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Cited by 461

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Mechanisms of circulatory and intestinal barrier dysfunction during whole body hyperthermia

Hall, David M., Buettner, Garry R., Oberley, Larry W., Xu, Linjing, Matthes, Ronald D., Gisolfi, Carl V.·2001·American Journal of Physiology-Heart and Circulatory Physiology
DOI 10.1152/ajpheart.2001.280.2.h509
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Abstract

This work tested the hypotheses that splanchnic oxidant generation is important in determining heat tolerance and that inappropriate ·NO production may be involved in circulatory dysfunction with heat stroke. We monitored colonic temperature (T c), heart rate, mean arterial pressure, and splanchnic blood flow (SBF) in anesthetized rats exposed to 40°C ambient temperature. Heating rate, heating time, and thermal load determined heat tolerance. Portal blood was regularly collected for determination of radical and endotoxin content. Elevating T c from 37 to 41.5°C reduced SBF by 40% and stimulated production of the radicals ceruloplasmin, semiquinone, and penta-coordinate iron(II) nitrosyl-heme (heme-·NO). Portal endotoxin concentration rose from 28 to 59 pg/ml ( P < 0.05). Compared with heat stress alone, heat plus treatment with the nitric oxide synthase (NOS) antagonist N ω-nitro-l-arginine methyl ester (l-NAME) dose dependently depressed heme-·NO production and increased ceruloplasmin and semiquinone levels. l-NAME also significantly reduced lowered SBF, increased portal endotoxin concentration, and reduced heat tolerance ( P < 0.05). The NOS II and diamine oxidase antagonist aminoguanidine, the superoxide anion scavenger superoxide dismutase, and the xanthine oxidase antagonist allopurinol slowed the rates of heme-·NO production, decreased ceruloplasmin and semiquinone levels, and preserved SBF. However, only aminoguanidine and allopurinol improved heat tolerance, and only allpourinol eliminated the rise in portal endotoxin content. We conclude that hyperthermia stimulates xanthine oxidase production of reactive oxygen species that activate metals and limit heat tolerance by promoting circulatory and intestinal barrier dysfunction. In addition, intact NOS activity is required for normal stress tolerance, whereas overproduction of ·NO may contribute to the nonprogrammed splanchnic dilation that precedes vascular collapse with heat stroke.

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Metadata

Authors
Hall, D. M., Buettner, G. R., Oberley, L. W., Xu, L., Matthes, R. D., & Gisolfi, C. V.
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Published
2001-02-01
Volume
280
Issue
2
Pages
H509-H521
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
DOI
10.1152/ajpheart.2001.280.2.h509
OpenAlex
W1858048769
Cited by
461
References
2
FWCI
5.53
Type
journal article
Language
en
Open access
closed

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