Bub-KAO tablet (50g) consisting of equimolar bicarbonate salt and succinate made it possible to use easily CO
2 bath at home. Since the obtained CO
2 concentration was not so high, we studied the circulatory effects of usual concentration of Bub-KAO bath in normal and hypertensive men.
Seven Bub-KAO tablets (KAO Co., Tokyo, Japan) were put into 350 l of 41°C simple hot spring bath (CO
2 conc. ≈300ppm). Eight normotensive subjects (32.2±4.2yrs) and 13 hypertensive patients (67.8±11.3yrs) took this artificial CO
2 bath for 10min. As a control, 12 normotensives (38.1±8.8yrs) and 12 hypertensives (51.0±8.2yrs) were immersed in 41°C simple hot spring bath for 10min. Hemodynamic functions and blood gas were followed before and after bathing for 30min in the supine position.
In normotensives, blood pressure (BP) was unchanged either by Bub-KAO or simple bath. The increase in heart rate (HR) and cardiac output (CO) and the decrease in total peripheral resistance (TPRi) after Bub-KAO bath were slightly but significantly greater than those of simple bath. In hypertensives, BP was significantly decrased after Bub-KAO bath (-17.2±6.4/-6.8±2.1mmHg) compared to simple bath. Although the increase in HR and CO (+0.55±0.22l/min) after Bub-KAO bath were not so remarkable, decrease in TPRi (-9.3±3.6 unit) was significantly greater than simple bath. Venous blood obtained 10min after Bub-KAO bath became fresh red showing a significant increase in pO
2 and pH (alkalosis) and significant decrease in pCO
2. In arterial blood, although pO
2 was unchanged, slight decrease in pCO
2 and increase in pH were also observed.
These results indicated that artificial CO
2 bath made by usual amounts of Bub-KAO tablets significantly reduced BP of the hypertensives due to vasodilating effect. Vasodilation by CO
2 bath was considered to be derived from the peripheral action of CO
2 as blood pCO
2 was rather reduced. As a basic mechanism of vasodilation by CO
2, we proposed the inhibitory effect on tissue enerqy metabolism of CO
2 as a product inhibtor of TCA cycle and subsequently, the onset of vascular autoregulation mechanism.
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