Cardiovascular Functions

Molecular Hydrogen Research on Cardiovascular Functions

Hydrogen-supplemented drinking water protects cardiac allografts from inflammation-associated deterioration
Graft injury as a result of oxidation and tissue inflammation is the major cause of allograft rejection and vasculopathy. Immunosuppressive regimens have demonstrated limited efficacy overall. Molecular hydrogen possesses antioxidant, anti-inflammatory, and anti-apoptotic properties. This study was conducted to determine the efficacy of molecular hydrogen in protecting cardiac allografts. Drinking molecular hydrogen water increased mitochondrial activity in allografts by more than 50%. It was confirmed through this study that drinking molecular hydrogen water prevented cardiac allograft rejection.

H2 Gas Improves Functional Outcome After Cardiac Arrest to an Extent Comparable to Therapeutic Hypothermia in a Rat Model
Cardiac arrest causes oxidative stress injury by ischemia-reperfusion. When cells are deprived of blood (ischemia) and then are suddenly given blood (reperfusion) severe electron leakage takes place which leads to free radical production. Since molecular hydrogen has many potential therapeutic applications as an antioxidant, it was used in this study to compare its effectiveness in improving functional outcome after a heart attack. One of the findings in this study was that the survival rate 24 hours after return of spontaneous circulation (ROSC) was 92% for the molecular hydrogen group compared to 43% for the control group.

Consumption of hydrogen water prevents atherosclerosis in apolipoprotein E knockout mice
Atherosclerosis is the build-up of plaque in the arteries that can lead to stroke, heart attack, and even death. The plaque consists of an accumulation of macrophages and oxidized products of low-density lipoproteins (LDLs). Oxidation caused by free radicals is one of the major factors in the prevalence of atherosclerosis. This study examined the hypothesis that since molecular hydrogen is an efficient antioxidant by gaseous diffusion into tissues and cells, it should potentially be able to prevent atherosclerosis. The results from the study showed that molecular hydrogen saturated water decreased oxidative stress level and prevented the formation of atherosclerosis, at least in mice.
Hydrogen-rich saline protects myocardium against ischemia/reperfusion injury in rats
Restoring blood flow to the heart after a heart attack is the most effective long-term therapy. Although restoration of blood flow is important, the rate at which the blood is reintroduced is more critical because oxygen triggers the generation of reactive oxygen species (ROS). This burst of ROS triggers signaling networks that lead to cellular necrosis and apoptosis (cell death). This study tests and confirms the hypothesis that molecular hydrogen will be effective in minimizing ROS generation during the reperfusion of the heart. The improvement in post-ischemic functional recovery was paralleled to a significant reduction in infarct size, decreased plasma and myocardium MDA concentration, attenuation of cardiac cell apoptosis and DNA oxidative stress in AAR. This cardiac improvement may result from radical oxygen species (ROS) scavenging effect of molecular hydrogen. Intermittent hypoxia increases free radical production. Molecular hydrogen (H2) may have an antioxidant effect by reducing hydroxyl radicals. This study examined the effects of molecular hydrogen gas on lipid metabolism and left ventricular remodeling induced by hypoxia in mice.
Inhalation of hydrogen gas attenuates left ventricular remodeling induced by intermittent hypoxia in mice
Sleep apnea syndrome increases the risk of cardiovascular morbidity and mortality. We previously reported that intermittent hypoxia increases superoxide production in a manner dependent on nicotinamide adenine dinucleotide phosphate and accelerates adverse left ventricular (LV) remodeling. Recent studies have suggested that hydrogen (H(2)) may have an antioxidant effect by reducing hydroxyl radicals. In this study, we investigated the effects of H(2) gas inhalation on lipid metabolism and LV remodeling induced by intermittent hypoxia in mice. Male C57BL/6J mice (n = 62) were exposed to intermittent hypoxia (repetitive cycle of 1-min periods of 5 and 21% oxygen for 8 h during daytime) for 7 days. H(2) gas (1.3 vol/100 vol) was given either at the time of reoxygenation, during hypoxic conditions, or throughout the experimental period. Mice kept under normoxic conditions served as controls (n = 13). Intermittent hypoxia significantly increased plasma levels of low- and very low-density cholesterol and the amount of 4-hydroxy-2-nonenal-modified protein adducts in the LV myocardium. It also upregulated mRNA expression of tissue necrosis factor-α, interleukin-6, and brain natriuretic peptide, increased production of superoxide, and induced cardiomyocyte hypertrophy, nuclear deformity, mitochondrial degeneration, and interstitial fibrosis. H(2) gas inhalation significantly suppressed these changes induced by intermittent hypoxia. In particular, H(2) gas inhaled at the timing of reoxygenation or throughout the experiment was effective in preventing dyslipidemia and suppressing superoxide production in the LV myocardium. These results suggest that inhalation of H(2) gas was effective for reducing oxidative stress and preventing LV remodeling induced by intermittent hypoxia relevant to sleep apnea.
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