So far two different theories one opposing the other have been forwarded concerning stimulus conduction in atrium, one that of a conduction through the definite passage namely the specific heart muscle and the other diffusible conduction through the normal heart muscle.The purpose of the study here is to make a minute investigation into the formation of the stimulus conduction in the atrium.First the author has made a foundamental experiment of the study using toad's heart. The E.C.G. were taken simultaneously by means of the unipolar lead with the different electrodes placed on the atrial surface and the sinus venosus and the indifferent electrode on the left hind limb, and calculated the activation time at different points on the atrial surface. In obedience to these results of calculation, author concluded the formation of the stimulus conduction in the atrium.Authorities differ as to which one of those points on the intrinsic deflection in the E.C.G. should be taken as the representative point indicating the arrival of excitation wave.The author has had recourse to Prof. Maekawa's views discussed in his "Chain-Doublet Theory".According to his theory, it is defined that the time of arrival of activation to the muscle region underlying electrode to lead is represented by the point where the downward deflection following initial positive peak crosses the zero-line in clinical E.C.G. In the simultaneously recorded E.C.G. above mentioned, the author calculated the activation times at different points on the atrial surface, taking for the activation times to lead points what were expended between the initial point of the P wave led from the sinus venosus and where the intrinsic deflection of the P wave led from the atrial surface crosses the zero-line. The summery and conclusion of this study are as follows.1) When stimulus is conducted from sinus venosus to atrium it is first conducted in a diffusing manner around the border between the sinus venosus and the right atrium.2) Stimulus conduction into the left atrium is performed a little later than in the former case but it is conducted in the same diffusing manner around the border between the sinus venosus and the left atrium. Moreover, it should be noted that conduction in the latter case is carried out not through the right atrium but directly from the sinus venosus.3) Stimulus conduction in the atria seems generally to propagate in a radial manner travelling towards the atrioventricular border, the rate of time expended being in proportion to the distance. So I think that there is not specific pathway of stimulus conduction in the atrium. Both the atria, however, seem to undergo conduction independently of the other with the septum intervening them and each of them is seen to contract by its own accord.4) It is observed that the time of arrival of activation differs considerably as the points on the atrioventricular border where the conduction take place vary. This is thought to be due to the fact that the distance between these points and the sinus venosus anatomically differs.

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It is widely accepted that the primary causative mechanism of such a heart failure as in a long termed anemia, coronary disease or peripheral circulatory shock and the like is the impairment of energy yielding metabolism due to the myocardial hypoxia.In the present paper, effects of hypoxia on myocardial metabolism were investigated with special reference to formation and utilization of some intermediates of Krebs cycle or energy rich phosphate.Myocardial tissue was obtained from rabbit or rat that was placed in a chamber of low oxygen content (7% O₂) with one atmospheric pressure for 24 hours before sucrifice.1) Exposing the rabbits to a low oxygen atmosphere caused the increase of lactic acid and citric acid in cardiac muscle as well as in venous in blood.2) Oxygen consumption of the myocardial homogenate taken out from rats exposed to hypoxia was only half that of normal ones, while the activities of succinic or lactic dehydrogenase determined manometricaly showed no significant difference between the control and experimental group.3) Spectrophotometric analysis of DPN and DPNH in cardiac muscle revealed a interesting fact that decrease of DPN and unchange of DPNH lead to the reduction of DPN/DPNH ratio in the hypoxic cardiac muscle.4) Those results described above introduced the next investigation about citric acid formation in vitro by cardiac tissue, and it was found that marked decrease in citrate formation from pyruvate and oxaloacetate by hypoxic myocardial homogenate was recovered nearly to the normal level when boiled heart extract, DPN, or DPN and cocarboxylase was supplemented.5) Besides the impairment of citric acid formation, uptake of citrate in vitro by hypoxic rabbit myocardial homogenate, which was remarkably reduced, was observed to be restored to normal by supplementation with boiled heart extract or DPN. These facts indicated the mareked reduction of Pyruvate and Citrate oxydation in cardiac tissue under hypoxic condition.6) When α-ketoglutarate served as the substrate, the oxydative phosphorylation quotient expressed in P/O ratio was proved to be between 1.5 to 3.0 with normal rabbit heart mitochondria, while the quotient with hypoxic one dropped nearly to 1.0 which indicated the reduced coefficiency in energy transformation.7) Against to these facts which showed a reduction of energy yielding metabolism in hypoxic cardiac tissue, determination of activity of ATP-ase in soluble extract of myocardial homogenate gave no evidence of any difference between normal and experimental group. This effect is considered to suggest that the failure in utilization of energy might well be ruled out as the primary causative for the heart failure in hypoxia.

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