H2’s Protective Effects on Brain in Cardiac ArrestScientific Research

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 hydrogen-treated 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 post-resuscitation (P<0.05). The neurological deficit scores at 24 and 48 h were lower in the hydrogen-treated 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 with 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.