Aims: 

Hyperbaric oxygen treatment (HBOT) is a beneficial therapy of ischemic stroke in animal models and humans. The objective of this paper is to describe the possible underlying mechanisms of neural and vascular protection induced by HBOT.

Methods: 

We searched the Medline using key words: stroke, neuroprotection, hyperbaric oxygen, microcirculation, vasoreactivity, angiogenesis, COX, NOS, arachidonic acid metabolites, reactive oxygen species (ROS), 20-HETE was conducted.

Results: 

Ischemia induces necrosis, autophagocytosis and apoptosis of brain tissue. After stroke, cerebrovascular resistance increases, this could be due - in part - to the increased release of the vasoconstrictor 20-hydroxyeicosatetraenoic acid (20-HETE. Inhibition of 20-HETE and/or increasing of epoxyeicosatrienoic acids (EETs) levels may decrease cerebral damage following stroke. Neuroprotection by HBOT improves brain metabolism by increasing ATP and decreasing lactate production. Also, HBOT may reduce blood–brain barrier (BBB) permeability and brain edema, thereby decreasing intracranial pressure, inflammatory responses and apoptotic cell death. For example, HBOT decreases hypoxia-inducible factor-la (HIF-la) and its targets: erythropoietin and vascular endothelial growth factor (VEGF). Also, HBOT prevents lipid peroxidation of membranes, reduces COX-2 expression and leukocyte adhesion during reperfusion and infiltration of neutrophils into the injured brain. It has also been shown that HBOT improves tissue healing by collagen matrix formation and angiogenesis. Interestingly, HBOT in normal tissues elicits significant vasoconstriction; in contrast, it improves microcirculation of ischemic tissues by inhibiting post-ischemic vasoconstriction. Our recent studies showed that in diabetic rats HBOT significantly improves dilation of cerebral vessels in response to ACh and hypoxia.

Conclusions: 

Thus HBOT likely elicits neuroprotection via two main pathways: one is improved targeted perfusion to increase oxygen delivery to ischemic tissue and two is, preventing apoptosis due to various changes in the metabolism of brain tissues; both could be due to altered production of vasoprotective and neuroprotective metabolites of arachidonic acid, such as 20-HETE, and EETs.

Support: 

HUHR Bilateral Collaboration Grant 2009-2011, Drenjancevic and Koller