Effects of hyperbaric oxygen therapy on cerebral oxygenation and mitochondrial function following moderate lateral fluid-percussion injury in rats

Abstract

Analysis of data in the current study demonstrates that HBO significantly increases brain tissue PO2 after injury. Nonetheless, treatment with HBO was insufficient to overcome injury-induced reductions in mitochondrial redox potential at 1 hour postinjury but was able to restore redox potential by 4 hours postinjury. Furthermore, HBO induced an increase in VO2 in both injured and sham-injured animals. Taken together, these data demonstrate that mitochondrial function is depressed by injury and that the recovery of aerobic metabolic function may be enhanced by treatment with HBO.

A prospective, randomized Phase II clinical trial to evaluate the effect of combined hyperbaric and normobaric hyperoxia on cerebral metabolism, intracranial pressure, oxygen toxicity, and clinical outcome in severe traumatic brain injury

“…These mechanisms have been demonstrated in both experimental and clinical investigations and include improved oxidative metabolism and mitochondrial function and reductions in intracranial hypertension, apoptosis, neuroinflammation, and free radical-mediated damage. 9,38,39,41,[44][45][46]50,52,[58][59][60][61]65 The results of the present randomized clinical trial help to support these findings.…”

“…Experimental investigations also support the concept of using HBO 2 followed by continued increased O 2 at normobaric pressures as a single treatment. 9 Daugherty et al, 9 in a lateral fluid percussion TBI rat model with 1 hour of HBO 2 treatment at 1.5 ATA followed by 3 hours of NBH, have documented significant improvement in mitochondrial function as measured by redox potential at the completion of the 4 hours of treatment but not at completion of 1 hour of HBO 2 . These data indicate that mitochondrial function is depressed after TBI but there is a potential for mitochondrial functional recovery and that the combination of HBO 2 and NBH can enhance this recovery.…”

“…Experimental investigations also support the concept of using HBO 2 followed by continued increased O 2 at normobaric pressures as a single treatment. 9,65 These studies have documented significant improvement in mitochondrial function, ATP production, reduced hippocampus cell loss, and functional recovery following a combined HBO 2 /NBH treatment as compared with NBH alone or control animals. The case for evaluating the combination of HBO 2 and NBH as a single treatment appeared compelling.…”

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

“…For example, in a mouse model with an intrinsic impairment of mitochondrial complex IV, HBOT at 2 atmospheres (atm) "significantly ameliorate[d] mitochondrial dysfunction" and delayed the onset of motor neuron disease when compared to control mice [108] . In animal studies, HBOT has been shown to increase the amount of work done by mitochondria [110] , improve mitochondrial function after brain injury [109] , and prevent mitochondrial deterioration [111] when compared to room air pressure and oxygen levels. HBOT also increased sperm motility by augmenting mitochondrial oxidative phosphorylation in fructolysis-inhibited sperm cells.…”

“…Since only approximately 0.3% of inhaled oxygen is ultimately delivered to mitochondria [107] , increasing the oxygen delivery to mitochondria by hyperbaric oxygen therapy (HBOT) may actually improve mitochondrial function [108,109] . For example, in a mouse model with an intrinsic impairment of mitochondrial complex IV, HBOT at 2 atmospheres (atm) "significantly ameliorate[d] mitochondrial dysfunction" and delayed the onset of motor neuron disease when compared to control mice [108] .…”