Hyperbaric oxygen (HBO 2 ) increases oxygen tension (PO 2 ) in blood but reduces blood flow by means of O 2 -induced vasoconstriction. Here we report the first quantitative evaluation of these opposing effects on tissue PO 2 in brain, using anesthetized rats exposed to HBO 2 at 2 to 6 atmospheres absolute (ATA). We assessed the contribution of regional cerebral blood flow (rCBF) to brain PO 2 as inspired PO 2 (PiO 2 ) exceeds 1 ATA. We measured rCBF and local PO 2 simultaneously in striatum using collocated platinum electrodes. Cerebral blood flow was computed from H 2 clearance curves in vivo and PO 2 from electrodes calibrated in vitro, before and after insertion. Arterial PCO 2 was controlled, and body temperature, blood pressure, and EEG were monitored. Scatter plots of rCBF versus PO 2 were nonlinear (R 2 ¼ 0.75) for rats breathing room air but nearly linear (R 2 ¼ 0.88-0.91) for O 2 at 2 to 6 ATA. The contribution of rCBF to brain PO 2 was estimated at constant inspired PO 2 , by increasing rCBF with acetazolamide (AZA) or decreasing it with N-nitro-L-arginine methyl ester (L-NAME). At basal rCBF (78 mL/100 g min), local PO 2 increased 7-to 33-fold at 2 to 6 ATA, compared with room air. A doubling of rCBF increased striatal PO 2 not quite two-fold in rats breathing room air but 13-to 64-fold in those breathing HBO 2 at 2 to 6 ATA. These findings support our hypothesis that HBO 2 increases PO 2 in brain in direct proportion to rCBF. IntroductionThe O 2 content of blood is the mathematical product of hemoglobin concentration and arterial hemoglobin O 2 saturation, the latter being a nonlinear function of arterial oxygen partial pressure (PaO 2 ). The small amount of O 2 dissolved in plasma is usually negligible. However, breathing hyperbaric oxygen (HBO 2 ), that is oxygen at pressures greater than 1 atmosphere absolute (ATA), raises PaO 2 beyond the point at which hemoglobin is fully saturated, so that the dissolved fraction becomes the main source of O 2 available to cells. But this does not assure enhanced O 2 delivery to brain, because tissue PO 2 also depends on regional blood flow.Tissue oxygen tension (PO 2 ) is a dynamic balance between O 2 delivery and consumption. Many authors have reported increased brain PO 2 in HBO 2 (Jamieson and Van Den Brenk, 1962;Bennett, 1965;Bean et al, 1971;Torbati et al, 1978;Hunt et al, 1978), and reviews are available (Jamieson, 1989;Camporesi et al, 1996;Dean et al, 2003). It is also known that total or regional cerebral blood flow (rCBF) decreases in HBO 2 as a function of pressure and time. But the contribution of CBF to brain PO 2 had never been quantified. Cerebral vasoconstriction and decreased total or rCBF have been shown in healthy volunteers and patients breathing O 2 at 3.5 ATA for brief periods (Lambertsen et al, 1953;Visser et al, 1996;Omae et al, 1998). In animals, in which HBO 2 is maintained for longer times and at higher pressures, the rCBF response is biphasic: the initial decrease in rCBF is followed by a secondary rise to www.jcbfm.com control leve...

No abstract

No abstract

Probabilistic models and maximum likelihood estimation have been used to predict the occurrence of decompression sickness (DCS). We indicate a means of extending the maximum likelihood parameter estimation procedure to make use of knowledge of the time at which DCS occurs. Two models were compared in fitting a data set of nearly 1,000 exposures, in which greater than 50 cases of DCS have known times of symptom onset. The additional information provided by the time at which DCS occurred gave us better estimates of model parameters. It was also possible to discriminate between good models, which predict both the occurrence of DCS and the time at which symptoms occur, and poorer models, which may predict only the overall occurrence. The refined models may be useful in new applications for customizing decompression strategies during complex dives involving various times at several different depths. Conditional probabilities of DCS for such dives may be reckoned as the dive is taking place and the decompression strategy adjusted to circumstance. Some of the mechanistic implications and the assumptions needed for safe application of decompression strategies on the basis of conditional probabilities are discussed.

Because carbon monoxide (CO) has been proposed to have anti-inflammatory properties, we sought protective effects of CO in pulmonary O(2) toxicity, which leads rapidly to lung inflammation and respiratory failure. Based on published studies, we hypothesized that CO protects the lung against O(2) by selectively increasing expression of antioxidant enzymes, thereby decreasing oxidative injury and inflammation. Rats exposed to O(2) with or without CO [50-500 parts/million (ppm)] for 60 h were compared for lung wet-to-dry weight ratio (W/D), pleural fluid volume, myeloperoxidase (MPO) activity, histology, expression of heme oxygenase-1 (HO-1), and manganese superoxide dismutase (Mn SOD) proteins. The brains were evaluated for histological evidence of damage from CO. In O(2)-exposed animals, lung W/D increased from 4.8 in normal rats to 6.3; however, only CO at 200 and 500 ppm decreased W/D significantly (to 5.9) during O(2) exposure. Large volumes of pleural fluid accumulated in all rats, with no significant CO treatment effect. Lung MPO values increased after O(2) and were not attenuated by CO treatment. CO did not enhance lung expression of oxidant-responsive proteins Mn SOD and HO-1. Animals receiving O(2) and CO at 200 or 500 ppm showed significant apoptotic cell death in the cortex and hippocampus by immunochemical staining. Thus significant protection by CO against O(2)-induced lung injury could not be confirmed in rats, even at CO concentrations associated with apoptosis in the brain.