Hyperbaric oxygen reduces neuronal death and improves neurological outcome after canine cardiac arrest.
OBJECTIVE
Studies suggest that hyperbaric oxygen (HBO) is neuroprotective after experimental cerebral ischemia, but the mechanism is unknown. This study tested the hypotheses that postischemic HBO affords clinical and histopathological neuroprotection after experimental cardiac arrest and resuscitation (A/R) and that this neuroprotection results from improved cerebral oxygen metabolism after A/R.


METHODS
Anesthetized adult female beagles underwent A/R and randomization to HBO (2.7-atm absolute [ATA] for 60 minutes, 1 hour after A/R) or control (Po2=80 to 100 mm Hg; 1 ATA). Animals underwent neurological deficit scoring (NDS) 23 hours after A/R. After euthanasia at 24 hours, neuronal death (necrotic and apoptotic) in representative animals was determined stereologically in hippocampus and cerebral neocortex. In experiment 2, arterial and sagittal sinus oxygenation and cerebral blood flow (CBF) were measured. Cerebral oxygen extraction ratio (ERc), oxygen delivery (Do2c), and metabolic rate for oxygen (CMRo2) were calculated (baseline and 2, 30, 60, 120, 180, 240, 300, and 360 minutes after restoration of spontaneous circulation).


RESULTS
NDS improved after A/R in HBO animals (HBO, 35+/-14; controls, 54+/-15; P=0.028). Histopathological examination revealed significantly fewer dying neurons in HBO animals; the magnitude of neuronal injury correlated well with NDS. HBO corrected elevations in ERc (peak, 60+/-14% for controls, 26+/-4% for HBO) but did not increase Do2c or CMRo2, which decreased approximately 50% after A/R in both groups.


CONCLUSIONS
HBO inhibits neuronal death and improves neurological outcome after A/R; the mechanism of HBO neuroprotection is not due to stimulation of oxidative cerebral energy metabolism.
Rosenthal
Robert E
RE
Program in Trauma, Department of Surgery, University of Maryland, Baltimore, USA. rrosenthal@umm.edu
Silbergleit
Robert
R
Hof
Patrick R
PR
Haywood
Yolanda
Y
Fiskum
Gary
G
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001925:Brain Damage, Chronic / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D002560:Cerebrovascular Circulation; D004285:Dogs; D004734:Energy Metabolism / Q000187:drug effects; D005260:Female; D006323:Heart Arrest / Q000473:pathology / Q000628:therapy*; D006624:Hippocampus / Q000098:blood supply / Q000473:pathology; D006931:Hyperbaric Oxygenation; D020925:Hypoxia-Ischemia, Brain / Q000209:etiology / Q000473:pathology / Q000517:prevention & control*; D023421:Models, Animal; D008954:Models, Biological; D009336:Necrosis; D019579:Neocortex / Q000098:blood supply / Q000473:pathology; D009474:Neurons / Q000187:drug effects* / Q000473:pathology; D010100:Oxygen / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects; D012151:Resuscitation
D010100:Oxygen