Affiliation:
1. From the Program in Trauma, Department of Surgery (R.E.R.), and Department of Anesthesiology (R.E.R., G.F.), University of Maryland, Baltimore; Department of Emergency Medicine, University of Michigan, Ann Arbor (R.S.); Kastor Neurobiology of Aging Laboratories and Fishberg Research Center for Neurobiology, and Departments of Geriatrics and Adult Development and Ophthalmology, Mount Sinai School of Medicine, New York, NY (P.R.H.); and Department of Emergency Medicine, George Washington University,...
Abstract
Background and Purpose—
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 (P
o
2
=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 (ER
c
), oxygen delivery (D
o
2
c), and metabolic rate for oxygen (CMR
o
2
) 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 ER
c
(peak, 60±14% for controls, 26±4% for HBO) but did not increase D
o
2
c or CMR
o
2
, which decreased ≈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.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Advanced and Specialised Nursing,Cardiology and Cardiovascular Medicine,Clinical Neurology
Cited by
82 articles.
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