2002
DOI: 10.1179/016164102101200861
|View full text |Cite
|
Sign up to set email alerts
|

Blood flow and ionic responses in the awake brain due to carbon monoxide

Abstract: This study examined the effect of 2000 ppm CO on the brain of an awake rat. Measurements of regional perfusion as well as metabolic, ionic and electrical activities were used to examine whether mechanisms responsible for changes in brain perfusion were separable from those attributable to compromises in neuronal metabolism. Exposure to 2000 ppm CO resulted in elevation of cerebral blood flow. The stability of mitochondrial NADH redox level during CO exposure indicated that tissue hypoxia did not develop. The e… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

0
6
0

Year Published

2004
2004
2019
2019

Publication Types

Select...
6
2
1

Relationship

1
8

Authors

Journals

citations
Cited by 14 publications
(6 citation statements)
references
References 25 publications
0
6
0
Order By: Relevance
“…Exchange transfusion with blood containing 80% CO-Hgb to otherwise healthy dogs resulted in no toxic effects, however, despite resultant CO-Hgb levels of 57% to 64%, suggesting that CO toxicity is not dependent on CO-Hgb formation. Other studies have corroborated the findings of morbidity and mortality due to CO poisoning independent of hypoxia or CO-Hgb formation [45][46][47][48][49].…”
Section: Direct Cellular Toxicitymentioning
confidence: 75%
“…Exchange transfusion with blood containing 80% CO-Hgb to otherwise healthy dogs resulted in no toxic effects, however, despite resultant CO-Hgb levels of 57% to 64%, suggesting that CO toxicity is not dependent on CO-Hgb formation. Other studies have corroborated the findings of morbidity and mortality due to CO poisoning independent of hypoxia or CO-Hgb formation [45][46][47][48][49].…”
Section: Direct Cellular Toxicitymentioning
confidence: 75%
“…Carbon monoxide (CO) is a toxic gas that can act as a cerebral vasodilator. 2 , 3 Increases in CBF with elevations in CO have been shown in animal models 3 7 as well as in humans. 8 , 9 Low-level CO exposure is common, through inhalation of cigarette smoke or air pollution.…”
Section: Introductionmentioning
confidence: 98%
“…Dora et al (68) were able to change the NADH redox state when CO was applied topically to the brain. Our group showed in detail the influence of various CO levels on the pathophysiology of the brain in vivo (173,186,188,212). When CO levels were low, the NADH remained the same; whereas Ͼ3,000 ppm, CO led to an increase in NADH due to the development of hypoxia.…”
Section: Hyperoxia or Normobaric And Hyperbaric Increase In Po2mentioning
confidence: 99%