Hyperbaric oxygen and hyperbaric air treatment result in comparable neuronal death reduction and improved behavioral outcome after transient forebrain ischemia in the gerbil

Abstract

Anoxic brain injury resulting from cardiac arrest is responsible for approximately two-thirds of deaths. Recent evidence suggests that increased oxygen delivered to the brain after cardiac arrest may be an important factor in preventing neuronal damage, resulting in an interest in hyperbaric oxygen (HBO) therapy. Interestingly, increased oxygen supply may be also reached by application of normobaric oxygen (NBO) or hyperbaric air (HBA). However, previous research also showed that the beneficial effect of hyperbaric treatment may not directly result from increased oxygen supply, leading to the conclusion that the mechanism of hyperbaric prevention of brain damage is not well understood. The aim of our study was to compare the effects of HBO, HBA and NBO treatment on gerbil brain condition after transient forebrain ischemia, serving as a model of cardiac arrest. Thereby, we investigated the effects of repetitive HBO, HBA and NBO treatment on hippocampal CA1 neuronal survival, brain temperature and gerbils behavior (the nest building), depending on the time of initiation of the therapy (1, 3 and 6 h after ischemia). HBO and HBA applied 1, 3 and 6 h after ischemia significantly increased neuronal survival and behavioral performance and abolished the ischemia-evoked brain temperature increase. NBO treatment was most effective when applied 1 h after ischemia; later application had a weak or no protective effect. The results show that HBO and HBA applied between 1 and 6 h after ischemia prevent ischemia-evoked neuronal damage, which may be due to the inhibition of brain temperature increase, as a result of the applied rise in ambient pressure, and just not due to the oxygen per se. This perspective is supported by the finding that NBO treatment was less effective than HBO or HBA therapy. The results presented in this paper may pave the way for future experimental studies dealing with pressure and temperature regulation.

Effects of High-Fat Diet on Neuronal Damage, Gliosis, Inflammatory Process and Oxidative Stress in the Hippocampus Induced by Transient Cerebral Ischemia

“…Among susceptible brain regions, the hippocampus is known as the most vulnerable region to cerebral ischemia, and extensive neuronal death occurs in this region [1][2][3][4]. In the hippocampus, pyramidal neurons of the CA1 region undergo neuronal death/ degeneration some days after the initial ischemic insult, which is referred to as ''delayed neuronal death'' [5].…”

Hyperbaric oxygen pre‐treatment impairs anoxic tolerance but improves hyperglycemic tolerance in peripheral nerve

“…During studies in which HBO was administered after hypoxic‐ischemic brain injury, Yin showed that HBO reduced apoptosis . Malek confirmed these positive effects of HBO and also found that hyperbaric air when given within 1–6 h after transient forebrain ischemia was also beneficial. Other studies have demonstrated that HBO can attenuate spinal cord injury, possibly through stimulation of the production of glial cell line‐derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF) and interleukin (IL)‐10.…”

“…The fixed factors in the analyses may include CONC, the concentration of glucose (5 mmol/L vs 55 mmol/L), ANOXIA, whether the nerve is continuously oxygenated (0) or subject to intermittent anoxia (1), as well as CYCLE which is an index of the time during the experiment from which the data is taken (1)(2)(3)(4)(5). In the anoxia experiments CYCLE is the number of anoxic periods preceding the time from which the measurements are taken.…”

Reply to “Comments on the Cerebral Edema After CPR: A Therapeutic Target Following Cardiac Arrest?”

“…We agree with them that hyperbaric oxygen may represent a potentially important therapeutic option for post-arrest encephalopathy as well as other forms of brain injury. We also agree that animal studies of global brain ischemia suggest that hyperbaric oxygen may be beneficial with regard to neurologic outcome [2,3], although not all preclinical studies concur [4]. However, we did not include hyperbaric oxygen in our review on cerebral edema after cardiac arrest for several reasons.…”