OBJECTIVE: To determine the role of hyperoxic and hyperbaric therapy following experimental subarachnoid hemorrhage (SAH). DESIGN: Prospective, randomized, controlled animal study. SUBJECTS: Thirty male Wistar rats. INTERVENTIONS: Thirty rats were assessed for an initial neurologic status as double-blinded by two different neurosurgeons using a neurologic severity score (NSS) and then underwent an initial angiographic examination. Two days later, 0.3 ml of homologous blood was injected into the cisterna magna to produce a SAH-induced cerebral vasospasm. The NSS and angiographic examination were then repeated. The rats having no spasm or a spasm under 50% (n=8) and 50% or over 50% (n=22) were grouped separately, as groups 1 and 2, respectively. The rats having 50% or more spasm were further divided randomly into group 2A and 2B. The rats in groups 1 and 2A (n=11) underwent a 60-min course of 100% oxygen at the atmospheric pressure 1 atmosphere absolute (ata), and group 2B (n=11) received 100% oxygen at 3 ata for 1 h. Neurologic assessment was repeated on the next day and 7 days later. MEASUREMENTS AND MAIN RESULTS: The animals having no spasm or less than 50% spasm had a better NSS and outcome when compared with the animals having 50% or more spasm. But the animals with 50% or more spasm which underwent hyperbaric therapy were shown to have a better outcome compared to the animals having hyperoxic therapy. CONCLUSION: Exposure to hyperbaric oxygen therapy seemed to accelerate the recovery of neurologic deficits secondary to experimental SAH.
OBJECTIVE: To determine the role of hyperoxic and hyperbaric therapy following experimental subarachnoid hemorrhage (SAH). DESIGN: Prospective, randomized, controlled animal study. SUBJECTS: Thirty male Wistar rats. INTERVENTIONS: Thirty rats were assessed for an initial neurologic status as double-blinded by two different neurosurgeons using a neurologic severity score (NSS) and then underwent an initial angiographic examination. Two days later, 0.3 ml of homologous blood was injected into the cisterna magna to produce a SAH-induced cerebral vasospasm. The NSS and angiographic examination were then repeated. The rats having no spasm or a spasm under 50% (n=8) and 50% or over 50% (n=22) were grouped separately, as groups 1 and 2, respectively. The rats having 50% or more spasm were further divided randomly into group 2A and 2B. The rats in groups 1 and 2A (n=11) underwent a 60-min course of 100% oxygen at the atmospheric pressure 1 atmosphere absolute (ata), and group 2B (n=11) received 100% oxygen at 3 ata for 1 h. Neurologic assessment was repeated on the next day and 7 days later. MEASUREMENTS AND MAIN RESULTS: The animals having no spasm or less than 50% spasm had a better NSS and outcome when compared with the animals having 50% or more spasm. But the animals with 50% or more spasm which underwent hyperbaric therapy were shown to have a better outcome compared to the animals having hyperoxic therapy. CONCLUSION: Exposure to hyperbaric oxygen therapy seemed to accelerate the recovery of neurologic deficits secondary to experimental SAH.
Authors: Peter Andrews; Elie Azoulay; Massimo Antonelli; Laurent Brochard; Christian Brun-Buisson; Geoffrey Dobb; Jean-Yves Fagon; Herwig Gerlach; Johan Groeneveld; Jordi Mancebo; Philipp Metnitz; Stefano Nava; Jerome Pugin; Michael Pinsky; Peter Radermacher; Christian Richard; Robert Tasker; Benoit Vallet Journal: Intensive Care Med Date: 2005-02-18 Impact factor: 17.440