We investigated the role of gastric prostacyclin (PGI₂) in water-immersion restraint stress-induced gastric mucosal injury in rats. Gastric 6-keto-PGF_1α levels were increased after 30min of stress, followed by a decrease to below baseline after 6 to 8h of stress. Gastric mucosal blood flow (GMBF) was decreased with time after stress. Gastric myeloperoxidase (MPO) activity was significantly increased after 8h of stress. Pretreatment of the animals with indomethacin (IM) prevented the increase in the gastric level of 6-keto-PGF_1α and markedly reduced the GMBF in animals subjected to stress. IM pretreatment markedly increased gastric MPO activity and exacerbated gastric mucosal injury in animals subjected to stress. Iloprost, a stable analog of PGI₂, inhibited these IM-induced changes in stressed rats. Although nitrogen mustard-induced leukocytopenia inhibited both exacerbation of gastric mucosal injury and the increase in the gastric accumulation of leukocytes induced by IM in stressed animals, the IM-induced decrease in GMBF was not prevented in leukocytopenic animals. These observations strongly suggest that gastric PGI₂ plays an important role in preventing formation of gastric mucosal lesions not only by maintaining the gastric mucosal blood flow, but by inhibiting the gastric accumulation of leukocytes.

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We prepared hemorrhagic shock models in dogs administered Neo Red Cell (NRC) instead of being given a blood transfusion to determine the effect of resuscitation fluid with respect to hemodynamic kinetics and oxygen kinetics. Under 50% oxygen inhalation, animals were exsanguinated at a rate of 30ml/min. Exsanguination was continued until systolic pressure decreased to 60 to 69mmHg and was followed by transfusion of NRC at the same rate. This cycle was repeated three times. First, we examined the mild shock in 6 dogs (group 1). In these experiments, NRC was transfused immediately after exsanguination. The required amount of NRC was tha same as that of the exsanguinated blood. On the other hand, we examined the more severe and irreversible shock in 7 dogs (group 2). Animals were left untreated for 30 minutes after exsanguination, then NRC was administered. NRC required 1.6 times the exsanguinated blood volume. Hemodynamically, vascular resistance decreased and the cardiac index increased in group 1 because of the low viscosity of NRC. However, vascular resistance increased gradually and the cardiandex decreased in group 2. In group 1, oxygen consumption did not increase. In group 2, oxygen consumption increased. NRC compensated for the decrease in cardiac output with an increase in the AV difference to deal with the increased oxygen consumption.

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Recently, an increasing number of patients are admitted to the emergency department with sudden cardiopulmonary arrest (CPA). When it is impossible to make a precise clinical diagnosis in patients who have died and cannot be resuscitated, the cause of death is usually recorded as acute heart failure. This was recorded for 212 of 384 adult (30∼80 years old) patients with non-traumatic CPA on arrival over the last 7 years in our department. In order to clarify the incidence and pathophysiology of acute myocardial infarction (AMI) in sudden CPA patients, a pathologic study including postmortem coronary angiography and hematoxylin-basic-fuchsin-picric acid staining of the myocardium was carried out in 64 patients with no vital signs on arrival and whose death had been ascribed to “acute heart failure”. Thirty-six (56.3%) out of the 64 autopsied cases were diagnosed with AMI. Assuming that this proportion of “acute heart failure” was due to AMI and adding these to the cases of clinically diagnosed AMI, 36.2% of sudden cardiopulmonary arrest patients admitted to our department as having CPA on arrival would be considered to be suffering AMI. Other causes of sudden death were arrhythmia (6), cardiomyopathy (4), aortic aneurysm rupture (6), pulmonary thrombus (2) and others (10). Postmortem coronary angiography revealed a high incidence of coronary obstruction and severe narrowing in the proximal segments of the left anterior descending (LAD), left circumflex (CX) and right coronary (RC) artery. The 36 AMI patients consisted of 19 with their first AMI and 17 with reattacks on healed myocardial infarctions. They also consisted of 18 with multi-vessel lesions and 18 with single-vessel lesions. First AMIs were composed of 13 cases with single vessel lesions and 6 cases with multi vessel lesions, while reattacks were composed of 5 cases with single vessel lesions and 12 cases with multi vessel lesions (p<0.05). Fresh thrombi were observed in 27 cases (75%). All 18 with single-vessel lesions were in the proximal portions of the LAD, CX or RC. An acute lesion in the proximal coronary artery often produces larger volumes of ischemic myocardium and is more likely to cause sudden cardiac death. In conclusion: 1) We estimate that 36.2% of adult sudden CPA victims suffer AMI. 2) Infarctions resulting in sudden cardiac death in AMI patients suffering single-vessel lesions were all in the proximal portions of the major coronary arteries.

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CPR was performed on a cardiac arrest victim who had received a kick to the side. We succeeded in reviving the victim after more than two-and-a-half hours of closed-chest cardiac massage (CCCM). One factor in success of CPR is initiation of CPR immediately after cardiac arrest. Other factors are early administration of oxygen and a young patient. It is thought that the reason the CPR took so long to succeed despite having been initiated immediately after arrest was because CCCM inside the ambulance proved to be ineffective. A CCCM machine (thumper) is essential for performance of in-ambulance CCCM. It is difficult to decide when to stop CPR in emergency situations where there is a lack of diagnostic equipment for vital signs.

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