In acute pulmonary embolism, because a thrombus which has developed in the venous system blocks the truncal pulmonary artery, fatal respiratory and circulatory arrest follows.
Although many researchers have attempted to establish medical and surgical treatment to eliminate such embolism, it is a fact that the effectiveness of the initial therapy to deal with unconsciousness and respiratory arrest determines whether the patient will recover or not. And this acute condition often occurs just before completion of treatment for the underlying disorder, with a high fatality rate-a misfortune not only for the patient but also for the medical staff, against whom legal action is often taken nowadays.
When the symptoms in the fatal condition and the state of the disease are analyzed, it is recognized that in many cases loss of consciousness and respiratory arrest, resulting from circulatory collapse, occur first, and this must be kept in mind when attempting to resuscitate the patient.

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The immunosuppressant FK 506 and cyclosporinA (CsA) have recently been reported to have neuroprotective effects, which are considered to be mediated by calcineurin inhibition consequently reduces NO production. Mitochondrial permeability transition pore (MPTpore), located on the mitochondrial inner membrane, opens under oxidative stress, and high calcium ion concentration, such as ischemic insult. The opening of the MPTpore, allowing free passage of solutes of less than 1500 Da through the inner mitochondrial membrane, causes disruption of the protonmotive force, cessation of ATP-production, release of apoptosis related molecules such as cytochrome C, apoptosis inducing factor (AIF), and cell death. CsA and it's non-immunosuppressave analog (MeValCsA), but not FK 506, prevent opening of the MPTpore.
The potent neuroprotection of CsA seems to be caused by both calcineurin inhibition and MPTpore blockade. FK 506 may have possible clinical use as an anti-stroke drug, because of its passage through blood-brain-barrier (BBB) . However, CsA has restricted passage through the undamaged BBB, therefore more research is needed to determine the clinical use of CsA as neuroprotective drug.

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Endotoxin (LPS) stimulates macrophages to activate NF-κB and to release large quantities of TNF and IL-1, which have been considered mediators in tissue injury and lethal shock. Sensitive responses to LPS require the GPI-anchored membrance protein CD 14. However, the mechanism by which the LPS signal is transduced across the plasma membranc remains unknown. Antagonists of TNF and IL-1 have shown limited efficacy in clinical trials for patients with sepsis. The occurrence of mental disturbance requires new mediators other than these cytokines.
Recently, Toll-like receptors (TLRs) containing the intracellular domain have been discovered and these signaling receptors are activated by LPS/LBP and enhanced by CD 14. Recent evidence indicates that macrophages and platelets generate different endogenous cannbinoids, anandamide and 2-arachidonyl glyceride, respectively, as potential immediate mediators before the release of these cytokine, and that both these cannaginoids may be paracrine mediators of LPS-induced hypotension via activation of vascular CB 1 receptors. Moreover, serum levels of high mobility group-1 protein (HMG-1) as a potential late mediator increase from 8 hours after LPS exposure in mice. Administration of HMG-1 itself was lethal and delayed administration of antibodies to HMG-1 attenuates LPS lethality. Moreover, septic patients have increased serum HMG-1 levels. In this aritcle, recent evidence conernig TLRs, endogenous cannaginoids and HMG-1 in pathogenesis of endotoxin shock is reviewed.

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In order to elucidate the relation between NO production and neuronal cell damage, changes in NO metabolites (NO₂ and NO₃) and cell injury were measured under LPS treatment. Also the effects of intravenous anesthetics on these changes were evaluated using the brain cell cultures.
Materials and Methods : Primary cultures of cerebellar granule cells, neuron-glia cocultured cells (neuron : glia=6: 4), were prepared from 8-day old Wistar rats. For assaying cell viability, cells were plated onto cultured dishes with non-fluorescent cover glass bottoms and cells containing calcein-AM were measured by a fluoro-platereader. Extracellular NO metabolites were continuously perfused using a special microdyalysis probe and automat-ically injected into a HPLC-system. The retention times of NO₂ and NO₃ were within 4 and 6 min, respectively.
Results : Increases of NO metabolites were detected after the application of LPS (10 and 20μg) in a timedependent manner. Increases in glia cell cultures were much greater than in glia excluded cell cultures, and marked NO₃ production was determined in the glia cell cultures. Under these conditions, over 40% of all cells were killed by incubations with LPS longer than 12 hr.NO metabolites were produced much earlier than the occurrence of cell death. In Ca²⁺ free medium, increases of NO metabolites were significantly suppressed. Also midazolam, pentobarbital and propofol blocked the increase of NO production and occurrence of cell injury.
Discussion and Conclusion : Neuronal NO production can be detected before the occurrence of cell injury and is related to the coexistence of glia cells. Furthermore, this production may be associated with cNOS and NO₃ production can be seen in glia cell, primarily. Some intravenous anesthetics may have neuroprotective functions.

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We investigated in five acutely ill septic patients the relationships among (1) parameters related with coagulopathy including blood level of tissue factor pathway inhibitor (TFPI), which is an inhibitor of the extrinsic coagulation pathway, (2) endothelial cell injury, and (3) multiple organ dysfunction syndrome (MODS) . The blood glucose levels were strictly controlled by means of the artificial pancreas in order to exclude the influence of blood glucose levels to the parameters related with coagulopathy. Measurements include plasma total TFPI level (total TFPI), platelet count (PLT), fibrin and fibrinogen degradation products (FDP), fibrinogen, prothrombin time ratio, thrombin and antithrombin-III complex (TAT), D-dimer, α₂plasmin inhibitor-plasmin complex (PIC), antithrombin-III (AT-III), plasminogen, protein C, protein S, and thrombomodulin (TM) . Multiple organ failure (MOF) score was calculated by using the MOF criteria of Japanese Association for Critical Care Medicine.Both MOF score and TM were positively and most strongly correlated with total TFPI, and negatively correlated with PLT, Plasminogen and PIC.
Hypercoagulability accompanied by decreased fibrinolysis was considered to be closely related with MODS and endothelial cell injury. Total TFPI seemed to be one of the indicators of the severity of the acutely ill septic patients.

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Blood glucose concentration measured by two types of portable glucometers were compared with three different inspired O₂ in vivo. One type of glucometer measures the blood glucose level by the electrode method. Another glucometer measures the glucose level by a colored spectrophotometer. At first, the blood glucose levels of 50 blood samples were measured by a blood gas analyzer system (ABL 625, RADIOMETER Co., COPENHAGEN) . In order to inspect the accuracy of ABL 625, we compared these results to the data obtained by the Department of Central Examination Center. The correlation coefficient between both data was 0.995, and so we decided to use ABL 625 as a standard meter in this study (Control) . The inspiratory oxygen concentration was adjusted at three different levels ; FIO₂=0.33 (n = 31), 0.50 (n = 32), 1.0 (n = 25) . Positive correlation coefficient was confirmed between both methods and Contorol. The values measured by either methods were not significantly influenced by different FIO₂. These results were statistically analysed by the Wilcoxon's test. The results obtained by the electrode method was significantly lower than those obtained by a colored spectrophotometer. Thus these results indicated that values measured by the electrode method is much closer to these of contorol compared to a colored specutrophotometer.

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A 65-year-old man admitted to our hospital because of atrial fibrillation with tachycardia. He had a one-year history of hyperthyroidism without any medications. The past history and the present symptoms (nausea, general-ized fatigue, weight loss) suggested thyrotoxic crisis to prompt antithyroid drug therapy combined with β-blockade. On the second hospital day, he developed dyspnea, confusion and hypotension. An echocardiographic study showed diffuse severe hypokinesis. The circulatory failure was rapidly progressive to cause profound shock refractory to inotropics and vasopressors. Percutaneous cardiopulmonary support (PCPS) was therefore initiated. The cardiac function was too seriously depressed to be estimated reliably by the echocardiography until the third hospital day. The echocardiographic studies showed improving cardiac function thereafter. The patient was readily weaned from PCPS because cardiac function was stable and improved with an estimated left ventricular ejection fraction (LVEF) of 30 percent on the eighth hospital day. Acute renal failure and hepatic insufficiency developed but resolved without blood purification. He was discharged from ICU on the 17 th hospital day. This case illustrates that the laboratory examinations showing low level of TSH and increased TSH receptor antibody strongly supported the diagnosis of thyrotoxicosis to account for severe depression of the systolic function, for which the echocardiography facilitated the early initiation and weaning of PCPS.

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A 57-year-old healthy man admitted to the hospital complaining of abdominal pain after vomiting and fever. Physical examination on admission was unremarkable, but one hour later, the patient developed hypotensive with increased pain. Echographical examination of the abdomen and a chest X-ray revealed a sign of pleural effusion in the left thorax. Diagnostic esophageal endoscopy demonstrated a deep ulcer in the lower portion of the esophagus. Since those examinations were suggestive of esophageal rupture, the emergency operation was performed.
General anesthesia was induced with midazolam 5 mg, thiamylal 125 mg, and vecuronium 8 mg, while continuous cricoid pressure was applied by an assistant. After the induction, the chest tube was inserted into the left thorax. A large amount of hemorrhagic pleural fluid and residural foods were aspirated through the chest tube. After aspiration of pleural effusion, he dramatically recoverd from hypotensive shock. The operation finished after closing the fissure of esophagus successfully.
Prompt diagnosis and treatment are necessary in the patient with Boerhaave syndrome.

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Acute epiglottitis is a serious disease because of its potential for sudden fatal airway obstruction in a previously healthy individual. We reported two cases of adult epiglottitis, who were not resuscitated. The patients complained of sore throat and dysphagia on the first visit to clinic. They were diagnosed as tonsillitis and given oral antibiotics. Upper airway obstruction occurred within hours after the first arrival. One patient died at home and second patient was exhibited severe brain damage. After this event, we reviewed the Japanese literature for study of the features of epiglottitis in Japan. Eight hundred fortysix cases were reported between 1979 and 1998, and 95.3% of the patients were adults. Male-female ratio was 2. 2: 1. Airway control was established in 11.1% of the patients and mortality rate was 1.4%. Mortality was very high in the reports not from otolaryngologists. Acute epiglottitis is not a common disease and patients often visit general clinicians other than otolaryngologists. Therefore, the risk of acute epiglottitis should be well realized by general physicians.

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A 67-year-old man (ASA physical status 2, 162 cm, 37 kg) with left bronchial stenosis due to invasion of esophageal carcinoma was scheduled for insertion of a Dumon tube under general anesthesia. After induction of anesthesia with propofol and vecuronium, the Dumon-Harrell Universal Bronchoscope (DRUB) was inserted into his trachea. Immediately after the DHUB was inserted, we were unable to continue with manual ventilation. Spp2 decreased siginif icantly to 54%. On examination with a fiberoptic bronchoscope (FOB), we found an obstruction of the left main bronchus that was composed of mucosal tissue and coagulated blood. A chest x-ray revealed atelectasis of the left lung. The hypoxia was improved by a high-frequency jet ventilation. We speculate that mucosal tissue tore off from the trachea when the DHUB was inserted. This mucosal tissue and the coagulated blood formed a mass that caused a left bronchial obstruction. The ventilatory state improved after the mucosal tissue was removed with forceps under solid bronchoscopy and the coagulated blood was aspirated under FOB. After proper ventilation was restored, we succeeded in placing the Dumon tube in the left bronchial stenotic area.

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