OBJECTIVE: To evaluate the effects of hyperbaric oxygen treatment after cerebral air embolism on intracranial pressure, brain oxygenation, brain glucose/lactate metabolism, and electroencephalograph. DESIGN: Prospective animal study. SETTING: Hyperbaric chamber. SUBJECTS: Eleven Landrace/Yorkshire pigs. INTERVENTIONS: In 11 anesthetized pigs, intracranial pressure and brain oxygenation were measured with microsensor technology, brain glucose/lactate by microdialysis, and electroencephalograph by conventional methods. After injection of air into the internal carotid artery, animals were treated immediately (at 3 mins; t = 3) or at 60 mins (t = 60) with U.S. Navy Treatment Table 6 for 4.48 hrs. RESULTS: At the end of hyperbaric oxygen treatment, intracranial pressure in the t = 60 group (39 +/- 8 mm Hg) was significantly higher than in the t = 3 group (27 +/- 6 mm Hg), brain oxygenation values for group t = 3 and t = 60 were 66 +/- 14 and 52 +/- 15 mm Hg, respectively (no significant difference from baseline), and there were no pathologic scores in the visually assessed electroencephalograph. However, there was a significant decrease in brain glucose and a significant increase in brain lactate in both groups at the end of the 5-hr study period. CONCLUSIONS: Hyperbaric oxygen treatment initiated at both 3 and 60 mins after embolization decreased the deleterious effects of cerebral air embolism on intracranial pressure and brain metabolism. Therefore, this model appears suitable to test the application of hyperbaric oxygen treatment with a delay >60 mins after embolization, as is often the case in the clinical situation.
OBJECTIVE: To evaluate the effects of hyperbaric oxygen treatment after cerebral air embolism on intracranial pressure, brain oxygenation, brain glucose/lactate metabolism, and electroencephalograph. DESIGN: Prospective animal study. SETTING: Hyperbaric chamber. SUBJECTS: Eleven Landrace/Yorkshire pigs. INTERVENTIONS: In 11 anesthetized pigs, intracranial pressure and brain oxygenation were measured with microsensor technology, brain glucose/lactate by microdialysis, and electroencephalograph by conventional methods. After injection of air into the internal carotid artery, animals were treated immediately (at 3 mins; t = 3) or at 60 mins (t = 60) with U.S. Navy Treatment Table 6 for 4.48 hrs. RESULTS: At the end of hyperbaric oxygen treatment, intracranial pressure in the t = 60 group (39 +/- 8 mm Hg) was significantly higher than in the t = 3 group (27 +/- 6 mm Hg), brain oxygenation values for group t = 3 and t = 60 were 66 +/- 14 and 52 +/- 15 mm Hg, respectively (no significant difference from baseline), and there were no pathologic scores in the visually assessed electroencephalograph. However, there was a significant decrease in brain glucose and a significant increase in brain lactate in both groups at the end of the 5-hr study period. CONCLUSIONS: Hyperbaric oxygen treatment initiated at both 3 and 60 mins after embolization decreased the deleterious effects of cerebral air embolism on intracranial pressure and brain metabolism. Therefore, this model appears suitable to test the application of hyperbaric oxygen treatment with a delay >60 mins after embolization, as is often the case in the clinical situation.
Authors: Wondwossen G Tekle; Cheryl D Adkinson; Saqib A Chaudhry; Vikram Jadhav; Ameer E Hassan; Gustavo J Rodriguez; Adnan I Qureshi Journal: Neurocrit Care Date: 2013-04 Impact factor: 3.210