Carbon dioxide balneotherapy and cardiovascular disease.
ABSTRACT Carbon dioxide (CO(2)) balneotherapy is a kind of remedy with a wide spectrum of applications which have been used since the Middle Ages. However, its potential use as an adjuvant therapeutic option in patients with cardiovascular disease is not yet fully clarified. We performed a thorough review of MEDLINE Database, EMBASE, ISI WEB of Knowledge, COCHRANE database and sites funded by balneotherapy centers across Europe in order to recognize relevant studies and aggregate evidence supporting the use of CO(2) baths in various cardiovascular diseases. The three main effects of CO(2) hydrotherapy during whole body or partial immersion, including decline in core temperature, an increase in cutaneous blood flow, and an elevation of the score on thermal sensation, are analyzed on a pathophysiology basis. Additionally, the indications and contra-indications of the method are presented in an evidence-based way, while the need for new methodologically sufficient studies examining the use of CO(2) baths in other cardiovascular substrates is discussed.
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ABSTRACT: Immersion in high concentrations of CO2 dissolved in freshwater (CO2-water) might induce peripheral vasodilatation in humans. In this study, we investigated whether such immersion could affect the autonomic nervous system in humans using spectral analysis of heart rate variability. Ten healthy men participated in this study. Tympanic temperature, cutaneous blood flow and electrocardiogram (ECG) were measured continuously during 20 min of immersion in CO2-water. The ECG was analyzed by spectral analysis of R-R intervals using the maximal entropy method. The decrease in tympanic temperature was significantly greater in CO2-water immersion than in freshwater immersion. Cutaneous blood flow at the immersed site was significantly increased with CO2-water immersion compared to freshwater. The high frequency component (HF: 0.15-0.40 Hz) was significantly higher in CO2-water immersion than in freshwater immersion, but the low frequency (LF: 0.04-0.15 Hz) /high frequency ratio (LF/HF ratio) was significantly lower in CO2-water immersion than in freshwater immersion. The present study contributes evidence supporting the hypothesis that CO2-water immersion activates parasympathetic nerve activity in humans.International Journal of Biometeorology 11/2008; 53(1):25-30. · 2.59 Impact Factor
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ABSTRACT: Carbon dioxide-rich water bathing has the effect of vasodilatation, whereas it remains undetermined whether this therapy exerts an angiogenic action associated with new vessel formation. Unilateral hindlimb ischemia was induced by resecting the femoral arteries of C57BL/J mice. Lower limbs were immersed in CO2-enriched water (CO2 concentration, 1000 to 1200 mg/L) or freshwater (control) at 37 degrees C for 10 minutes once a day. Laser Doppler imaging revealed increased blood perfusion in ischemic limbs of CO2 bathing (38% increase at day 28, P<0.001), whereas N(G)-nitro-L-arginine methyl ester treatment abolished this effect. Angiography or immunohistochemistry revealed that collateral vessel formation and capillary densities were increased (4.1-fold and 3.7-fold, P<0.001, respectively). Plasma vascular endothelial growth factor (VEGF) levels were elevated at day 14 (18%, P<0.05). VEGF mRNA levels, phosphorylation of NO synthase, and cGMP accumulation in the CO2-bathed hindlimb muscles were increased (2.7-fold, 2.4-fold, and 3.4-fold, respectively) but not in forelimb muscles. The number of circulating Lin-/Flk-1+/CD34- endothelial-lineage progenitor cells was markedly increased by CO2 bathing (24-fold at day 14, P<0.001). The Lin-/Flk-1+/CD34- cells express other endothelial antigens (endoglin and VE-cadherin) and incorporated acetylated LDL. Our present study demonstrates that CO2 bathing of ischemic hindlimb causes the induction of local VEGF synthesis, resulting in an NO-dependent neocapillary formation associated with mobilization of endothelial progenitor cells.Circulation 03/2005; 111(12):1523-9. · 15.20 Impact Factor
- American Heart Journal - AMER HEART J. 01/1942; 23(3):349-361.