endotracheal tube (SET), regarding the time of intubation during conventional orotracheal intubation and the incidence of postoperative sore throat and hoarseness. One hundred and thirty-four patients scheduled for elective anesthesia using orotracheal intubation were randomized to either the PFT or SET and 132 completed the study. The intubators were classified into three groups: staff anesthesiologists, inexperienced anesthesiologists, and anesthesia trainees. The tube was selected by another anesthesiologist and the time required for intubation was measured. PFT did not shorten the time required for intubation and did not reduce the incidence of sore throat and hoarseness. However, a detailed analysis revealed that the PFT decreased the time required for intubation in the anesthesia trainee group. The PFT may help novice intubators to conduct a smooth intubation.

The aim of this study was to test our hypothesis that both phasic cardiac vagal activity and tonic pulmonary vagal activity, estimated as respiratory sinus arrhythmia (RSA) and anatomical dead space volume, respectively, contribute to improve the efficiency of pulmonary gas exchange in humans. We examined the effect of blocking vagal nerve activity with atropine on pulmonary gas exchange. Ten healthy volunteers inhaled hypoxic gas with constant tidal volume and respiratory frequency through a respiratory circuit with a respiratory analyser. Arterial partial pressure of O(2) (P(aO(2))) and arterial oxygen saturation (S(pO(2))) were measured, and alveolar-to-arterial P(O(2)) difference (D(A-aO(2))) was calculated. Anatomical dead space (V(D,an)), alveolar dead space (V(D,alv)) and the ratio of physiological dead space to tidal volume (V(D,phys)/V(T)) were measured. Electrocardiogram was recorded, and the amplitude of R-R interval variability in the high-frequency component (RRIHF) was utilized as an index of RSA magnitude. These parameters of pulmonary function were measured before and after administration of atropine (0.02 mg kg(-1)). Decreased RRIHF (P < 0.01) was accompanied by decreases in P(aO(2)) and S(pO(2)) (P < 0.05 and P < 0.01, respectively) and an increase in D(A-aO(2)) (P < 0.05). Anatomical dead space, V(D,alv) and V(D,phys)/V(T) increased (P < 0.01, P < 0.05 and P < 0.01, respectively) after atropine administration. The blockade of the vagal nerve with atropine resulted in an increase in V(D,an) and V(D,alv) and a deterioration of pulmonary oxygenation, accompanied by attenuation of RSA. Our findings suggest that both phasic cardiac and tonic pulmonary vagal nerve activity contribute to improve the efficiency of pulmonary gas exchange in hypoxic conscious humans.

We describe a case of inadvertent intrathecal cannulation with a central venous catheter in an infant, confirmed by three-dimensional computed tomography, which clearly demonstrated the track of the catheter. We believe that this complication could have been related to two major factors: depth of needle insertion and penetration of the vein by a straight-tip guidewire. To avoid this complication, the depth of needle insertion must be carefully checked, a "J"-tipped rather than a straight-tipped guidewire should be used, and puncture should be guided by ultrasound.

This study was undertaken to determine whether long-term in vivo administration of nitroglycerine (NTG) downregulates the hyperpolarization induced by acetylcholine (ACh) in aortic valve endothelial cells (AVECs) of the rabbit and, if so, whether antioxidant agents can normalize this downregulated hyperpolarization. ACh (0.03-3 microM) induced a hyperpolarization through activations of both apamin- and charybdotoxin-sensitive Ca2+-activated K+ channels (K(Ca)) in rabbit AVECs. The intermediate-conductance K(Ca) channel (IK(Ca)) activator 1-ethyl-2-benzimidazolinone (1-EBIO, 0.3 mM) induced a hyperpolarization of the same magnitude as ACh (3 microM). The ACh-induced hyperpolarization was significantly weaker, although the ACh-induced [Ca2+]i increase was unchanged, in NTG-treated rabbits (versus NTG-untreated control rabbits). The hyperpolarization induced by 1-EBIO was also weaker in NTG-treated rabbits. The reduced ACh-induced hyperpolarization seen in NTG-treated rabbits was not modified by in vitro application of the superoxide scavengers Mn-TBAP, tiron or ascorbate, but it was normalized when ascorbate was coadministered with NTG in vivo. Superoxide production within the endothelial cell (estimated by ethidium fluorescence) was increased in NTG-treated rabbits and this increased production was normalized by in vivo coadministration of ascorbate with the NTG. It is suggested that long-term in vivo administration of NTG downregulates the ACh-induced hyperpolarization in rabbit AVECs, possibly through chronic actions mediated by superoxide.

1 This study was undertaken to determine whether long-term in vivo administration of nitroglycerine (NTG) downregulates the endothelium-dependent relaxation induced by acetylcholine (ACh) in the rabbit intrapulmonary vein and, if so, whether the type 1 angiotensin II receptor (AT1R) blocker valsartan normalizes this downregulated relaxation. 2 In strips treated with the cyclooxygenase inhibitor diclofenac, ACh induced a relaxation only when the endothelium was intact. A small part of this ACh-induced relaxation was inhibited by coapplication of two Ca2+-activated K+-channel blockers (charybdotoxin (CTX)+apamin) and the greater part of the response was inhibited by the nitric-oxide-synthase inhibitor Nω-nitro-L-arginine (L-NNA). 3 The endothelium-dependent relaxation induced by ACh, but not the endothelium-independent relaxation induced by the nitric oxide donor NOC-7, was significantly reduced in NTG-treated rabbits (versus those in NTG-nontreated control rabbits). The attenuated relaxation was normalized by coapplication of valsartan with the NTG. 4 In the vascular wall, both the amount of localized angiotensin II and the production of superoxide anion were increased by in vivo NTG treatment. These variables were normalized by coapplication of valsartan with the NTG. 5 It is suggested that long-term in vivo administration of NTG downregulates the ACh-induced endothelium-dependent relaxation, mainly through an inhibition of endothelial nitric oxide production in the rabbit intrapulmonary vein. A possible role for AT1R is proposed in the mechanism underlying this effect. British Journal of Pharmacology (2005) 145, 193–202. doi:10.1038/sj.bjp.0706178

維持透析患者38例の体外循環下冠動脈バイパス術(coronary artery bypass graft, CABG)における術後合併症と短期予後について,非透析患者231例と比較検討した。透析群の周術期管理として,術前は2日連続の血液透析(hemodialysis,HD)を施行し,術中は限外濾過装置を使用,術後は術翌日よりHDを開始することを原則とし,循環が不安定な症例には持続血液濾過を施行し,この方法で管理可能であった。縦隔炎の発生率は透析群で有意に高かったが,出血再開胸,術後脳梗塞の頻度は両群で有意差はなかった。また,術前の貧血は透析群で有意に進んでおり,輸血率も透析群で有意に高かった。透析群の病院死亡率は15.8%と有意に高く,敗血症を死因としたものが多かったため,更なる成績向上には感染予防を主体とした,よりきめ細かい患者管理が必要である。

巨大卵巣腫瘍摘出術の術中・術後管理に難渋した症例を経験した. 症例は22歳, 女性. 術前体重が92kgに対し, 摘出された腫瘍の重量は40kg近くあった. 麻酔導入前に起坐位で局所麻酔下に液状の腫瘍内容物を吸引し, 腹部膨満を軽減した後, 仰臥位にして全身麻酔を導入した. 術後, 酸素化能が低下したためICUに入室した. 仰臥位では酸素化は低下を認めたが, 起坐位になることで改善したため, 抜管した. 喀痰排出困難のため, 翌日右上葉の無気肺を認めた. 気管支ファイバー下に喀痰を吸引した. 巨大腹部腫瘤摘出術の術中・術後管理においては, 術前から合併している肺機能低下を考慮した呼吸管理が必要と考えられた.

To describe cardiovascular collapse during a cemented hip hemiarthroplasty in a patient who, despite a successful cardiopulmonary resuscitation, remained in a persistent vegetative state due to cerebral fat embolism diagnosed by magnetic resonance imaging (MRI).A 75-yr-old woman with no medical history underwent cemented hip hemiarthroplasty under spinal anesthesia for a right femoral neck fracture. Shortly after insertion of the prosthesis, a sudden oxygen desaturation, hypotension, bradycardia, and cardiac arrest occurred. The patient was successfully resuscitated, but did not regain consciousness. The patient developed high-grade fever, thrombocytopenia, anemia, and oliguria. MRI scans of the brain revealed multiple high intensity signals throughout the white matter, the basal ganglia, the cerebellum, and the brain stem. The diagnosis of fat embolism was made on the basis of clinical findings and MRI images. Although her cardiorespiratory status improved over the next week, the patient remained in a persistent vegetative state.When fat embolism is suspected, serial MRI scans of the brain should be performed to diagnose the etiology of cerebral embolism as well as to evaluate the severity of brain damage.

Aquaporins (AQPs) are a family of water-selective transporting proteins with homology to the major intrinsic protein (MIP) of lens, that increase plasma membrane water permeability in secretory and absorptive cells. In this study, we investigated the effect of mild hypothermia on the expression of AQP4, AQP5 and AQP9 in rat astrocytes cultured under hypoxic conditions. At 37 degrees C, a marked decrease in the expression of AQP4, AQP5 and AQP9 mRNAs was observed. However, at 32 degrees C (mild hypothermia), the expression of AQP5 mRNA was restored to its basal level. Interestingly, under mild hypothermia AQP4 mRNA expression transiently decreased and then increased about two-fold; while AQP9 mRNA expression decreased the same as at 37 degrees C. The changes in the expression of AQP4 and AQP9 proteins were confirmed by Western blot analysis. The restoration of the AQP4 and AQP5 expression at 32 degrees C from the hypoxia-induced decrease at 37 degrees C may play an important role in the reduction of brain edema under hypothermic conditions.

Tissue ischemia and inflammation result in localized acidosis, and acidic pH can trigger a sensation of pain. Pain is known to be often modified by the tissue temperature. The purpose of this study is to clarify the thermal behavior of nociceptors in response to acidification using intracellular recordings from cultured rat primary afferent neurons. Extracellular acidification induced depolarization of two types, transient and sustained responses. The former (to pH 6.3 and 5.2) was augmented at lower temperature (26, 16 degrees C) and amiloride blocked the response to pH 6.3 at 26 degrees C. On the other hand, the sustained depolarization, which often followed the transient one, in response to pH 6.3 was greater at 36 degrees C and significantly blocked by capsazepine at 36 degrees C, but not at 26 degrees C. The sustained response to pH 5.2 was blocked even at 26 degrees C. These results suggest that the low pH evoked depolarization is temperature-dependent, and the contribution of transient receptor potential V1 (vanilloid receptor 1) to proton-induced response is greater in the physiological body temperature range, while that of the acid-sensing-ion-channel family is greater at room temperature or lower.

The effects of H(2)O(2) on the membrane potential of smooth muscle cells of rabbit mesenteric resistance arteries were investigated. H(2)O(2) (3-30 microM) concentration-dependently hyperpolarized the membrane; this was inhibited by catalase but not by superoxide dismutase or the hydroxyl-radical scavenger dimethylthiourea. The cyclooxygenase inhibitor diclofenac partly inhibited the responses; the subsequent addition of the 5-lipoxygenase inhibitor 2-(12-hydroxydodeca-5,10-diynyl)-3,5,6-trimethyl-p-benzoquinone (AA-861) (but not the cytochrome P(450) inhibitor 17-octadecynoic acid) further attenuated H(2)O(2)-induced hyperpolarizations. The sarcolemmal ATP-sensitive K(+) (K(ATP)) channel inhibitor 1-[5-[2-(5-chloro-o-anisamido)ethyl]-2-methoxyphenylsulfonyl]-3-methylthiourea, sodium salt (HMR-1098), blocked the H(2)O(2)-induced hyperpolarization in the absence and presence of diclofenac. H(2)O(2) increased the production of prostaglandin E(2) and prostacyclin (estimated from its stable metabolite 6-keto-prostaglandin F(1alpha)), both of which produce a HMR-1098-sensitive hyperpolarization in the smooth muscle cells. It is concluded that, in smooth muscle cells of rabbit mesenteric artery, H(2)O(2) increases the synthesis of vasodilator prostaglandins and possibly 5-lipoxygenase products, which produce a hyperpolarization by activating sarcolemmal K(ATP) channels.

Parkinsonism is a rare complication in patients with organophosphate poisoning. To date there have been two cases of transient parkinsonism after acute and severe cholinergic crisis, both of which were successfully treated using amantadine, an anti-parkinsonism drug. We report on an 81-year-old woman who was admitted for the treatment of acute severe organophosphate poisoning. Although acute cholinergic crisis was treated successfully with large doses of atropine and 2-pyridine aldoxime methiodide (PAM), extrapyramidal manifestations were noticed on hospital day 6. The neurological symptoms worsened, and the diagnosis of parkinsonism was made by a neurologist on hospital day 9. Immediately, biperiden (5 mg), an anti-parkinsonism drug, was administered intravenously, and her symptoms markedly improved. From the following day, biperiden (5 mg/day) was given intramuscularly for eight days. Subsequently, neurological symptoms did not relapse, and no drugs were required. Our patient is the third case of parkinsonism developing after an acute severe cholinergic crisis and the first case successfully treated with biperiden. Patients should be carefully observed for the presence of neurological signs in this kind of poisoning. If present, an anti-parkinsonism drug should be considered.

Objective: To evaluate the usefulness of transesophageal echocardiography (TEE) for cardiac surgery in children. Design: Prospective clinical study. Setting: Nagoya City University Hospital. Participants: Children who had cardiac surgery from January 1998 to December 2000 (n = 90). Interventions: TEE was used to the extent permitted by the probe size and the position of the patient during surgery. Measurements and Main Results: TEE monitoring was performed safely without any complications in 88 of the patients. Based on the TEE findings, the anesthesiologists conferred with the surgeon about the efficacy of the surgical procedures in 11 patients (11 of 88 [12.5%]). The cardiac surgeons altered the surgical repair in 2 patients based on the TEE findings (2 of 88 [2.4%]). Conclusion: TEE is a valuable diagnostic tool for monitoring during cardiac surgery in children. The person who performs the TEE should use it carefully after obtaining thorough knowledge of the pathophysiology of pediatric cardiac diseases, their surgical indications, and how specific surgical procedures are done. Copyright 2002, Elsevier Science (USA). All rights reserved.

Bradykinin (BK) is an inflammatory mediator that plays a pivotal role in pain and hyperalgesia to heat in inflamed tissues by exciting nociceptors and sensitizing them to heat through activation of protein kinase C (PKC). It has been suggested that the capsaicin receptor (VR1), a nociceptor-specific cation channel sensitive to noxious heat, protons, and capsaicin, is a channel that is modified by BK in these effects. In this study, we examined how BK modulates the activity of VR1. We measured VR1 currents using the patch-clamp technique in human embryonic kidney-derived (HEK293) cells expressing VR1 and B2 BK receptor. We found that BK lowered the threshold temperature for activation of VR1 currents in HEK cells down to well below the physiological body temperature in a concentration-dependent manner through PKC activation. We also demonstrated that in capsaicin-sensitive dorsal root ganglion (DRG) neurons the activation threshold of heat-induced current, which is considered to be VR-1 mediated, was lowered by BK and that this effect was also mediated by PKC. These data further support the supposition that modulation of VR1 is a mechanism for the BK-induced excitation of nociceptors and their sensitization to heat.

Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching the pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2directly affects RSA in conscious humans even when changes in tidal volume (VT) and breathing frequency ( F B), which indirectly affect RSA, are prevented. In seven healthy subjects, we adjusted end-tidal Pco 2 (Pet CO2 ) to 30, 40, or 50 mmHg in random order at constant VT and F B. The mean amplitude of the high-frequency component of R-R interval variation was used as a quantitative assessment of RSA magnitude. RSA magnitude increased progressively with Pet CO2 ( P < 0.001). Mean R-R interval did not differ at Pet CO2 of 40 and 50 mmHg but was less at 30 mmHg ( P < 0.05). Because VT and F B were constant, these results support our hypothesis that increased CO2directly increases RSA magnitude, probably via a direct effect on medullary mechanisms generating RSA.

Objective To compare the utilization and outcomes of critical care services in a cohort of hospitals in the United States and Japan. Design Prospective data collection on 5,107 patients and detailed organizational characteristics from each of the participating Japanese study hospitals between 1993 and 1995, with comparisons made to prospectively collected data on the 17,440 patients included in the US APACHE (acute physiology and chronic health evaluation) III database. Setting Twenty-two Japanese and 40 US hospitals. Patients Consecutive, unselected patients from medical, surgical, and mixed medical/surgical ICUs. Measurements Severity of illness, predicted risk of in-hospital death, and ICU and hospital length of stay (LOS) were assessed using APACHE III. Japanese ICU directors completed a detailed survey describing their units. Main results US and Japanese ICUs have a similar array of modalities available for care. Only 1.0% (range, 0.56 to 2.7%) of beds in Japanese hospitals were designated as ICUs. The organization of the Japanese and US ICUs varied by hospital, but Japanese ICUs were more likely to be organized to care for heterogeneous diagnostic populations. Sample case-mix differences reflect different disease prevalence. ICU utilization for women is significantly lower (35.5% vs 44.8% of patients) and there were relatively fewer patients ≥85 years old in the Japanese ICU cohort (1.2% vs 4.6%), despite a higher per capita rate of individuals ≥85 years old in Japan. The utilization of ICUs for patients at low risk of death significantly less in Japan (10.2%) than in the United States (12.9%). The APACHE III score stratified patient risk. Overall mortality was similar in both national samples after accounting for differences in hospital LOS, utilizing a model that was highly discriminating (receiver operating characteristic, 0.87) when applied to the Japanese sample. The application of a US-based mortality model to a Japanese sample overpredicted mortality across all but the highest (> 90%) deciles of risk. Significant variation in expected performance was noted between hospitals. Risk-adjusted ICU LOS was not significantly longer in Japan; however, total hospital stay was nearly twice that found in the US hospitals, reflecting differences in hospital utilization philosophies. Conclusions Similar high-technology critical care is available in both countries. Variations in ICU utilization reflect differences in case-mix and bed availability. Japanese ICU utilization by gender reflects differences in disease prevalence, whereas differences in utilization by age may reflect differences in cultural norms regarding the limits of care. Such differences provide context from which to assess the delivery of care across international borders. Miscalibration of predictive models applied to international data samples highlight the impact that differences in resource use and local practice cultures have on outcomes. Models may require modification in order to account for these differences. Nevertheless, with large databases, it is possible to assess critical care delivery systems between countries accounting for differences in case-mix, severity of illness, and cultural normative standards facilitating the design and management such systems.

当院は,2000年2月環境管理における国際標準規格であるISO(International standardization for organization) 14001を取得した。ISO14001の命題は,地球環境の保全である。そのために国内外の法規制,協定などを遵守,尊重した自主活動による継続的改善のためのシステムを構築し,運用管理することが要求されている。麻酔科では環境影響評価の結果,「著しい環境側面」と認められた以下の4項目,1)電気消費の削減,2)廃棄物の削減,3)コピー紙購入の削減,4)亜酸化窒素使用量の削減,に取り組んだ。特に亜酸化窒素に関しては使用を全廃できる見通しとなった。

Aquaporins (AQPs) are a family of water-selective transporting proteins with homology to the major intrinsic protein (MIP) of lens [6] , that increase plasma membrane water permeability in secretory and absorptive cells. In astrocytes of the central nervous system (CNS), using the reverse transcription-polymerase chain reaction (RT-PCR), we previously detected AQP3, 5 and 8 mRNAs in addition to the reported AQP4 and 9. However the mechanisms regulating the expression of these AQPs are not known. In this study, we investigated the effects of a protein kinase C (PKC) activator on the expression of AQP4, 5 and 9 in cultured rat astrocytes. Treatment of the cells with TPA caused decreases in AQP4 and 9 mRNAs and proteins in time- and concentration-dependent manners. The TPA-induced decreases in AQP4 and 9 mRNAs were inhibited by PKC inhibitors. Moreover, prolonged treatment of the cells with TPA eliminated the subsequent decreases in AQP4 and 9 mRNAs caused by TPA. Pretreatment of cells with an inhibitor of protein synthesis, cycloheximide, did not inhibit the decreases in AQP4 and 9 mRNAs induced by TPA. These results suggest that signal transduction via PKC may play important roles in regulating the expression of AQP4 and 9.

Aquaporins (AQPs) are a family of water-selective transporting proteins with homology to the major intrinsic protein (MIP) of lens [Cell 39 (1984) 49], that increase plasma membrane water permeability in secretory and absorptive cells. In the central nervous system (CNS), we detected the transcripts of AQP3, 5 and 8 in addition to the previously reported transcripts of AQP4 and 9 in astrocytes, of AQP3, 5 and 8 in neurons, of AQP8 in oligodendrocytes, and none of them in microglia using RNase protection assay and the reverse transcription-polymerase chain reaction (RT-PCR). Hypoxia evoked a marked decrease in the expression levels of AQP4, 5 and 9, but not of AQP3 and 8 mRNAs, and in astrocytes in vitro subsequent reoxygenation elicited the restoration of the expression of AQP4 and 9 to their basal levels. Interestingly, AQP5 showed a transient up-regulation (about 3-fold) and subsequent down-regulation of its expression within 20 h of reoxygenation after hypoxia. The changes in the profiles of AQP expression during hypoxia and reoxygenation were also observed by Western blot analysis. These results suggest that AQP5 may be one of the candidates for inducing the intracranial edema in the CNS after ischemia injury.

麻酔器に接続した圧縮空気ホースの結露を発見して,中央監視室における圧縮空気供給装置の異常を指摘できた事例を経験した-医療ガス管理者が毎日の医療ガス保守点検指針を守っていても,空気加圧装置の付属品である排水装置に不備があると除水されない圧縮空気が送気される可能性があることが判明した.今回の経験から,圧縮空気の異常を末端で知るためには,圧縮空気ホースは結露がわかりやすいように透明な材質にする必要があり,また圧縮空気ホースの麻酔器接続部に気水分離器を標準装備する必要があると考えられる.

We report a case of a ruptured pulmonary arteriovenous fistula (PAVF) which caused shock. A 72-year-old woman was transferred from a local hospital to our hospital because of sudden onset of left chest pain that followed hypotension and left pleural effusion. A suspended rupture of an aortic aneurysm was suggested, but results of transesophageal echocardiography and enhanced computed tomography provided no evidence of this diagnosis. Also, aortography performed on the 2nd hospital day, revealed no abnormalities of the intercostal and bronchial arteries, nor the source of the hemothorax. On the 3rd hospital day, she developed shock due to recurrent bleeding, therefore, probe thoracotomy was performed. Pulsative bleeding from the lung surface of the left S8 segment was observed and a diagnosis of a ruptured PAVF was confirmed. Left lower lobectomy was carried out and she was discharged on the 26th hospital day. There are few reports describing the intrapleural rupture of PAVF. This case suggests that pulmonary arteriography should be considered in addition to aortography in patients with sudden onset of chest pain and hemothorax.

手術室で使用中のETCO2モニタ機器の汚染状況を調査したところ,細菌が高頻度に検出された.そこで,手術室において1ヵ月間あるいは2ヵ月間の期間別に複数患者に使用したところ,ETCO2モニタ機器の使用期間が長くなるにつれて細菌汚染がより高頻度となる傾向にあった.さらに,気道感染を有するICU長期入室患者1名に対してETCO2モニタの経時的汚染状況を調査したところ,24時間で患者からモニタへの細菌の移行が生じた.つまり,患者からモニタへの細菌汚染は比較的短時間に,高頻度に生じることが示唆され,単一ETCO2モニタ回路の複数患者への使用は問題があると考えられた.複数患者への使用には,細菌除去フィルタの使用等の対策が必要である.

Two cDNA isoforms of bovine aquaporin-4 (bAQP4-A and bAQP4-B) were newly isolated. Sequence analysis of both cDNAs revealed open reading frames of 972 (bAQP4-A) and 906 nucleotides (bAQP4-B) with deduced proteins of 323 (bAQP4-A) and 301 amino acid residues (bAQP4-B). Partial 5'-genomic sequence analysis showed that the 5'-noncoding sequences specific to bAQP4-A and -B transcripts were contained in distinct exons, exon 0 for bAQP4-A and new exon X for bAQP4-B. RNase protection assay demonstrated the definite expression of both isoforms in bovine brain. The deduced amino acid sequence of bAQP4-A was highly homologous to the human (97%), rat (95%), and mouse (93%) AQP4. Reverse transcription-PCR detected the expression of AQP4 mRNAs in bovine brain endothelial cells as well as in a variety of bovine organs such as brain, lung, spleen, and kidney. Northern blot analysis indicated that a 6.0 kb message is predominantly expressed in bovine brain and lung.

The blood-brain barrier (B-BB) protects the free passage of substances into the brain and maintains the homeostasis of the central nervous system. It is commonly accepted that astrocytes surrounding brain endothelial cells influence the B-BB formation and the exhibition of B-BB function of capillaries. To begin the in vitro study on the B-BB, it is essential to obtain a homogenous and sufficient supply of brain endothelial cells as well as astrocytes. We thus immortalized the bovine brain endothelial cell (BBEC) by transfection of the SV40 large T antigen and obtained a single clone, t-BBEC-117, which retained the brain endothelial cell phenotype. Astrocyte in co-culture was found to tighten the intercellular contacts of the immortal cells resulting in a reduced L-glucose permeability, and its conditioned medium (CM) augmented a B-BB phenotype, alkaline phosphatase (ALP) activity. Among known astrocytic factors, only fibroblast growth factor-basic (bFGF) could mimic the actions of astrocytes as measured by L-glucose permeability and ALP activity. Moreover, anti-bFGF antibody canceled 90% of ALP activation by astrocyte CM. Basic FGF, however, failed to induce other B-BB phenotypes such as the expressions of multidrug resistance (mdr) and glucose transporter (GLUT-1) genes. These data suggest that bFGF is one of the most plausible astrocytic factors to induce the B-BB properties of immortal brain endothelial cells together with some unknown factors in the astrocyte CM.

Earlobe skin blood flow measured by laser Doppler flowmetry often shows low-frequency oscillations with a frequency around 0.1 Hz. We evaluated the effects of different sympathetic blocking techniques on the oscillations. Power spectrum of 5-min time series of beat-to-beat peak earlobe skin blood flow showed a distinct spectral peak at a frequency around 0.1 Hz (mean +/- SD, 0.107+/-0.016 Hz). The power of the spectral peak measured as coefficient of component variance (CCV) was diminished with total spinal anesthesia (TSA, n = 4) and cervicothoracic epidural anesthesia (CTEA, n = 4; P0.05 for both). The CCV was unchanged significantly with bilateral thoracic sympathetic ganglionic excision (TSGE, n = 5). Right stellate ganglion block (RSGB, n = 6) caused a trend towards an increase in the CCV on the right (blocked)-side (P = 0.072) but no change on the left (intact)-side. Cross-spectrum analysis revealed that the low-frequency oscillations were not coherent between the right- and left-side earlobes or with low-frequency oscillations in systolic blood pressure either before or after RSGB. TSA and CTEA are known to cause extensive sympathetic nerve blockade in a broad area, while TSGE and RSGB are known to cause local and partial sympathetic blockade. Our results suggest that although the low-frequency oscillations in earlobe skin blood flow may be mediated non-neurally, magnitude of the oscillations may be modified by sympathetic vasomotor tone.

高齢者で多彩な精神・神経症状を示した甲状腺クリーゼの1症例を経験した。患者は69歳,女性。3ヵ月前より全身倦怠感があった。その後,悪心,嘔吐,食事摂取困難となり入院した。入院時より抑うつ症状が認められ,しだいに夜間せん妄,多弁,独語,妄想が出現し,不穏,錯乱状態となった。その後,突然の意識消失,呼吸停止をきたし,ICUへ収容した。収容時の意識レベルは,Japan Coma Scale (JCS) III-200,右方共同偏視,右半身不全麻痺が認められた。甲状腺の腫大および眼球突出より甲状腺クリーゼを疑い,チアマゾール,ヨードグリセリンを投与し,心臓交感神経抑制の目的で持続胸部硬膜外ブロックを施行した。3日後には意識レベルJCS I-1に回復し,同時に共同偏視,右半身不全麻痺も消失した。甲状腺クリーゼによる頻脈の改善に持続胸部硬膜外ブロックが有効であった。

術前ACE阻害薬服用患者(54歳,女性)の僧帽弁置換術中に,白血球除去フィルターを用いた血小板輸血を行なったところ,収縮期血圧が90mmHgから40mmHgに急激に低下した.術後の検索で,副作用のあった濃厚血小板製剤のフィルター濾過後ブラジキニン濃度は著しく高値(61,500Pg/ml)であった.患者血清のACE活性は低値(3.1IU/l)を示した.血漿が陰性荷電に接触すると,ブラジキニンが産生されることが知られている.本症例の血圧低下は,ACE活性が低くブラジキニンの分解が不十分な患者に,陰性荷電を有するフィルターとの接触でブラジキニン濃度が高まった濃厚血小板製剤が輸血されたことが原因と考えられた.

Background Propofol (2,6-diisopropylphenol) possesses vasodilating activity in vivo and in vitro. The propofol-induced relaxation of agonist-induced contractions in small resistance arteries has not been clarified. Methods The effect of propofol was examined on the contractions induced by norepinephrine and high K+ in endothelium-denuded rabbit mesenteric resistance artery in vitro. The effects of propofol on the [Ca2+]i mobilization induced by norepinephrine and high K+ were studied by simultaneous measurement of [Ca2+]i using Fura 2 and isometric force in ryanodine-treated strips. Results Propofol attenuated the contractions induced by high K+ and norepinephrine, the effect being greater on the high K+-induced contraction than on the norepinephrine-induced contraction. In Ca2+-free solution, norepinephrine produced a transient contraction resulting from the release of Ca2+ from storage sites that propofol attenuated. In ryanodine-treated strips, propofol increased the resting [Ca2+]i but attenuated the increases in [Ca2+]i and force induced by both high K+ and norepinephrine. In the presence of nicardipine, propofol had no inhibitory action on the residual norepinephrine-induced [Ca2+]i increase, whereas it still modestly increased resting [Ca2+]i, as in the absence of nicardipine. Conclusions In smooth muscle of the rabbit mesenteric resistance artery, propofol attenuates norepinephrine-induced contractions due to an inhibition both of Ca2+ release and of Ca2+ influx through L-type Ca2+ channels. Propofol also increased resting [Ca2+]i, possibly as a result of an inhibition of [Ca2+]i removal mechanisms. These results may explain in part the variety of actions seen with propofol in various types of vascular smooth muscle.

腹腔鏡下胆嚢摘出術の肝機能に及ぼす影響をアルコール脱水素酵素とグルタチオンS転移酵素αの血清活性と門脈血流量の変化から検討した.術中の血圧を吸入麻酔薬のみで術前の安静時血圧に近い値に維持した群と,吸入麻酔薬にジルチアゼムを併用し術前の安静時平均血圧の80%前後に低下させた群で比較した.両酵素活性は2群とも術前値と比較し術中有意に増加し,術後には術前値と有意差はなくなった.門脈血流量は気腹解除直前にそれぞれ術前値の30.3±9.4%, 37.9±9.5%と有意(p

We describe our experience with use of variable-flow nasal continuous positive airway pressure (NCPAP) to manage postextubation stridor in a 31-month-old child with Down syndrome (DS). Although it has been recognized that children with DS tend to develop obstruction of the upper airway postoperatively, little is known concerning appropriate management of this situation. Although there are surprisingly few reports of use of variable-flow NCPAP for children older than preterm infants, we successfully treated postextubation ventilatory complications by providing variable-flow NCPAP without complications such as pneumothorax.

病院前救急医療のひとつの試みとして救急指令台に医師を常駐させる,いわゆる救急指令台指導医の制度を取り入れている地域がある。この方法によればひとりの指導医を勤務させるだけで比較的広域の救急医療に対応可能であるという利点があり,救急専門医が不足する本邦では大変有効と考えられる。しかしながら,この指導医に求められている業務の内容ばかりか,実際に病院前救急の主な担い手である救急隊員が,指令台指導医を求めているのかどうかすら調査した報告が見あたらない。そこで今回このような制度のない名古屋市消防局の指令台オペレータ,救急隊(救急救命士が乗務した場合には救急救命士,乗務していなかった場合には救急隊員)の救急出動179事例にアンケートを行って,彼らがどの程度指令台指導医の必要を感じたか調査した。その結果,オペレータは59.9%の事例で指導医の必要を感じており,救急救命士が乗務していた場合56.0%,救急隊員のみの場合64.5%と,救急救命士が乗務しない場合の方が指導医の必要を感じる事が多いようであったが統計的に有意ではなかった。一方出動した隊員は,59.2%の事例で指導医の必要を感じており,救急救命士が乗務した場合60.6%,救急隊員のみの場合57.5%とむしろ救急救命士の方が若干多く指導医を望んでいたが,これも有意ではなかった。つぎに傷病者重症度別の指導医必要度を分析した。オペレータはCPA群の90.9%,重症群の72.7%,中等症群の65.8%,軽症群の47.3%に指導医の必要を感じており,重症例ほど有意に多く指導医を求める結果となった。救急隊でも同様にCPA群の100%,重症群の95.5%,中等症群の66.7%,軽症群の43.3%に指導医を求めており,やはり重症例ほど有意に多くの事例で指導医を必要としていた。それぞれの重症度において,オペレータと現場の救急隊で指導医を求める頻度には有意差は認められなかった。

加圧時測定型自動血圧測定モジュール(M-21C,日本コーリン社)は,減圧時に圧測定する従来のオシロメトリック式血圧計と異なり,カフ加圧と同時に血圧を測定する方法を採用している.このM-21Cの精度を観血的血圧と臨床的に比較検討した.収縮期圧,拡張期圧の誤差平均はそれぞれ0.43,3.36mmHg,標準偏差は5.30,7.10mmHgであり,精度においては十分臨床使用に耐えうることがわかった.また加圧時の平均血圧測定時間は19.2±4.2secであり,減圧時平均測定時間の30.8±4.6secより有意に測定時間の短縮を認め,頻回測定やカフ加圧による合併症の軽減に有用であろう.

ベクロニウムは循環抑制の比較的少ない筋弛緩薬とされているが,sympathetic overactivityを呈した重症破傷風の1症例においてベクロニウムが著明な血圧低下をきたした.自律神経機能異常を有する症例においてはベクロニウムは予想外の低血圧を呈することがある.

われわれは,大量に産生されるサイトカインを制御し,病態改善を図るため抑制性biological response modifier (BRM)としてのmethylprednisolone (MPS)の比較的,短時間持続投与を敗血症患者4例に行なった.すなわちMPSの初回投与量は5mg/kgとし,その後0.65mg/kg・hを48時間持続投与した.また,MPSの血中濃度の推移を測定した.われわれの投与方法ではMPSの濃度は投与後30分で2μg/mlに達し,以後2～4μg/ml前後で推移した.MPS投与により血中のTNFα,IL-6,IL-8は一様に低下した.臨床症状と各種検査値は投与後24時間には有意に改善された.以上より,敗血症症例での高サイトカイン血症が原因である臓器機能不全に対して,MPSの比較的少量持続投与は有効な治療手段の一つとなりうることが示唆された.

We investigated the efficacy of thrombolytic therapy with recombinant tissue plasminogen activator (t-PA) from the standpoint of changes in hemodynamics and pulmonary oxygenation in 9 patients suffering from massive pulmonary embolism. Eight of the 9 patients presented with shock symptoms, and 4 of them required cardiopulmonary resuscitation. We immediately administered 20 million units of t-PA over the course of an hour. Systolic blood pressure (SBP), heart rate (HR), central venous pressure (CVP), systolic pulmonary arterial pressure (SPAP), PaO2/FiO2 ratio (P/F ratio), cardiac index (CI) and pulmonary vascular resistance (PVR) were recorded before and after t-PA administration. After t-PA infusion, HR, SPAP, CI and PVR showed significant improvement, but SBP and CVP did not change significantly.The results demonstrated the rapid thrombolytic capability of t-PA, and as early as possible administration seemed crucial to saving the lives of patients with massive pulmonary embolism complicated by shock. Since t-PA infusion did save critically ill pulmonary embolism patients without any side effects, we believe that early thrombolytic therapy with t-PA is a life saving treatment for massive pulmonary embolism.

抗リン脂質抗体症候群(61歳,男性)の左下腿切断術に対する麻酔管理を経験した。術前検査で,出血傾向を伴わない,活性化部分トロンボプラスチン時間(A-PTT)の高度の延長を認めたため,凝固因子定量とA-PTT補正試験を施行し,lupus anticoagulants (LA)陽性により本疾患と診断した。麻酔管理の主眼を病態の急性増悪予防と疾患に対する治療におき,術前よりステロイドホルモンを投与した。麻酔は,塞栓症状の早期発見が可能で,麻酔による侵襲が少ないと考えられた脊椎麻酔を選択した。術後にはヘパリンなどによる抗血小板,抗凝固療法にて管理した。以上により周術期を病態を悪化させることなく良好に管理しえた。

IMPLICATIONS: Airway compression from insertion of a transesophageal echocardiography (TEE) probe has been mostly limited to pediatric patients. We present a case of TEE-associated airway obstruction in an adult patient undergoing surgery for repair of a giant ascending aortic pseudoaneurysm.

IMPLICATIONS Nicardipine-induced bradycardia has been reported in experimental animals but not in clinical patients. We report a clinical case of unexpected bradycardia caused by nicardipine. The mechanism of this bradycardia was not clear, and depression of sympathetic tone by epidural anesthesia, hypothermia, and paroxysmal atrial fibrillation might have been contributory.