Using a highly concentrated CO₂-bathing, authors studied an effect of the bathing (CO₂: 1, 000ppm, for 10min at 40°C) on circadian blood pressure in six cases of antihypertensive drug-refractory hypertension. The patients were females, ranging from 62 to 70 years old (mean age: 65.8±2.6). All of the patients were diagnosed as the III stage of essential hypertension (according to WHO criteria) and have been treated with captopril, nifedipine or α-methyl DOPA since three to ten years ago. Out of six cases five showed non-dipper pattern in circadian blood pressure. All bathings were done at 16:30 and comparative study of circadian blood pressure between plain water and CO₂-bathing was carried out.
The results obtained were as follows.
1) In five cases of non-dippers CO₂-bathing exerted the therapeutic effect upon the high blood pressure at night and resulted in the significant decrease in hyperbaric indici of systolic, mean and diastolic blood pressure, comparing with plain water-bathing. However, no significant difference of heart rate was observed between plain water and CO₂-bathing.
2) In a case of good responder to antihypertensive drug, a relatively low blood pressure continued all day after CO₂-bathing.
From these results it is expected that a highly concentrated CO₂-bathing is useful as supportive therapy to essential hypertension, specially to non-dipper.

Effects of hot-spring bathing on plasma concentrations of diuresis-related hormones were examined. Four healthy males were asked to bath in either 47°C hot-spring water for 3 minutes (jikan-yu) or 42°C hot-spring water for 10 min. Plasma levels of human atrial natriuretic polypeptide (HANP), anti-diuretic hormone (ADH), aldosterone (ALD), and endothelin (ET) were measured at 0, 5, 15, and 30 minutes after the start of the immersion. A transient rise was found only in plasma HANP at 5 minutes in the 42°C bath, which may have been induced by the hydrostatic pressure. Plasma concentrations of ADH, ALD, and ET hormones showed no remarkable change.
These results suggest that a few minutes of hot-spring bathing may have little influence on the amount of these hormones secreted.

Effects of hyperthermia on the formation of platelet-derived microparticles (MP) and the expression of surface CD62 antigen were examined in normal human platelets. Venous blood from healthy subjects, anticoagulated with 1 volume of 3.8% sodium citrate, was heated at 37°C (control), 42°C and 47°C for 15 minutes. Then 2μl of each sample was incubated with FITC or PE-conjugated anti-human CD42b or CD62 antibodies, and assayed for MP and CD62 by flow cytometry. The percentage of MP after the incubation was not significantly different from that before the incubation nor that of control (9.9±0.6% before incubation, 10.2±0.6% at 37°C, 10.8±0.4% at 42°C and 10.3±0.3% at 47°C), CD62 positive-platelets slightly increased after the incubation, but no significant differences were observed between the control value and the values at 42°C and 47°C (1.6±0.3% at 37°C, 1.9±0.5% at 42°C and 1.7±0.3% at 47°C). These data suggest that hyperthermia has only a weak stimulatory effect on platelets and is unable to induce MP formation.

The change in the skin surface temperature after taking a 3-minute 47°C hot-spring bath was examined in five healthy male volunteers whose mean age was 29.5 years and body mass index was 22.6kg/m², As a control, they took a 10-minute 42°C hot-spring bath after 4 days. Skin surface temperature was measured by a thermotracer in a room where the ambient temperature was maintained at 25°C and relative humidity at 38%. To eliminate any effect of diurnal variation in skin surface temperature, the experiment was started at 1 p.m. of each day. There was no significant difference in the highest value of skin surface temperature of the face, chest, arm, hand, leg and foot between both bathings. However, the abdominal skin surface temperature was slightly higher after the 3-minute 47°C bath than after the 10-minute 42°C bath. The skin surface temperature of the chest was transiently decreased after the 3-minute 47°C bath. The highest value of skin surface temperature of all areas examined after the 3-minute 47°C bath was about 34°C and did not differ from that after the 10-minute 42°C bath. These findings suggest that external heat stress gives no influence on the skin surface temperature and the transient decline of the skin surface temperature of the chest after the 3-minute 47°C bath may be due to some pathophysiological change in the vascular and respiratory systems.

The effect of hot spring bathing on nocturnal blood pressure was investigated in 6 normotensive young individuals at Kusatsu. Blood pressure and heart rate were measured at 1-hour intervals from 18:00 one day until 12:00 the following day. The experiments were performed on 2 consecutive days. Three subjects took a 10-minute 42°C hot-spring bath at 20:00 on the first experimental day but did not on the second experimental day. The order of experiments was inverted in the other 3 subjects. While not statistically significant, the nocturnal blood pressure on the “bathing” day tended to be decreased more than that on the control day. However, there was no difference in the heart rate. These findings may suggest possible involvement of hot spring bathing in the initiation of thrombotic diseases occurred in the morning hours at Kusatsu.

To clarify possible involvement of hot spring bathing in the occurrence of acute myocardial infarction and cerebral infarction at Kusatsu, its effects on blood pressure, heart rate, plasma cortisol and hematocrit were examined in 9 healthy young men. Abrupt increase in systolic blood pressure was observed immediately after starting a 3-minute 47°C or a 10-minute 42°C hot-spring bath. Both systolic and diastolic blood pressure were abruptly decreased one minute after completing either 47°C or 42°C bathing. The heart rate was increased gradually after the start of either 47°C or 42°C bathing and was decreased gradually after the completion of either 47°C or 42°C bathing. It was considered that the plasma Cortisol level was increased 15 minutes after starting 47°C bathing and the hematocrit was increased 15 minutes after starting 42°C bathing. We have already reported that fibrinolytic activity was decreased and platelet function was activated by 47°C bathing. Taken together, it is suggested that the mechanism of the occurrence of thrombotic diseases after hot spring bathing may be explained by considering transient changes in blood pressure, heart rate, blood viscosity, fibrinolytic activity and platelet function induced by hyperthermal stress.