Hydrogen Therapy Protects Brain During Heart Surgery in Rats

Hydrogen-rich saline demonstrates significant cerebroprotective effects in DHCA-induced brain injury through multiple mechanisms including reduction of oxidative stress, suppression of inflammatory cytokines (IL-1β, TNF-α), and inhibition of apoptotic pathways. This therapeutic approach shows promise for mitigating postoperative neurological complications in cardiac and neurosurgical procedures requiring deep hypothermic circulatory arrest.

Plain-Language Summary

This study tested whether hydrogen-rich saline (a salt solution containing dissolved hydrogen) could protect the brain during deep hypothermic circulatory arrest (DHCA), a surgical procedure that stops blood flow and cools the body to protect organs during complex heart and brain surgeries). In rats undergoing DHCA, hydrogen-rich saline reduced brain damage, decreased harmful inflammatory molecules and cell death markers, and improved antioxidant activity compared to untreated animals.

Abstract

Deep hypothermic circulatory arrest (DHCA) has been widely used in the operations involving the aortic arch and brain aneurysm since 1950s; but prolonged DHCA contributes significantly to neurological deficit which remains a major cause of postoperative morbidity and mortality. It has been reported that hydrogen exerts a therapeutic antioxidant activity by selectively reducing hydroxyl radical. In this study, DHCA treated rats developed a significant oxidative stress, inflammatory reaction and apoptosis. The administration of HRS resulted in a significant decrease in the brain injury, together with lower production of IL-1β, TNF-α, 8-OHdG and MDA as well as decreased activity of NOS while increased activity of SOD. The apoptotic index as well as the expressions of caspase-3 in brain tissue was significantly decreased after treatment. HRS administration significantly attenuated the severity of DHCA induced brain injury by mechanisms involving amelioration of oxidative stress, down-regulation of inflammatory factors and reduction of apoptosis.

DOI: 10.1007/s11064-011-0476-4