Studies were made on the hemodynamics in the liver and kidney during hemorrhage and retransfusion, using 20 dogs with or without hepatic periarterial nerve plexus, anaesthetized with sodium pentobarbital. The results were as follows. In 14 dogs in which the hepatic periarterial nerve plexus was left intact (Group A), the averages of the hepatic arterial flow (HAF), portal venous pressure (PVP), portal venous flow (PVF), and flow in the right renal artery (RAF) decreased significantly to 38, 64, 35, and 25%, respectively of the control levels when the abdominal aortic pressure (ABP) fell to 40 mm Hg (36% of the control level) during hemorrhage. At the same time the portal venous resistance (PVR) and the right renal vascular resistance (RVR) increased greatly and the hepatic arterial resistance (HAR) either increased or decreased in different dogs. During retransfusion, the ABP and vascular resistance returned to nearly the control levels, the PVF increased beyond the control level. In 6 dogs in which the nerve plexus was resected (Group B), the decreases in the HAF and RAF during hemorrhage were not significantly different from those in Group A. These results may suggest the following. The decrease in the HAF during hemorrhage seems to be mostly a passive change resulting from decrease in the systemic blood pressure. Neurogenic regulation may be a little. Further, the existence of the humoral regulation and autoregulation in the HAF were suggested in some cases. While, the responsibilities to hemorrhage and retransfusion appear to be different among the examined three vessels, i.e. the hepatic artery, portal vein, and renal artery. No definite interrelation was seen between the hepatic and renal circulations.

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Left ventricular performance and coronary flow in isolated dog hearts were observed for to discuss whether lungs have any nonrespiratory function. The results of our experiments showed the fact that pulmonary circulation seemed to have some metabolic functions to prevent the increase in coronary flow and the decline in ventricular performance. And it was also suggested that isolated lungs removed a factor responsible for coronary vasodilation and the decline of ven-tricular performance. But it could not be fully negrected that the pulmonary circulation added a factor which prevents the increase in coronary flow.

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Bovine tendon collagen suspension (4.5mg/kg) was injected rapidly into the femoral vein of 14 normal (untreated) and 8 busulfan treated rats. Trasient effects included decreased platelet counts and arterial PO₂, increased central venous pressure, apnea, bradycardia and variable A-V block. These findings were most prominent within 1 minute after injection and subsided or disappeared by 10 minutes. During this period, ADP and ATP in platelet-free plasma from carotid arterial blood were measured in a liquid scientillation counter using the firefly luciferase assay. In normal (untreated) rats, collagen injection was followed by increases in plasma ADP and ATP, a rise in plasma hemoglobin and minimal changes of fibrinogen and hematcrit. Pathological observations indicated the platelet emboli in pulmonary vessels. In contrast, rats made thrombocytopenic by intraperitoneally injected busulfan prior to collagen injection had minimal or no change in platelet count, plasma ADP, ATP, hemoglobin, fibrinogen, or cardiopulmonary functions following collagen injection. These finding suggest that collagen injection causes release of ADP and ATP from platelets; released ADP induces platelets to form aggregates which lodge in the coronary and pulmonary microcirculations and elsewhere, resulting in thrombocytopenia and the cardiopulmonary dysfunction, in the presence of shear, of red cells with vessel surfaces altered by platelet aggregates.

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A 22-year-old female patient presenting complete atrioventricular block and giant P waves in electrocardiogram had anomalous pulmonary venous drainage from the entire left lung. There was normal drainage from the right lung and no associated atrial septal defect or other intracardiac abnormalities. After a permanent pacemaker was implanted, she manifested signs and symptoms of heart failure. Although the anomalous pulmonary vein was anastomosed to the left atrium, intractable heart failure continued. She died six months later after surgical intervention. Postmortem examination revealed diffuse interstitial fibrosis throughout the myocardium.

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Five interesting autopsy cases of post-valvular replacement death are reported and discussed with special reference to disturbances of the conduction system. The most important acute changes are hemorrhages; the significance of a venous hemorrhage is emphasized. Chronic changes are collagenization of conduction system. One case of mycotic valvulitis, probably due to aspergillus, and one case of dissecting aneurysm probably related to previous valve replacement surgery are included.

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Electrocardiogram and coronary angiography play an important role in the diagnosis of ischemic heart disease. However, ischemic heart disease should be evaluated intrinsically on the basis of myocardial metabolism for its diagnosis because it is the pathophysiological state of myocardial hypoxia. Although various metabolic indicators of myocardial hypoxia such as excess lactate and redox-potential etc. have been advocated so far by many investigators, a number It has been suggested that electron spin resonance (ESR) spectrometry was an useful method for detecting of the mechanism of biological reactions, particularly an involvement in enzymatic oxidation-reduction processes. Yamazaki examined pathophysiological state in oxidation-reduction system in ischemic myocardium by means of ESR spectrometry, and proposed a new metabolic indicator of myocardial hypoxia based on the myocardial free The left descending coronary artery distal to radical metabolism. Yamawoto reported myocardial free radical metabolism during coronary insufficiency induced by exercise, and observed an increase in the free radical of coronary sinus plasm after exercise. Exercise, the most physiological myocardial stress, has its own intrinsic direct effects on metabolism. It is therefore not always appropriate to the examination of myocardial metabolism. On the other hand, atrial pacing, which enables to apply a controllable stress to the heart, is a simple, repeatable and safe procedure without the hemodynamic and metabolic changes that accompany exercise. It has there-fore been employed in the study of pathological states during coronary insufficiency. The present study was undertaken to investigate alterations in coronary circulation and myocardial metabolism, especially free radical and lactate metabolism, during atrial pacing-induced tachycardia in dogs with experimental acute and chronic coronary insufficiency, and to define the clinical application of ESR spectrometry in combination with atrial pacing to the diagnosis of ischemic heart disease.

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