[abstract] EFFECTS OF DECOMPRESSION AND VENOUS GAS EMBOLISM ON CEREBRAL BLOOD FLOW RESPONSES TO HYPEROXIA MEASURED BY PERFUSION MAGNETIC RESONANCE IMAGING

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[abstract] EFFECTS OF DECOMPRESSION AND VENOUS GAS EMBOLISM ON CEREBRAL BLOOD FLOW RESPONSES TO HYPEROXIA MEASURED BY PERFUSION MAGNETIC RESONANCE IMAGING

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Title: [abstract] EFFECTS OF DECOMPRESSION AND VENOUS GAS EMBOLISM ON CEREBRAL BLOOD FLOW RESPONSES TO HYPEROXIA MEASURED BY PERFUSION MAGNETIC RESONANCE IMAGING
Author: Clark, JM; Gelfand, R; Floyd, TF; Cameron, BA; Guvakov, D; Eckenhoff, RG
Abstract: BACKGROUND: Decompression and associated venous gas embolism (VGE) may alter baseline vascular tone and physiologic responses to vascular stimuli. The sparse innervation of the cerebral circulation, in conjunction with available methods for quantitative measurement of cerebral blood flow (CBF), provides an opportunity for assessing effects of decompression on a specific vascular bed. A model for human decompression was provided by previous studies (JAP 1990; 69:914-918), which showed that saturation exposure at 25 fsw followed by direct decompression produced VGE in all subjects without symptoms of decompression sickness. METHODS: Perfusion MRI with continuous arterial spin labeling was used to measure CBF during air and O2 breathing in 4 men (to date) before and after exposure for 12 h at 25 fsw (76.6 kPa) with decompression over 2-3 min. Precordial Doppler ultrasound with Kisman-Masurel coding was used to monitor VGE. RESULTS: CBF values (Mean SEM) during air and O2 breathing before exposure were 48.7 5.1 and 32.2 4.9 ml/100 g/min, respectively, at end-tidal PCO2 levels of 42.4 1.1 and 39.9 0.7 mm Hg. CBF values at 2-3 h after decompression were 55.2 7.1 and 40.4 3.5 ml/100 g/min at PCO2 levels of 43.1 1.6 and 40.7 1.9 mm Hg. Relative CBF decrements during O2 breathing were 34.9 5.0 percent before exposure and 25.5 3.5 percent after decompression. Grade 3 VGE on movement were detected in 3 subjects within 1 h post-decompression and in all 4 subjects within 4 h. Two subjects still had VGE 9 h after decompression. CONCLUSIONS: Preliminary results are consistent with a reduced cerebral vasoconstrictor response to hyperoxia after rapid decompression from shallow saturation exposure. Furthermore, because the cerebral vasculature is largely isolated from venous bubbles, an indirect humoral influence may be responsible for the observed CBF effects. (Supported by NAVSEA N61331-99-C-0040-P001) embolism, cerebral blood flow, MRI, hyperoxia, bubbles
Description: Undersea and Hyperbaric Medical Society, Inc. (http://www.uhms.org )
URI: http://archive.rubicon-foundation.org/1135
Date: 2002

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  • UHMS Meeting Abstracts
    This is a collection of the published abstracts from the Undersea and Hyperbaric Medical Society (UHMS) annual meetings.

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