Pathophysiology of shock was fundamentaly investigated in several different ways. 1. Fractional distribution of cardiac output was measured, using radioactive microsphere technique. Hemorrhagic, endotoxin and trime-thapan hypotension were compared to each other in their fractional distribution of cardiac output. As a whole, cardiac output was distributed in the way to maintain cerebral or coronary blood flow, whatever the cause of shock may be. This "centralization" was rather well maintained even shock progressed. Splanchinic blood flow, especially the pancreas flow were decreased significantly. This may be related to the production of vasoactive or toxic substances from these organs. 2. Myocardial depressant factor was identified both in plasma and pancreas in advanced shock. Gel-chormatographic analysis was applied to separate the myocardial depressant factor. It is also demonstrated that myocardial depressant factor was produced in pancreas, transported via blood stream to the hear and caused cardiac depression. 3. In vivo cardiac contractility was measured by the change of Vmax sequentially as shock advanced. Left ventricular pressure was measured, using catheter tip transducer. In hemorrhagic shock, cardiac contractility began to decrease 4 hours after bleeding and continued to deteriorate progressively thereafter. 4. Regional coronary blood flow distribution was also measured by radioactive microsphere method. 2 hours after bleeding, endocardial fractional distribution already began to decrease and remained in the same distributional pattern even 4 hours after bleeding, while the myocardial contractility did not show any deterioration in 2 hours after bleeding. So it may be said that endo-cardial ischemia had no significant relationship with this cardic dysfunction. 5. Phagocytic function was decreased progressively when shock advanced. Reticuloendothelial depressing substance was also analyzed using gel-chromatographic method. Bioassay of RDS was shown by the decrease of phagocytic index after administering this fraction to healthy rats. 6. Closed loop, negative feed back mechanism (Fig.24) was suggested with relation to the above mentioned results. Decrease of cardiac output, followed by decrease of splanchinic blood flow, might cause the production of myocardial depressant factor. And this MDF might exert again decrease of cardiac contractility, thus closed negative feed-back loop was established. This mechanism might be called as "peripheral theory" for cardiac deterioration in shock. MDF, lysozomal enzymes or other vasoactive substances could not be phagocytized because of the reticuloendothelial system dysfunction, which may be caused by the decrease in opsonin activity or the release of reticuloendothelial depressing substance.

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Severe respiratory failure may develop in patients following or during various types of shock. A number of mechanisms for the genesis of this syndrome have been proposed. The exact role of each of these etiologies is unknown, but a combination of these and others may be the actual causative factors. Prevention of respiratory failure consists of prompt resuscitation of shock, and prevention of hypoventilation or atelectasis, embolism, and infection. Judicious use of oxygen and electrolyte fluids is also important in prophylactic therapy. At the present the principal feature in treatment consists of IPPV with adequate inspired oxygen concentration. If progressive pulmonary deterioration occurs in patients on IPPV, the CPPV may be indicated. Judicious use of CPPV may result in an apparent improvement of shock lung in some instances.

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Relationship between shock and disseminated intravascular coagulation (DIC) was investigated in 699 consecutive autopsied cases. The diagnosis of DIC was made when consumption coagulopathy was observed. Among these patients, 106 cases had evidences of DIC and 30 ones had clinical and pathological findings highly suggestive of DIC although the coagulation findings were nonspecific. Shock was complicated in 38 of the former and in 10 of the latter. In 32 of these 48 cases with shock coagulation abnormalities were observed simultaneously with or after the development of the shock. The most common underlying disease in these patients was gram-negative septicaemia, while shock in gram-positive septicaemia, gastrointestinal hemorrhage and myocardial infarction caused DIC less frequently. In the other 16 cases, about 70% of which was patients with metastatic cancer of the gastrointestinal or biliary tracts, shock developed after the diagnosis of DIC was established, although marked exaggeration of the coagulation findings was observed following the shock. Levels of factor XII and C3 in plasma decreased in DIC. Especially, depletion of factor XII was remarkable in cases with septic shock. The most important clinical symptom in patients with DIC associated with shock was acute renal failure. Administration of low does of heparin to DIC improved coagulation abnormalities frequently, however no beneficial effects on symptoms other than bleeding, i.e. acute renal failure, were observed. Examination of autopsy material showed that fibrin thrombi were present in about 70% of these cases. It is concluded that shock is frequently accompanied with DIC and the patients with shock should be treated with heparin as soon as possible whenever DIC was suspected.

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Clinical study was conducted in the course of treatment of patients with hypovolemic and septic shock at Department of Traumatology, Osaka University Hospital. We have found large difference between date obtained in our study and experimental results obtained in animals. In hypovolemic shock of man, we could not observe "taking up phenomenon" to abdominal organs. Therefore, if the shock does not respond to transfusion and infusion, we must look for other causes. In patients whose shock state persisted more than 10 hours, death related to shock organs increased remarkably. The nature of septic shock in man is hyperdynamic state. Hemodynamic change during the development of septic shock from sepsis was described and the difference from experimental research on endotoxin shock in animals was discussed.

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Five children under 10 years of age were operated on with a Bjork-Shiley disc valve. The mitral valve was replaced in four patients and the tricuspid valve in one. No hospital death, late death, or thromboembolic episode was observed during the 155 patient-months of the follow-up. Moreover, a marked reduction in cardiomegaly was demonstrated to parallel the clinical improvement and low risk seen in adult. We feel that our experience might justify a more aggressive approach in the management of valvular disease in children of the younger age group.

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