Hypotensive and Circulatory Effects of Artificial CO₂ Bathing (Bub-KAO Bath) in Normal and Hypertensive Men

Abstract

Bub-KAO tablet (50g) consisting of equimolar bicarbonate salt and succinate made it possible to use easily CO₂ bath at home. Since the obtained CO₂ 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 (CO₂ conc. ≈300ppm). Eight normotensive subjects (32.2±4.2yrs) and 13 hypertensive patients (67.8±11.3yrs) took this artificial CO₂ 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 pO₂ and pH (alkalosis) and significant decrease in pCO₂. In arterial blood, although pO₂ was unchanged, slight decrease in pCO₂ and increase in pH were also observed.
These results indicated that artificial CO₂ bath made by usual amounts of Bub-KAO tablets significantly reduced BP of the hypertensives due to vasodilating effect. Vasodilation by CO₂ bath was considered to be derived from the peripheral action of CO₂ as blood pCO₂ was rather reduced. As a basic mechanism of vasodilation by CO₂, we proposed the inhibitory effect on tissue enerqy metabolism of CO₂ as a product inhibtor of TCA cycle and subsequently, the onset of vascular autoregulation mechanism.