Transient ischemia causes a peculiar type of cell death, referred to as delayed neuronal death, which is restricted to the hippocampal CA1 layer, and its mechanism is still controversial. This study addressed the molecular mechanism of delayed neuronal death using a transient ischemia-model of mongolian gerbil, focusing particularly on the induction of apoptosis by means of nitric oxide (NO·) and superoxide (O^-/⋅₂) . DNA fragmentation was demon-strated by both terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) method and DNA-ladder formation in the hippocampal CA 1 pyramidal neurons showing delayed neuronal death. Analysis of apoptosis-related genes at both protein and message levels revealed a decrease of bcl-2, an overexpres-sion of bax, and induction of the caspases in the hippocampal CA1 layer between 24 to 48 hours following transient ischemia. In the hippocampal CAl pyramidal neurons, inducible NO synthase (iNOS) was induced by transient ischemia at the message level at 6 hours, and at the protein level at 24 hours following ischemia. Nitrotyrosine formation was detected in the hippocampal CAl layer, indicating that a cytotoxic oxidant, peroxy-nitrite (ONOO^-), was produced from NO· by the interaction with O^-/⋅₂. Furthermore, activation of NF-κB, one of the important inducers of the iNOS gene, was shown in the hippocampal CA1 layer at 20 to 30 min after transient ischemia. These results clearly show that apoptosis is the main mechanism of delayed neuronal death in the hippocampus, and that down-regulation of bc1-2 is involved in the induction of apoptosis; this is followed by transcriptional activation of the caspase genes, which are common mediators of apoptosis. These findings suggested that iNOS induced in the hippocampal CA1 pyramidal neurons soon after transient ischemia may play an important role in the induction of apoptosis; NO· and O^-/⋅₂ may show multiple functions. Transcription of the iNOS gene seems to be upregulated by NF-κB, which is activated by calcium-signaling due to excitatory amino acid neurotoxicity.

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The effects of vasodilators on cerebral blood flow (CBF) are summarized. Vasodilators may affect CBF as a result of decreased cerebral vascular resistance and cerebra perfusion pressure.
Trimetaphan has few effect on CBF or intra-cranial pressure (ICP), but decrease in cardiac output, tachycardia, tachyphylaxis and mydriasis limit the clinical use of the drug. Trinitroglycerin (TNG) dilates intracranial capacitance vessels. TNG has variable effects on CBF and may increase ICP to dangerous levels in patients with intracranial pathology. Sodium nitroprusside (SNP) induces vasodilation in both cerebral resistance and capacitance vessels, so cerebral blood volume and ICP may increase. A mixture of SNP and other drugs are effective to avoid the cyanide toxicity. Prostaglandin E₁ (PGE₁) is a potent vasodilator that causes direct relaxation of vascular smooth muscle. Both ICP and CBF are well-maintained despite a reduction in blood pressure.
Resent studies have suggested that some kinds of vasodilators may present a new therapeutic role for the management of ischemic stroke. Nitric oxide donor TNG or SNP may ameliorate cerebral ischemic damage because of its cerebrovasodilation and inhibitory effects of platelet aggregation. PGE₁ has protective effects against the delayed death of neural cells, and it might be due to direct protective effects of cell membrane in addition to its microcirculatory improvement.

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Our hospital staff had opportunities to take basic cardiac life support (BCLS) courses three times, once every 3 months. The total number of participants in the course was 54. The course participants were evaluated for their acquired skill level during manikin training using a check-list consisting of 15 items corresponding to the American Heart Association 8-step BCLS course. The maximum score was set 28. A videocamera was used to revise the BCLS skill evaluation. The evaluation was done before starting the BCSL course (T₀), just before starting the second course (T₁), and just after the final BCLS course (T₂) . Scores at both T₁ (20.7±5.2) and T₂ (27.3±0.9) were significantly higher (P<0.05) than the total score point at To (6.5±3.8) . Seventeen participants had previously attended other BCLS courses, and had better scores than those who had never attended similar BCLS courses. However, the BCLS skill of those who had experienced previous other BCLS courses was far less than we expected. It is most important that BCLS courses should be taken repeatedly and regularly, if individuals are appropriately to carry out actual cardiopulmonary resuscitation.

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We measured circulating blood volume (CBV) in 42 elective surgical patients (24 male and 18 female, 19-74 years old) after induction of anesthesia (before the start of surgery) using DDG-2001 (Nihon Kohden Corp.), which enabled us to monitor arterial concentration of indocyanine green and provided CBV calculation. CBV and CBV per body weight were 4.7±1.1l and 81±18 ml/kg (Mean±SD), respectively. CBV had a significant but weak correlation with body weight and body surface area (r=0.494, P=0.0009 and r=0.557, P=0.0001, respectively), with the maximum value of 6.5l observed in obese patients whose weight exceeded 80 kg. There were no significant differences in CBV per body weight (ml/kg) between sexes (81±17 in male, 88±32 in female), and among ages (83±30 in 65 y>, 85±19 in 65 y≤) . The instrument used in the present study facilitated simple and minimally invasive bed-side monitoring of CBV and has been shown to provide reliable CBV values comparable to the values obtained with the conventional radioisotope method. Measurement of CBV is useful not only for circulatory management but also for determination of appropriate drugs doses.

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Although low output syndrome (LOS) is often found mainly due to left ventricular failure, recent development in cardiac imaging including echocardiography is able to detect right ventricular dysfunction in the presence of LOS. We reported three cases which developed right ventricular dysfunctions after cardiac surgery despite conventional cardiac support. All cases were diagnosed by transesophageal echocardiography. Additional intraaortic balloon pumping (IABP) in all cases and artificial veno-arterio bypass (VAB) in two cases were necessary to support right ventricular function. One case of which need VAB could not survive. Early diagnosis and treatments including VAB should be indispensable for right ventricular dysfunction.

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The three cases reported here illustrate the effect of ventilation during cardiopulmonary resuscitation (CPR) in infants with congenital heart disease accompanied with high pulmonary blood flow such as endocardial cushion defect, hypoplastic left heart, and large ventricular septal defect. Although use of high fraction of inspiratory oxygen (F_IO2) and/or hyperventilation are performed in principle during CPR, these treatment can conversely break the balance between pulmonary and systemic vascular resistance in those peculiar hemodynamics. From clinical expe-riences we emphasize four practical purposes as follows: (1) temporary use of 100% oxygen and/or manual hyper-ventilation can be approved at the beginning of CPR, (2) to lower F_IO2, if possible is desirable after the diagnosis of heart disease accompanied with high pulmonary blood flow or dependence of patent ductus arteriosus referring to oxygen saturation, (3) the method of ventilation without less reduction of pulmonary vascular resistance may be decided carefully considering into central nervous system, and (4) echocardiography should be performed not only during CPR but after recovery from cardiovascular instability to evaluate pulmonary blood flow. The artificial ventilation in regard to FIO2 and the method of ventilation during CPR should be carefully managed in patients with congenital heart disease.

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A 57-year-old female was admitted to Chiba-nishi General Hospital complaining of exertional dyspnea. Severe hypoxemia and right ventricular dilatation were observed, which were consistent with acute pulmonary thromboembolism. Multiple large thrombi were detected in the bilateral main pulmonary arteries by angiography. Both thrombolytic therapy with urokinase and transcatheter suction maneuver were unsuccessful. An insertion of percutaneous cardiopulmonary support system (PCPS) was attempted only to fail because of peripheral vascular disease and her further deterioration, which resulted in sudden cardio-pulmonary arrest.
The patient was immediately transferred to the operating room under cardiopulmonary resuscitation, and emergency open-heart thrombectomy was successfully performed.
The postoperative recovery was uneventful and she discharged without any clinical sequellae following six weeks admission.

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We have experienced 2 cases of cardio-pulmonary arrest (CPA) occurred in our hospital, and we success-fully resuscitated both cases by switching the resuscitation methods from standard (STD) CPR to ACD-CPR. We recorded the wave forms of arterial pressure during the CPRs in these 2 cases. ACD-CPR raised both arterial systolic and diastolic pressure (STD: 60-70/20-30 mmHg, ACD: 120-140/40-50 mmHg) and markedly augmented pulse pressure. Chest compression frequency during ACD-CPR decreased compared with STD-CPR (STD: 120-130 beat/min., ACD: 100-110 beat/min.) due to fatigue of the operator in ACD-CPR. These 2 cases indicate that the chance of ROSC (return of spontaneous circulation) by ACD-CPR seems higher than that of STD-CPR in Cardio-pulmonary arrest (CPA) .

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We have experienced a case of acute renal failure caused by paroxysmal nocturnal hemoglobinuria, in which blood purification therapy was effective.
A 44-year-old male patient complained abdominal pain with fever and cough 2 days before his admission. He was anuretic complicated with severe hemolytic crisis. Steroid pulse therapy, administration of haptoglobin, and volume loading with diuretics all failed to improve oliguria. Con-tinuous hemodiafiltration (CHDF) was started on ICU Day 1, followed by continuous equilibration peritoneal dialysis (CEPD) on Day 11. The patient was placed on ventilator, and was successfully weaned from it at 18 th day. Then, he regained normal urinary output, and per-itoneal dialysis was discontinued on Day 21.
The concentration of C 3 a in post-hemofilter blood was less when polyacrylonitrile (PAN) was used than when polymethyl methacrylate (PMMA) was used.
Acute renal failure is not frequently associated with paroxysmal nocturnal hemoglobinuria. With this patient, upper respiratory tract infection would trigger severe hemolytic crisis, and dehydration from fever and vomiting exacervated his physical condition, leading to acute renal failure. Early intensive care with CHDF/CEPD provided favorable outcome for this patient.

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Nafamostat mesilate has been known to induce hyperkalemia, but the mechanism has been unidentified. It was reported that nafamostat mesilate and/or its derivatives may induce hyperkalemia only in non-anuric state by affecting renal potassium excretion. We reported here two cases of acute pancreatitis associated with nafamostat mesilate-induced hyperkalemia during continuous hemofiltration. In the first case in which the patient became anuric, only serum K+ value increased despite that the other biochemical parameters stayed within normal limit. In the second case, patient was non-oliguric. It is suggested that nafamostat mesilate and/or its derivatives may induce hyperkalemia by affecting the extrarenal potassium regulatory system instead of affecting renal potassium excretion.

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