Effects of environmental temperature on enzyme values were studied in both whole animal and excised heart in rabbits. When the temperature increased from 20 to 40°C with a constant humidity (60%) in the controlled climate chamber, significant increase of GOT and CPK values was observed. LDH2, LDH3 and LDH4 increased compared to LDH1. GOT and GPT increased more in 35°C than in 25°C. Hypoxia and elevated potassium markedly decreased GOT and GPT values in the medium. It was suggested that thermal stress may disturb the homeostasis to increase the serum enzyme and have some relation with high incidence of patients of myocardial infarction during hot summer.

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In a previous experiment, the pressor action of propranolol was observed in the spinal rat in which the β-receptor vascular tone was induced by infusions of β-adrenergic stimulating agents. This pressor action is considered to be due to the blockade of the β-adrenoceptive vasodilator tone provided by β-stimulants in the peripheral vessel. In this experiment, the pressor action of propranolol was used to investigate the mechanism of the vasodilator action of some vasodilators. Nylidrin, isoxsuprine, bamethan, acetylcholine and papaverine were used as vasodilators. Propranolol produced a pressor action in the spinal rat during infusions of the mixture of nylidrin, isoxsuprine or bamethan and vasopressin, but not during infusions of the mixture of papaverine or acetylcholine and vasopressin. This observation suggests that nylidrin, isoxsuprine and bamethan caused vasodilation through stimulation of β-vascular receptors. This method could be used to ascertian the role of β-receptor activation as a mechanism for the vasodilator action of some drugs.

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A factor in the kidney which forms the transcellular (pleural and peritoneal fluid, when injected into the bilaterally nephrectomized animals, has been reported. This factor might be identical with renin, or the pathogenesis of hypertension. We determined the transcellular forming and renin activity in hypertensive or salt-loaded rats.)

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Kidney extract forms the transcellular (pleural and peritoneal) fluid and increases hematocrti, when injected into the bilaterally nephrectomized animals. It is not evident that these actions are due to angiotensin formed by renin. We determined transcellular formation and hematocrit increase in rats by infusion of Asp¹-Ile⁵-angiotensin I and II, the native forms of rat angiotensin.

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The ascending limb of left ventricular pressure curve and its first dervative obtained by the routine cardiac catheterization were carefully analyzed in 74 patients with varying heart diseases. The ratio of an instantaneous rate (dP/dt), to the mean rate (P/t), of left ventricular pressure rise, for a given patient was resonably constant during the pre-ejection phase (coefficient of variable=10.1±4.5 (sd, %). The value of the ratio (dP/dt)/(P/t) obtained in each patient was compared to the cardiac function assessed by routine hemodynamic data. Patients with normal cardiac function (60 cases) and those with abnormal one (14 cases) had the ratio of 2.49±0.39 sd and 1.84±0.33 sd, respectively, and the diference between two patinet-group was statistically significant (p<0.001). The usefulness of the ratio (dP/dt)/(P/t) as an indicator for evaluating the LV performance was emphasized. The theoretical significance of the ratio was also discussed, suggesting that the LV pressure rises with increasing acceleration or decreasing one when the ratio is greater, or smaller than "2", respectively.

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