Hydrogen Gas Protects Brain After Heart Attack in Animal Study
- Authors
- Guoqing Huang, Xiangmin Li, Yongxiang Tang, Zhengbin Yao, Shuo Hu, Hui Zhou, Xiaoye Mo, Changshou She, Xiaoqin Lu
- Journal
- Current Medical Imaging Formerly Current Medical Imaging Reviews
- Year
- 2022
- DOI
- 10.2174/1573405618666220321122214
- Study Type
- Rabbit
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Cardiac Arrest
- Body System
- Cardiovascular
TL;DR
Hydrogen treatment helps protect the brain from damage after a heart stops beating, as shown by brain scans and blood tests in rabbits.
Key Finding
Hydrogen-treated rabbits showed significantly better brain glucose metabolism and lower neurological deficits after cardiac arrest compared to control rabbits, with reduced markers of brain cell injury in the blood.
Summary
Researchers studied whether hydrogen gas could protect the brain after cardiac arrest (when the heart stops) in rabbits. They used a special imaging technique called PET/CT to measure brain activity and also checked blood markers of brain damage. Rabbits treated with hydrogen showed better brain glucose metabolism (energy use), lower neurological damage scores, and less brain tissue damage compared to untreated rabbits.
Practical Takeaway
This early-stage animal study suggests hydrogen gas may have protective effects on the brain after cardiac arrest, but these findings are from rabbits only and have not been tested in humans. Much more research would be needed before any conclusions could be drawn about hydrogen's potential benefits for people recovering from cardiac arrest.
Abstract
Background: Anatomical imaging methods and histological examinations have limited clinical value for early monitoring of brain function damage after cardiac arrest (CA) in vivo. Objective: We aimed to assess the cerebral protective effects of hydrogen in rabbits with CA by using fluorodeoxyglucose-positron emission tomography/computed tomography (FDG-PET/CT). Methods: Male rabbits were divided into the hydrogen-treated (n=6), control (n=6), and sham (n=3) groups. Maximum standardized uptake values (SUVmax) were measured by FDG-PET/CT at baseline and post-resuscitation. Blood Ubiquitin C-terminal hydrolase-L1 (UCH-L1) and neuron-specific enolase (NSE) were measured before and after the operation. After surgical euthanasia, brain tissues were extracted for Nissl staining. Results: SUVmax values first decreased at 2 and 24 h after resuscitation before rising in the hydrogentreated and control groups. SUVmax values in the frontal, occipital, and left temporal lobes and in the whole brain were significantly different between the hydrogen and control groups at 2 and 24 h postresuscitation (P<0.05). The neurological deficit scores at 24 and 48 h were lower in the hydrogentreated group (P<0.05). At 24 h, the serum UCH-L1 and NSE levels were increased in the hydrogen and control groups (P<0.05), but not in the sham group. At 48 and 72 h post-CA, the plasma UCH-L1 and NSE levels in the hydrogen and control groups gradually decreased. Neuronal damage was smaller in the hydrogen group compared to the control group at 72 h. Conclusion: FDG-PET/CT could be used to monitor early cerebral damage, indicating a novel method for evaluating the protective effects of hydrogen on the brain after CA.