Hydrogen Therapy Protects Brain During Heart Surgery in Rats

Authors
Journal
Neurochemical Research
Year
DOI
10.1007/s11064-011-0476-4
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Brain Injury
Body System
Nervous System

TL;DR

Inhaling hydrogen-rich saline (HRS) can significantly reduce brain damage caused by deep hypothermic circulatory arrest (DHCA), a technique used in certain surgeries.

Key Finding

Hydrogen-rich saline significantly reduced brain injury in rats undergoing deep hypothermic circulatory arrest by decreasing oxidative stress, inflammatory molecules, and cell death pathways.

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.

Practical Takeaway

While this rat study suggests hydrogen may have protective effects on the brain during surgical procedures involving circulatory arrest, it is a preliminary animal-only study and does not demonstrate safety or effectiveness in humans. Any potential clinical application would require human trials before hydrogen-rich saline could be considered for this purpose.

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.