Cerebral white matter, which is composed of myelinated axons and glials, is demonstrated to be as vulnerable as grey matter to ischemia, and the mechanisms of white matter damage are distinct in some points from those of grey matter damage. However, attention has focused almost exclusively on the damage to grey matter in rodent models of brain injury while the assessment of white matter damage has been neglected. Because an explanation for the lack of efficacy of most of neuroprotective drugs for clinical use is that neuroprotective strategies have primarily targeted grey but not white matter damage, the efficacy of a drug or a method should be dependent on its ability to protect against not only grey but also white matter damage.

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Neuroprotection means to describe the putative effect of interventions protecting the brain under pathological condition, such as global ischemia, stroke, traumatic brain injury, brain hypoxia and so on. The main concept of neuroprotection is to prevent the cascades of pathological molecular events following ischemia that leads to massive calcium influx, activation of free radical reaction and cell death. This review article describes the mechanisms of ischemic brain damage and summarize the neuroprotection trials to date. We also try to consider the perspectives of drug therapies. Clinical trials should use randomization techniques, which reduce imbalance of prognostically important baseline variables and choose the proper sample size of trial should be based on expectations of a clinical effect.

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Patients resuscitated from cardiac arrest have only a very short time window for therapy. This makes it crucial to quickly recognize the severity of brain damage in post-resuscitated patients and make therapeutic plans. In this study we measured auditory brain stem responses (ABRs) and took continuous measurements of jugular oxygen saturation (SjO₂) during therapeutic hypothermia after resuscitation from cardiac arrest in order to evaluate the severity of brain damage and the effectiveness of the therapeutic hypothermia. Our findings demonstrated that an absence of V waves in the ABRs of patients after the return of spontaneous circulation (ROSC) is a possible indication of severe brain damage and limits the chances of improved outcome after therapeutic hypothermia. In case of SjO₂> 80% on admission, outcome was poor even if the ABR V wave was present after ROSC or when ABR V wave disappeared after the time course. We conclude that it is important, when planning therapeutic strategies, to recognize the severity of brain damage and the pathophysiology after ROSC in post-resuscitative patients.

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The effect of nitrous oxide on neuronal cells during cerebral ischemia was evaluated by direct current (DC) potential, neuronal damage and dynamic change in extracellular glutamate concentration.
Under 1 % halothane anesthesia, forty-six male gerbils were randomly assigned to a group receiving 70% nitrous oxide (N₂O group) and a group receiving 70% nitrogen (N₂ group) . Forebrain ischemia was performed by occlusion of bilateral common carotid arteries for 3, 5 or 7 minutes. DC potential was recorded from the bilateral hippocampal CA1 regions. Histological evaluation was performed 5 days after the ischemia. Dynamic change in hippocampal extracellular glutamate in 5-minutes ischemia was also measured.
Onset time of ischemic depolarization was shorter in the N₂O group (p<0.01) . In the case of 5-minute ischemia, the percentage of damaged neurons in the N₂O group was higher (p<0.01) . However, the difference of dynamic changes in extracellular glutamate concentrations in both groups was not significant.
Nitrous oxide increased neuronal damage at 5-minutes ischemia in gerbils. However, there was no significant difference between the dynamic changes in extracellular glutamate concentration in both groups. The increase of neuronal damage by nitrous oxide was affected by reduction of onset time and a factor other than the amount of extracellular glutamate release.

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We compared the data of between 128 out-of-hospital cardiac arrest patients before the introduction of the comprehensive defibrillation on April 2003 and 419 cases after that. We examined prognosis, the first identified cardiac rhythm, the witnessed, bystander CPR, cardiogenic cases, and time from dispatch to the first defibrillation (TDD) .
1.6% of 128 cases in the former and 4.8% of 419 cases in the latter recovered to their usual lives. The first identified cardiac rhythm was VF in 7% of the former and in 8.8% of the latter. In the former, there were no significant differences among the prognosis according to the cardiac rhythm, but in the latter, recovery rate to their usual lives in VF rhythm was higher than those of PEA and asystole. The rates of by-stander CPR (60%) and the witnessed (91%) of the full-recover patients were significantly higher than those in the worse conditions. Cardiogenic arrest was 65.6% of the former and 54.7% in the latter. TDD was shorten from 11.7 ±3.8 min in the former to 8.8±3.0 min in the latter.
Increase of the rate of witnessed by-stander CPR and enhancement of prehospital care would improve the full-recovery rate of out-of-hospital cardiac arrest patients.

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It is necessary for nurses to acquire the skills for Basic Life Support (BLS) with the increasing number of patients requiring resuscitation among hospitalized patients. This seminar on BLS for nurses was created in 2003 with an Objective Structured Clinical Examination (OSCE), with the objective of imparting the precise skills of BLS. We evaluated whether such education might be useful for imparting sustained knowledge of and skills for BLS.
The study results revealed that the knowledge and skills of the nurses could be sustained for a longer period of time with a follow-up-seminar conducted after 6 months followed by self-education before the OSCE on BLS.
In conclusion, to sustain the skills for and knowledge of BLS for a longer period of time, it would be important to hold a follow-up seminar after a 6-month period and to recommend self education.

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It is a very important thing that staff members at the hospital can perform basic life support correctly and quickly at the time of in-hospital emergency. The cardiopulmonary resuscitation training for hospital staff has been held every month from June, 2004. 21 month (year and nine month) has passed since it began; a questionnaire of “how the awareness and the knowledge to cardiopulmonary resuscitation have changed” was carried out. The rate who answered that they knew how to do the cardiopulmonary resuscitation was increased from the initial 82% to 93%. The rate who answered that they could perform the cardiopulmonary resuscitation alone was increased from 30% to 52%. The interest and knowledge about cardiopulmonary resuscitation were increasing steadily. But it is going to take more time for all staff to attend the lecture. Then, because there was a revision of guideline for cardiopulmonary resuscitation (guideline 2005), it is also necessary for the participants who have already participated in the lecture to reconfirm their knowledge and skills, and we must continue the high quality education courses in the hospital.

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There are two methods of tracheostomy commonly performed in clinical practice: conventional surgical tracheostomy and percutaneous tracheostomy. Percutaneous tracheostomy is getting popular because of its better cost-effectiveness, safety and simplicity. There have been several reports regarding the perioperative complications of percutaneous tracheostomy. However, little is known about the late complications. We now report two cases of suprastomal stenosis occurred after percutaneous tracheostomy (Ciaglia Blue Rhino technique) . In one patient, the second percutaneous tracheostomy was performed. The incidence of the suprastomal stenosis is 4% (2 out of 47 cases performed in our institute during the last year and a half) with Ciaglia Blue Rhino technique that may catch the upper tissues into the trachea, the incidence of tracheal stenosis may become higher than with the surgical tracheostomy. Long term follow-up is needed to assess the late complications after percutaneous tracheostomy.

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An eight year old boy had been cared with home oxygen therapy (HOT) and administered PGI₂ due to primary pulmonary hypertension, underwent cardiac catheterization to evaluate his cardiac performance.
The injection of contrast medium into the left atrium induced severe bradycardia and hypotension abruptly, and then necessitated cardiopulmonary resuscitation. Although he temporarily recovered, the transnasal intubation resulted in severe bradycardia and hypoxemia again. Cardiopulmonary resuscitation was re-started, however inhalation of nitric oxide could gradually ameliorate him and he was transferred to the ICU. He was eventually discharged from the hospital on the 17th day without any sequelae. We recognized this event during cardiac catheterization was consequent upon pulmonary hypertensive crisis, because he had been suffered from severe pulmonary hypertension and the inhalation of nitric oxide was effective.

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A 43-year-old man developed suddenly dyspnea and syncope on third day of his hospital stay for traffic accident. After echocardiographic and computed tomographic examination, he was diagnosed as submassive pulmonary embolism with right atrial large thrombus. We introduced percutaneous cardiopulmonary support (PCPS) because free-floating thrombus could result in recurrent emboli. Therefore, we administered with monteplase. After two hours, he developed recurrent embolic event proved by echocardiogram, but hemodynamic disturbance was slight by PCPS. He underwent percutaneous catheter-based aspiration of thrombus. Therefore, he was improved and discharged on 31 day.

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Massive pulmonary embolism is a major cause of cardiac arrest. Standard CPR is not effective for cardiac arrest caused by massive pulmonary embolism.
We report resuscitated severe pulmonary embolism with cardiac arrest. The first case occurred after arterial angiography by femoral arterial approach and the second case occurred four days after abdominal surgery.
Thrombolitic therapy using tPA was effective to the second case, and he was recovered completely. without neurological deficiency
We report a case of successful thrombolitic therapy using tPA for cardiac arrest patient caused by massive pulmonary embolism.

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