To clarify the effects of acupuncture treatment on acute and chronic shoulder-hand syndrome, 20 minutes of manual acupuncture was applied to 14 patients with posthemiplegic shoulder-hand syndrome at the hemiplegic arm and hand (eight points of keiketsu) twice a week for 5 weeks. Thermographic and laser doppler measurements showed the increases in skin temperature and blood flow of the affected hand. Although manual acupuncture produced long-lasting increases in skin temperature and blood flow of both hands, its effects were inhibited when 10-mg alpha-blocker phentolamine was injected beforehand. After 5 weeks of the acupuncture therapy, the increased skin temperature and blood flow of the affected hand were gradually reduced to normal levels. Subjective and objective symptoms such as pain, local heating, and swelling showed positive improvement in 10 out of 14 patients after the 5 weeks of acupuncture therapy. These results may suggest that the shulder-hand syndrome is produced by unknown sympathetic vasodilating mechanisms and that acupuncture plays a therapeutic role through the suppression of increased sympathetic tone.
To find the correlation between the inhibitory effects of hot-spring water on blood-pressure and its chemical composition, the effects of artificial spa bathing on lowering blood pressure were compared with those of hot-spring bathing on spontaneously hypertensive rats (SHR). Further, the induction of heat-shock proteins (HSP) in rat organs was quantitatively examined in order to clarify the mechanism of its action. Artificial spa (Na2SO4-Na2HCO3) bathing showed almost the same inhibitory effects on blood pressure as those of hot-spring bathing. There was no significant difference in the catecholamine value in blood between both types of spa bathing, nor was there any difference from the values of the control group. It was found that HSP molecules were induced in the brain, liver, and kidneys not only by hot-spring bathing but also by artificial spa bathing, with different inductive profiles from one organ to another.
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.
Promethazine-HCl was used to suppress histamine production in the skin by Na2SO4·NaHCO3 bathing, confirming the previous data that the small amount of histamine released as a chemical mediator may have caused the warming effect, as observed in type I allergic reaction. The skin histamine contents after serial bathings with Na2SO4·NaHCO3 under medication of Promethazine-HCl for 3 weeks were significantly reduced compared with that of tap water (p<0.05). The skin histamine produced by physical stimulation of Na2SO4·NaHCO3 bathing was suppressed with H1-blocker (Promethazine), verifying that the warming effect with Na2SO4·NaHCO3 bathing was caused by histamine released as a chemical mediator, as observed in type I allergic reaction.