There have been many works on cerebral electrical activity (EEG) during convulsion, however, very few on cerebral blood flow (CBF) because of lack of adequate method for CBF during convulsion. Since CBF is influenced by blood pressure and vascular resistance which is greatly influenced by metabolic activity, measurement of metabolic activity should simultaneously be made. Method of continuous recording of CBF by thermistor, of metabolic activity by PO₂, PCO₂ pH, and Na⁺ have been developed in our laboratory and these methods were applied to the study of convulsion induced by Megimide.

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Hypersensitive reaction to penicillin, or anaphylactic shock is a clinical problem of increasing magnitude. Although hepatic circulation in secondary shock due to trauma or hemorrhage has been extensively studied in animals especially on its irreversibility, hepatic circulation in anaphylactic shock has not yet been fully understood. In this paper, hepatic circulation in anaphylactic shock is discussed in correlation with systemic hemodynamics and the plasma concentration of catecholamines in dogs. The mechanism of the change of hepatic circulation is also mentioned. I HEPATIC CIRCULATION IN ANAPHY-LACTIC SHOCK Systemic and hepatic circulatory dynamics were examined simultaneously, for the furtherclarification of the possible relationship between those two systems. Material and Methods The observations reported in this paper were made on sensitized dogs under thiopentobarbital sodium anesthesia.(1) Adult dogs were sensitized by horse serum. At subsequent intervals after the last sensitization, anaphylaxis were provoked by a intravenous injection of horse serum.(2) Hepatic blood flow were determined by the modified Frank's method. A catheter was introduced from the right creasing magnitude. jugular vein into the hepatic vein and advanced as far as possible. Blood flow from the catheter, which is proved to be proportional to total hepatic flow, was measured directly and then the sampling blood was returned through the left jugular vein. Small amounts of heparin were used to prevent blood clotting in the catheter. (3) Cardiac output was determined by the method of STEWERT-HAMILTON using radio-iodinated serum albumin (RISA). RISA was rapidly introduced into the left ventricle or ascending aorta through a catheter advanced from the carotid artery. Counting of radio-activity changes in blood, which was sampled from the femoral artery, were made by using the Well type scintillation counter. (4) Mean artery pressure was measured by means of a strain gauge manometer connected with a tube in the femoral artery. Portal vein pressure was obtained by a catheter advanced into the vessel from a splenic branch vein and by attaching it to a water manometer. Inferior vena cava pressure was measured at the level of the vena caval ostia of the hepatic vein. (5) Total peripheral resistance was estimated by dividing mean artery pressure by cardiac out put. Splanchnic resistance was also calculated by the same principle.

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Purpose Many reports have been documented in the literature dealing with hepatic circulatory changes and associated injury of the liver function in secondary shock. Several investigators have stressed the significance of blood pooling phenomenon in splanchnic area as one of the most characteristic features representing the irreversible state of hemorrhagic shock. However, the mechanism responsible for this phenomenon still remains to be solved. In this paper, we would attempt to clarify the effect of endogenous catecholamines on systemic and hepatic circulatory changes during hemorrhagic shock and to discuss the possible significance of these pressor amines in determining the course and severity of this condition. Method (1) A total of 25 mongrel dogs were used with anesthesia of intravenously infused thiopento-barbital sodium. (2) Portal vein pressure was obtained by a catheter advanced into the vessel from a splenic branch vein and by attaching the catheter to a water manomater. Inferior vena cava pressure was measured at the level of the vena cava ostia of the hepatic vein. (3) Total peripheral resistance was calculated by dividing mean arterial pressure by cardiac output. Splanchnic resistance was also calculated on the same principle. (4) After observing the control status, blood was removed gradually from the dog juglar vein, until mean arterial pressure was lowered to 50-60 mmHg up to 90 minutes from the onset of bleeding. Thereafter, no further hemorrhage was performed and arterial pressure was sustained at that level as possible. (5) Blood catecholamines were determined fluorometricaly by the improved BERTLER, CARLSSON and ROSENGREN'S method. Results (1) Inferior cava vein pressure and portal pressure With the beginning of hemorrhage, inferior cava vein pressure is reduced, while portal pressure remains unchanged or rather slightly rises, so that the resultant increase in porto-caval pressure gradient is observed despite a marked fall in arterial pressure.

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