Two experiments were performed to clarify the effects of balneotherapy on platelet glutathione metabolism. One experiment, in which healthy men were subjected to water immersion at temperatures of 25°C, 36°C, and 42°C for 10min, showed that the level of platelet lipid peroxides (LPO) tended to increase at 25°C and 42°C, suggesting the presence of oxidative stress at these temperatures. When an antioxidative defense system was induced at these temperatures, the levels of platelet glutathione (GSH), glutathione peroxidase (GPX) and glutathione reductase (GR) activities increased. The other experiment, in which 4 weeks of balneotherapy was applied to type II (non-insulin-dependent) diabetic patients, showed that the level of GSH on admission correlated well with that of fasting plasma glucose (FPG, r=0.692, p<0.050). After 4 weeks of balneotherpy, the level of GSH increased (p<0.01) in well-controlled patients (FPG<150mg/dl) and decreased (p<0.05) in poorly controlled patients (FPG≥150mg/dl), There was a negative correlation between GPX activities and the level of FPG (r=-0.430, p<0.05). After the balneotherapy, the activity increased in five patients, decreased in three patients, and showed no changes in four patients. These results indicate that, in diabetic patients, 1) platelet GSH synthesis is obviously induced in response to oxidative stress, 2) lowered GPX activities suggest an impaired antioxidative defense system, and 3) platelet glutathione metabolism was partly improved by 4 weeks of balneotherapy but depended on the control status of plasma glucose levels. From these findings, we conclude that 1) patients whose platelet antioxidative defense system is damaged such as those with diabetes mellitus should not take hot or cold bath, and that 2) balneotherapy improves platelet glutathione metabolism, leading to normalization of platelet aggregability.
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.
To study the adrenocortical function in fever, we examined the effect of high temperatures on the corticoidogenesis (CG) in isolated bovine adrenocortical cells. To evoke CG, a stimulus was given using adrenocorticotropic hormone (ACTH, 1pM to 10nM), which stimulates the receptor operated Ca2+ channel (ROC) and adenylate cyclase activity; dibutyryl cyclic AMP (db-cAMP, 1mM), which mimics intracellular action of cyclic AMP; and high (30mM) K+, which activates the voltage dependent Ca2+ channel (VDC). Cells were incubated for 1 hour with each of the above mentioned secretaogues at 37°C, 40°C, and 42°C (only for ACTH). Compared with incubation at 37°C, the log dose response curve of ACTH shifted to the right, the maximal effect decreased to about 60% at 40°C, and CG ceased at 42°C. The use of Ca2+ (1.2mM) alone evoked CG via the nonspecific Ca2+ channel (NSC) at 37°C, but not at 40°C. 30mM K+-induced CG decreased to below 50% at 40°C, but 1mM db-cAMP-induced CG decreased only to 80%. However, the conversion of 25-hydroxycholesterol to corticoid was not affected at 40°C The results of these experiments show that VDC and NSC are not the main factors of CG at 40°C and that the enzyme activity beyond the side chain cleavage of cholesterol is not affected. Since the increases in cyclic AMP production and intracellular Ca2+ are essential in various stimulants-induced CGs, it is suggested that adenylate cyclase and ROC play a more important role in CG at 40°C than VDC and NSC.
We recently conducted 10-minute axillary temperature measurements on 699 healthy individuals, ranging in age from 5 to 83 years (mean: 36.5±15.3 years). Axillary temperature readings are sometimes inaccurate because the thermometer is not inserted in the correct place (i.e. the point of the highest temperature) or due to incomplete closure of the axilla during measurement. As the result of analysis of temperature rises during the 10-minute axillary temperature measurement, we found that the results are not always accurate because of incorrect conditions of measurement such as when the thermometer reading does not reflect the surrounding temperature. In this study, the following temperature readings were regarded to be inaccurate when: (1) the temperature temporarily fell during the rising phase; and (2) the rise in temperature was accelerated during measurement and the temperature had not become stable after 10 minutes. As a result of analyzing 10-minute axillary temperature measurements, we believe the temperature rise during the measurement must be considered to obtain more accurate readings. When analyzing the readings of short-term temperature measurements using a predictive algorithm, awareness required of possible errors which may be caused by the measurement method employed. Error factors other than the algorithm used for prediction become large when the thermometer is temporarily withdrawn from the axillary pit or its direction is changed during measurement to check an interim reading. After error factors associated with the measurement method have been eliminated, high accuracy is obtained and the difference between predicted reading and 10-minute becomes 0.01±0.13°C. A difference smaller than±0.2°C has been achieved in 98.0% of all measurements. Such a difference causes no problem from a clinical point of view.
There are three hot springs having distinctive water quality in the Tohoku district of Japan. They are described below. 1) Tamagawa hot spring Acidic hot sulfur spring, pH: 1.3. Main components: H2SO4 and HCl. Headspring temperature: 98°C. Effect on the skin (during bathing at 42°C): stimulation, sedation of itching, bacteriocidal function, crust formation, etc. Dermatological curative indications: Neurodermatitis constitutionalis or chronic prurigos, impetigo, trichophytia, psoriasis vulgaris, etc. 2) Hikage hot spring Neutral hot sulfur spring, pH: 6.5. Evaporated residue (NaCl, CaCl2, Mg(HCO3)2, KCl, MgCl2): 14g/1, H2S: 136mg/1, Headspring temperature: 43°C Effect on the skin: sedation of itching, bacteriocidal function, high osmotic pressure, regeneration of skin, etc. Dermatological curative indications: contact dermatitis (eczema), chronic prurigos, urticaria, psoriasis vulgaris, acne, scabies, etc. 3) Shin-Appi hot spring Brine, pH: 7.0. NaCl: 20g/1. Headspring temperature: 53°C. Effect on the skin: High osmotic pressure, coagulation of protein, bacteriocidal function, crust formation, etc. Dermatological curative indications: psoriasis vulgaris, chronic prurigos, pernio, erythema exsudativa multiforme, burn, pemphigus vulgaris, hemorrhoids, bedsores, etc.