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The acute effects of carbon monoxide (CO) on cardiac metabolism at the mitochondrial level were investigated. Rats were exposed to 4% CO for 4 minutes in a closed chamber. Immediately after exposure, hearts were removed and frozen with a precooled clamp. Blood from the thoracic cavity was sampled for analysis. Gas analysis of arterial blood taken from the abdominal aorta demonstrated severe hypoxia with oxygen partial pressure less than 20 mmHg, metabolic acidosis and reduced pH value. There were no significant changes in the plasma level of glucose and non esterified fatty acids (NEFA). In the myocardium, ATP levels decreased significantly, and concomitantly, a significant increase in the plasma uric acid level was observed. Although no significant change was observed in short chain acyl carnitine, free carnitine levels decreased to one fourth of the control value. Long chain acylcarnitine increased 11-fold. Coenzyme Q9 (CoQ9) level decreased significantly, but there was no significant change in Coenzyme Q10 (CoQ10).

-255 -Surface and deep electroencephalograms , electrocardiogram and behavior of 10 male rabbits were studied by infusing fresh water or sea water slowly at a speed of 0.5-2.0 ml/min, by means of a dripping apparatus, into the canulated trachea until the death of the animals.From the behavior of the animal and EEG and ECG findings, the course was divided into 4 stages. The 1st, alert stage; 2nd, adapted or calm stage; 3rd, dyspnea stage; and 4th, covering from the agonal spasm to ECG silence. The course of this drowning death was quite different from that due to a large amount of water aspirated within a short period. The volume of fresh water needed to kill the animals was 7 times larger than that of the sea water in this method, and the latter was less than half of the volume of sea water necessary for the death due to short period aspira tion. The mechanism of death seems to be slow and prolonged asphyxia and, among the terminal events in fresh water drowning, there might occur marked pulmonary hypertension that results in a high degree of lung edema.In the ECG at terminal stage, final bradycardia (84.4% of normal pulse rate) at around the time of surface EEG disappearance, and final tachycardia (142.7% of normal pulse rate) about 120 sec later than final bradycardia and 40 min later than deep EEG disappearance were observed consistently. After clinical signs of death ECG still continued to beat slowly for 1-2 hr.slowly induced sea and fresh water drowning; permanent electrode; EEG; ECG Since the first heart transplantation was performed in 1967 in our country, the donor-problem has been widely discussed all over Japan, not only from the medical but also from the ethical and moral aspects. One of the authors, as a surgeon, has experienced an operative death case in which continuous ECG tracing was taken for more than one hr after the clinical signs of death. But the courses of events around the time of death of living creatures were not clearly documented so as to be readily applied for the resuscitation and/or organ transplantation etc. by any physicians or surgeons.