The fact that in the patients of beri-beri the increase in the blood during muscular exercise is considerably greater than that after the recovery of the disease or in normal persons, may be based on the relaxation of peripheral blood vessels, dilatation of the blood vessels through acidosis, in addition to the increased cardiac function brought about by the accelerated secretion of adrenaline, and if the acidcsis is markedly increased, the adrenaline copiously secreted during the exercise can act dilating on the peripheral blood vessels, as above described, thus bringing in the further light augmentation of the blood flow.
Now, in reflecting on the mechanism of the circulatory disturbance in beri-beri, it is well known that the disorder in the circulatory apparatus in patients of experimental B-avitaminosis is slight, as compared with that in the patients of beri-beri, but it can be, as we have already mentioned, deteriorated as much as in beri-beri by giving a certain muscular exercise to the patients.
M. Miura,
38) Nagayo
39) and Honda
40) missed hypertrophy and dilatation of the heart in cascs of pucrperal beri-beri, in which the patients are accustomed to remain always in a quiet condition and to perform no noticeable muscle work.
There is no agreement up to the present in the various theories as to the reason why the right heart becomes hypertrophic and dilated in beri-beri. Besides the paralysis of the respiratory muscles which was supported by M. Miura,
41) Kure and Hiramatsu,
42) a cause for this fact may be that the right heart whose muscúlar wall is thinner than that of the left heart, must labour in excess in order to transport the blood to the pulmonary circulation because of the augmented minute volume in presence of the paralysis of respiratory muscles.
Evidence that in acting muscles, as has been pointed out by Krogh,
33) the arterioles and praecapillaries are considerably dilated and lead to increased local blood flow, thus giving rise to lowering of the resistance in systemic circulation as compared with pulmonary one, may be regarded as an auxiliary cause for the preponderance of the right heart in hypertrophy.
The increased stream equivalent in beri-beri suggests that the heart of the patients of beri-beri is forced to work more excessively and less economically than in normal people in order to transport the same quantity of oxygen into the tissue and especially during the muscular exercise which is accompanied by increased oxygen consumption and thus becomes an important factor for the cardiac hypertrophy. Eppinger,
43) relying on his animal experiment in which notwithstanding the minute volume was increased by artificial connection of the descending aorta with the vena cava inferior the heart showed only slight hypertrophy, maintains that the augmentation of the minute volume is not the only cause of the cardiac hypertrophy. Gaskell,
26) however, demonstrated that the heart is dilated when acids are added to the perfusing fluid in perfusion experiment on an isolated heart and Eppinger
32) that the heart of dogs showed a noticeable dilatation when they inhaled 20-30% CO
2 for an hour.
Reviewing these facts the latter author attributed the dilatation of the heart in the patients of cardiac disease observed after muscular exercise to an accumulation of lactic acid in the blood.
Evidence that beri-beri with marked circulatory symptoms is accompanied by a considerable acidosis suggests together with those observations above mentioned, that in beri-beri the weakness of the cardiac muscles due to acidosis may have an etiologic relation to the dilatation of the heart. The latter seems to be further urged by muscular exercise which increases the acidosis.
Since “shoshin”
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