Distribution of peripheral blood flow in primary tissue hypoxia induced by inhalation of carbon monoxide

Chalmers, John; Korner, Paul I.; White, Saxon William

doi:10.1113/jphysiol.1967.sp008316

Cited by 14 publications

(3 citation statements)

References 16 publications

(11 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies comparing responses to hypoxia or various types of CO interaction have disclosed significant differences. Since arterial Po2 may be normal despite a reduced oxygen-carrying capacity, reflexes which normally increase respiratory rate and tissue blood flow may not be activated (10,11). Recovery from hypoxia associated with CO intoxication is greatly prolonged in comparison to recovery from hypoxia alone (12,13).…”

Section: The Escape Responsementioning

confidence: 99%

Physiological and toxicological aspects of smoke produced during the combustion of polymeric materials.

Einhorn¹

1975

Environ Health Perspect

View full text Add to dashboard Cite

Normally one expects that flame contact is the major cause of injury and death during fires. Analysis of the factors involved in numerous fires has revealed that most deaths were not due to flame contact, but were a consequence of the production of carbon monoxide, nitrogen oxides, and other combustion products, such as aldehydes, low molecular weight alcohols, hydrogen cyanide, and other noxious species. The major emphasis within the scope of this paper relates to the physiological and toxicological aspects of smoke produced during the combustion of materials. Special emphasis is directed toward laboratory procedures which have been developed to determine the qualitative and quantitative analysis of smoke, factors pertaining to smoke development, and to measure the response of laboratory animals exposed to smoke. The effects that fire retardants, incorporated into polymeric materials as a means of improving flammability characteristics, may have on smoke development, the mechanism of polymer degradation, and on the survival response of laboratory animals are also considered.ImagesFIGURE 1.FIGURE 2.FIGURE 3.FIGURE 4.FIGURE 5.FIGURE 6.FIGURE 7.FIGURE 8.FIGURE 9.

show abstract

Section: The Escape Responsementioning

confidence: 99%

Physiological and toxicological aspects of smoke produced during the combustion of polymeric materials.

Einhorn¹

1975

Environ Health Perspect

View full text Add to dashboard Cite

show abstract

“…In cellular level, shortage of oxygen supply suppresses the respiratory chains of mitochondria and causes subsequently less energy generation (13,14). In contrast, we demonstrate for the first time that direct delivery of CO can increase the ATP availability in primary hepatocytes.…”

Section: Discussionmentioning

confidence: 82%

Carbon Monoxide Inhalation Rescues Mice From Fulminant Hepatitis Through Improving Hepatic Energy Metabolism

Tsui¹,

Obed²,

Siu

et al. 2007

Shock

View full text Add to dashboard Cite

Heme oxygenase 1 (HO-1) enhances cellular antioxidative capability by increasing the cleavage of the endogenous and exogenous heme. Besides the biochemical activities of HO, the products of heme degradation significantly contribute to the cytoprotective effects of HO. Here, we show that HO-1 deficiency significantly increases the susceptibility of mice to apoptotic insults, whereas expression of HO-1 significantly increased the resistance of primary hepatocyte to apoptosis. This phenomenon was correlated with the production of one of its catalytic products-carbon monoxide (CO). Surprisingly, exposing the primary mouse hepatocyte to CO could improve the cellular energy metabolism in a soluble guanylyl cyclase-dependent manner. One-hour inhalation of low-dose CO enhanced the hepatic soluble guanylyl cyclase activities in mice. In parallel, the levels of hepatic adenosine triphosphate increased significantly and were associated with a marked reduction of TNF-alpha-induced apoptosis in the liver of D-galactosamine-sensitized mice. In addition, CO inhalation for 1 h significantly improved the survival of mice after initiation of fulminant hepatitis. Up to 90% of mice given CO survived for more than 7 days, whereas control mice died within 12 h. The data provide novel insight of CO-mediated cytoprotection.

show abstract

“…Since arterial Po2 may be normal despite a reduced oxygen-carrying capacity, reflexes which normally increase respiratory rate and tissue blood flow may not be activated (10,11). Since arterial Po2 may be normal despite a reduced oxygen-carrying capacity, reflexes which normally increase respiratory rate and tissue blood flow may not be activated (10,11).…”

Section: The Escape Responsementioning

confidence: 99%

Physiological and Toxicological Aspects of Smoke Produced during the Combustion of Polymeric Materials

Einhorn¹

1975

Environmental Health Perspectives

View full text Add to dashboard Cite

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) andBrogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.Normally one expects that flame contact is the major cause of injury and death during fires. Analysis of the factors involved in numerous fires has revealed that most deaths were not due to flame contact, but were a consequence of the production of carbon monoxide, nitrogen oxides, and other combustion products, such as aldehydes, low molecular weight alcohols, hydrogen cyanide, and other noxious species.The major emphasis within the scope of this paper relates to the physiological and toxicological aspects of smoke produced during the combustion of materials. Special emphasis is directed toward laboratory procedures which have been developed to determine the qualitative and quantitative analysis of smoke, factors pertaining to smoke development, and to measure the response of laboratory animals exposed to smoke. The effects that fire retardants, incorporated into polymeric materials as a means of improving flammability characteristics, may have on smoke development, the mechanism of polymer degradation, and on the survival response of laboratory animals are also considered.

show abstract

Distribution of peripheral blood flow in primary tissue hypoxia induced by inhalation of carbon monoxide

Cited by 14 publications

References 16 publications

Physiological and toxicological aspects of smoke produced during the combustion of polymeric materials.

Physiological and toxicological aspects of smoke produced during the combustion of polymeric materials.

Carbon Monoxide Inhalation Rescues Mice From Fulminant Hepatitis Through Improving Hepatic Energy Metabolism

Physiological and Toxicological Aspects of Smoke Produced during the Combustion of Polymeric Materials

Contact Info

Product

Resources

About