Effect of Hyperbaric Oxygen Treatment on Nitric Oxide and Oxygen Free Radicals in Rat Brain

2000 ◽  
Vol 83 (4) ◽  
pp. 2022-2029 ◽  
Author(s):  
Ikram M. Elayan ◽  
Milton J. Axley ◽  
Paruchuri V. Prasad ◽  
Stephen T. Ahlers ◽  
Charles R. Auker
Keyword(s):  
Nitric Oxide ◽  
Free Radicals ◽  
Rat Brain ◽  
Hyperbaric Oxygen ◽  
High Pressures ◽  
Oxygen Free Radicals ◽  
In Vivo Microdialysis ◽  
Sprague Dawley ◽  
Fourfold Increase

Oxygen (O2) at high pressures acts as a neurotoxic agent leading to convulsions. The mechanism of this neurotoxicity is not known; however, oxygen free radicals and nitric oxide (NO) have been suggested as contributors. This study was designed to follow the formation of oxygen free radicals and NO in the rat brain under hyperbaric oxygen (HBO) conditions using in vivo microdialysis. Male Sprague-Dawley rats were exposed to 100% O2 at a pressure of 3 atm absolute for 2 h. The formation of 2,3-dihydroxybenzoic acid (2,3-DHBA) as a result of perfusing sodium salicylate was followed as an indicator for the formation of hydroxyl radicals. 2,3-DHBA levels in hippocampal and striatal dialysates of animals exposed to HBO conditions were not significantly different from controls. However, rats treated under the same conditions showed a six- and fourfold increase in nitrite/nitrate, break down products of NO decomposition, in hippocampal and striatal dialysates, respectively. This increase was completely blocked by the nitric oxide synthase (NOS) inhibitor l-nitroarginine methyl ester (l-NAME). Using neuronal NOS, we determined the NOS O2 K m to be 158 ± 28 (SD) mmHg, a value which suggests that production of NO by NOS would increase approximately four- to fivefold under hyperbaric O2 conditions, closely matching the measured increase in vivo. The increase in NO levels may be partially responsible for some of the detrimental effects of HBO conditions.

The influence of nitric oxide synthase 1 on blood flow and interstitial nitric oxide in the kidney

2001 ◽  
Vol 281 (1) ◽  
pp. R91-R97 ◽  
Author(s):  
Masao Kakoki ◽  
Ai-Ping Zou ◽  
David L. Mattson
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Renal Cortex ◽  
In Vivo Microdialysis ◽  
Sprague Dawley ◽  
Selective Inhibitors ◽  
Renal Vasculature ◽  
Doppler Flowmetry ◽  
Arterial Blood

The role of nitric oxide (NO) produced by NO synthase 1 (NOS1) in the renal vasculature remains undetermined. In the present study, we investigated the influence of systemic inhibition of NOS1 by intravenous administration of N ω-propyl-l-arginine (l-NPA; 1 mg · kg−1 · h−1) and N 5-(1-imino-3-butenyl)-l-ornithine (v-NIO; 1 mg · kg−1 · h−1), highly selective NOS1 inhibitors, on renal cortical and medullary blood flow and interstitial NO concentration in Sprague-Dawley rats. Arterial blood pressure was significantly decreased by administration of both NOS1-selective inhibitors (−11 ± 1 mmHg with l-NPA and −7 ± 1 mmHg with v-NIO; n = 9/group). Laser-Doppler flowmetry experiments demonstrated that blood flow in the renal cortex and medulla was not significantly altered following administration of either NOS1-selective inhibitor. In contrast, the renal interstitial level of NO assessed by an in vivo microdialysis oxyhemoglobin-trapping technique was significantly decreased in both the renal cortex (by 36–42%) and medulla (by 32–40%) following administration of l-NPA ( n = 8) or v-NIO ( n = 8). Subsequent infusion of the nonspecific NOS inhibitor N ω-nitro-l-arginine methyl ester (l-NAME; 50 mg · kg−1 · h−1) to rats pretreated with either of the NOS1-selective inhibitors significantly increased mean arterial pressure by 38–45 mmHg and significantly decreased cortical (25–29%) and medullary (37–43%) blood flow. In addition, l-NAME further decreased NO in the renal cortex (73–77%) and medulla (62–71%). To determine if a 40% decrease in NO could alter renal blood flow, a lower dose ofl-NAME (5 mg · kg−1 · h−1; n = 8) was administered to a separate group of rats. The low dose of l-NAME reduced interstitial NO (cortex 39%, medulla 38%) and significantly decreased blood flow (cortex 23–24%, medulla 31–33%). These results suggest that NOS1 does not regulate basal blood flow in the renal cortex or medulla, despite the observation that a considerable portion of NO in the renal interstitial space appears to be produced by NOS1.

Ethane production as a measure of lipid peroxidation after renal ischemia

1986 ◽  
Vol 251 (5) ◽  
pp. F839-F843 ◽  
Author(s):  
M. S. Paller ◽  
R. P. Hebbel
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Superoxide Radical ◽  
Oxygen Free Radicals ◽  
Tissue Injury ◽  
Renal Ischemia ◽  
Radical Scavenger ◽  
Base Line ◽  
Ethane Production

After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.

scholarly journals EFFECT OF ANOXIA ON STRIATAL MONOAMINE METABOLISM IN IMMATURE RAT BRAIN COMPARED WITH THAT OF HYPOXIA : AN IN VIVO MICRODIALYSIS STUDY† 1378

1996 ◽  
Vol 39 ◽  
pp. 232-232
Author(s):  
Wako Nakajima ◽  
Akira Ishida ◽  
Hirokazu Arai ◽  
Yasushi Takahashi ◽  
Tadahiko Ito ◽  
...  
Keyword(s):  
Rat Brain ◽  
In Vivo Microdialysis ◽  
Monoamine Metabolism ◽  
Immature Rat ◽  
Microdialysis Study
Sign in / Sign up

Export Citation Format

Share Document