Severinghaus' equation can safely be used for the indirect estimation of oxygen half saturation pressure (P₅₀) on the basis of blood gas parameters in normal subjects. However, in 139 blood samples from 65 patients with severe injuries, the estimated P₅₀ values differed significantly from directly measured values. The difference is highly correlated to the molar ratio of 2, 3-diphosphoglycerate to hemoglobin tetramer (2, 3-DPG ratio, [DPG]). Using this correlation, a modified Severinghaus'equation, including 2, 3-DPG molar ratio, was derived:i. e.,
Δlog Po₂=+0.48 (7.4-pH)+0.024 (T-37) +0.0013BE+0.135 [DPG]-0.116
where Δlog Po₂ is the shift from the standard oxygen dissociation curve, pH is plasma pH, and T and BE refer to temperature and base excess of blood, respectively. The modified equation enables one to indirectly estimate P₅₀ and oxygen saturation with an accuracy of ±2.5 mmHg and ±5%, respectively, based on blood gas parameters and 2, 3-DPG molar ratio in most clinical cases. The limitations of the equation was discussed.

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In anesthetized dogs venous return was drained into a blood reservoir from which blood was pumped to the right atrium at a variable perfusion rate, which was equal to cardiac output in the steady state. When cardiac output was decreased or increased by 25 or 50% of the control, the blood volume in the dog's body was changed in the same direction in the intact reflexic state as well as in the areflexic state prepared by hexamethonium and norepinephrine infusion. The volume change in the reflexic state was twice that in the areflexic state when compared 5 min after stepwise changes in cardiac output. When only the flow through the right heart and lungs was changed by-50%, with systemic flow unchanged, the decrease in blood volume was about one-fifth of that observed on a 50% decrease of cardiac output and not affected by ablation of the reflexes. It is concluded that, on a change in cardiac output, the passive change in blood volume is as large as the active or reflexic change, that the majority of the change in blood volume takes place in the systemic circulation rather than in the pulmonary circulation, and that the receptors for the reflexic change are located in the systemic circulation.

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The main bronchi of excised dog lobes were obstructed with beads, 5 to 6cm from their origin so that they did not communicate with the peripheral air spaces.Both pulmonary artery and vein were cannulated and both pulmonary vascular pressures were controlled. With the lobe held at constant transpulmonary pressure, bronchial pressurevolume curves were studied during acute pulmonary vascular engorgement. The bronchial compliance was reduced at higher vascular pressure and the effect of vascular engorgement on the bronchial collapsibility was larger at higher transpulmonary pressure: bronchial compliance at vascular pressure 10cm H2O were 70, 84, 98, and 100% of the bronchial compliance at vascular pressure-40cm H₂O at transpulmonary pressure 20, 10, 5, and 0cm H₂O, respectively. We concluded that vascular engorgement increased parenchymal radial traction to the bronchi when the bronchi reduced its diameter, although it appeared that vascular engorgement resulted in little change in the lung elastic recoil pressure.

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The contractility of the ventricular muscle of bullfrog in Ca-free Sr Ringer was investigated. The well-known depression of the rate of rise of twitch tension as well as prolongation of the time to peak tension were observed. The latter change was closely related to the lengthening of the action potential duration. The washout of muscle with a divalent cation-free perfusate caused a more rapid decline of the twitch contraction in the muscle preparation preloaded with Sr than in that preloaded with Ca. High potassium solution containing 30 mM caffeine produced a contracture in the muscle preloaded with Sr even after prolonged divalent cation-free perfusion although its magnitude was smaller than in the muscle preloaded with Ca.
The pattern of the potassium contracture of the muscle perfused with Sr was quite different from that perfused with Ca. In the former condition the initial transient component was suppressed while the secondary sustained component was prominently augmented. Noradrenaline in 10^-5g/ml exerted a negative inotropic effect on the potassium contracture of the Ca-perfused muscle whereas it did not demonstrate any inhibitory effect on the potassium contracture of the Sr-perfused muscle although a marked prolongation as well as a positive inotropism of the twitch contraction were observed in the latter condition.
An electron microscopic study revealed that electron-opaque granules, identified as Sr by means of X-ray spectrum microanalysis, are located both in the sarcoplasmic reticulum and mitochondria.
From these results it was concluded that Sr replaces Ca in maintaining the electrical and mechanical activities of the heart muscle. It is also suggested that Sr suppresses the inactivation kinetics of the slow ionic channel and exerts some inhibitory effects on myofibrillar ATPase activity. The possibility of contribution of the intracellular binding sites to the regulation of contraction is discussed.Noradrenaline seems to stimulate Ca uptake by the sequestering system but appears to be ineffective in Sr uptake.

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The transmembrane potential of female rat liver cells in situ was-52.4 mV. This was decreased to-42.9 mV by ethacrynic acid (4 mg/100 g), but not by ouabain (1 mg). DL-Ethionine (25-100mg) caused a decrease in the membrane potential and tissue ATP content. A high dose ethionine (100 mg) increased tissue Na content and decreased K content. By applying adenine (25 mg) to the animals treated with ethionine (100 mg), the membrane potential, ATP content and K content were increased and the Na content was decreased. The repolarized membrane potential in the animals treated with adenine following the ethionine was again depolarized by the administration of ouabain, but not by the administration of ethacrynic acid. These results suggest that two kinds of active ion transport mechanisms, ethacrynic acid-sensitive and ouabain-sensitive mechanisms, may be involved in maintenance of the membrane potential of rat liver cells.

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The effects of catecholamines (adrenaline and isoproterenol), dibutyryl cyclic AMP and propranolol on mechanical and electrical responses in curarized frog twitch fiber were investigated. Twitch tension and potassium contracture were potentiated by catecholamines or by dibutyryl cyclic AMP, without exerting any effect on the magnitude of the resting potential, the amplitude and duration of the action potential and the negative afterpotential. The effect on twitch tension was more pronounced with isoproterenol than with adrenaline. The action of isoproterenol was antagonized by propranolol in optimal concentrations. Caffeine contracture was not affected by catecholamines or by dibutyryl cyclic AMP. Dibutyryl cyclic AMP itself did not induce contracture, even in phospholipase A-treated fibers.On the other hand, twitch tension was abolished and potassium contracture was inhibited by propranolol in relatively higher concentrations (50μm), whereas the caffeine contracture and the resting and action potentials were not affected. The twitch tension once abolished in a solution with 50μm propranolol was completely recovered after immersion of the fibers in a solution with propranolol and either isoproterenol or dibutyryl cyclic AMP in high concentrations. Adenylate cyclase could not be detected in frog sartorius muscle, whereas the presence of the enzyme was found electron microscopically in guinea pig psoas muscle. On the basis of these results, the actions of catecholamines and their antagonist on excitation-contraction coupling in frog twitch fiber and the mechanism of their actions were discussed.

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Exposing frog's toe muscles to Ringer's solution made hypertonic with 400mM urea for 60min followed by placing the muscles back in Ringer's (urea-removal treatment) completely blocks the twitch without disrupting the surface openings of the T-tubules. The urea-removal treatment also increased the triadic junction width.Placing the muscles in Ringer's with an elevated calcium concentration (5mM) following exposure to the hypertonic solution prevented the block of the twitch response but not the increase in the triadic junction width.Exposing untreated muscles to Ringer's with 5mM calcium either had no effect on the twitch or reduced it by 30% or less.These results suggest the possibility that increasing the width of the triadic junction decreases the amount of calcium ions reaching the terminal cisternae during an action potential thereby blocking the twitch.Elevating the calcium concentration in the T-tubules would increase the amount of calcium which enters the triadic junction during an action potential and thus antagonize the above effects.

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Thin sections of guinea pig cerebellum were incubated in an artificial medium and responses of neurons in the granular layer to glutamic acid were studied. About half of these neurons were inhibited by glutamate administered electrophoretically (GI cells) and others were excited (GE cells). The GI cells were also inhibited in a medium containing glutamate. Gamma-amino butyric acid inhibited the GI as well as the GE cells. The inhibition in the GI cells induced by glutamate was not susceptible to picrotoxin or strychnine medication, and was not blocked in a Cl-free medium or in a medium containing Ca²⁺ in low concentrations and Mg²⁺ in high concentrations. Some GI cells showed high-amplitude spikes which were recordable at distances of tens of micrometer from the cell. These observations indicate that at least some of the GI cells were large Golgi cells and that the inhibition induced by glutamate in the GI cells was not mediated by inhibitory interneurons.

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Some properties of late after-potentials which appear following a train of impulses were examined in frog skeletal muscle fiber. The decay of the late after-potential followed a simple exponential time course. The time constant of the decay was larger in a viscous solution than in normal Ringer solution. It was proved by physical experiments that the diffusion of K ions was delayed in the viscous medium at the same rate as the decay. The effect of temperature on the decay was low and the Q₁₀ for the time constant was 1.2. When the late after-potentials were recorded at membrane potentials variedly controlled by the polarizing current, the reversal potential shifted in the positive direction with the increase of impulses. These results suggest that the late after-potential may be dependent on K ions accumulated in the T system. During the initial 300msec period immediately after the onset of the decay, the amplitude was smaller than expected by a simple exponential time course. This effect was especially apparent in the sucrose hypertonic Ringer solution in which the decay was extremely extended. The cause of this non-exponential component was discussed with respect to the K accumulation hypothesis.

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The role of Ca in stimulus-secretion coupling has been analysed in an isolated adrenal gland of the rat perfused in the reverse direction through the adrenolumbar vein.
The omission of [Ca] _o virtually abolished the release of adrenaline in response to continuous stimulation with acetylcholine (ACh;5μm). A quantitative relation was found between the amount of adrenaline release by ACh and [Ca] _o over a range 0.5-4mM in the perfusion fluid: the amount was a saturable function of [Ca] _o. A similar relation was also observed when [Mg] o in the perfusion fluid was increased from 1mM to 20mM, but the responses in the presence of 20mM Mg were reduced to about one-half of those observed with 1mM Mg.
The relation between the reciprocal of [Ca] _o and the reciprocal of AChinduced adrenaline release in the presence of 1 or 20mM Mg corresponds to that of noncompetitive inhibition in a kinetic scheme of Michaelis-Menten.
The relation is in harmony with the view that carrier-mediated Ca influx is the major contributor to the stimulus-secretion coupling process in the adrenal chromaffin cell. The present results, however, may also be explained by another mechanism: a fixed pore mechanism may be involved in the facilitated diffusion of Ca. The relation obtained by antidromic perfusion was not reproduced in preparations in situ perfused in the orthodromic direction. Possible explanation of this discrepancy is discussed.

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