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Interleukin-1 beta peptides induce cerebral pial arteriolar dilation in anesthetized newborn pigs

Interleukin-1 beta peptides induce cerebral pial arteriolar dilation in anesthetized newborn pigs pial arteriolar SHIBATA, HELENA PARFENOVA, SAMUEL L. ZUCKERMAN, M. SEYER, JAMES M. KRUEGER, AND CHARLES W. LEFFLER for Research in Neonatal Physiology, Department of Physiology and Biophysics, of Tennessee, Memphis 38163; Division of Critical Care Medicine, St. Jude Research Hospital, Memphis 38101; and Veterans Affairs Medical Center, Tennessee 38163 induced by the secondary release of inflammatory cytokines, such as interleukin (IL)-lcx, p, IL-6, and tumor necrosis factor-a (TNF-cw). To investigate potential individual components of the pathogenesis of bacterial meningitis in a neonatal model, we previously infused IL-b and TNF-(x onto the exposed cortex of piglets using a closed cranial window technique (33-35). The results suggested that these inflammatory cytokines dilate pial arterioles by mechanisms that involve , nitric oxide, adenosine 3’,5’cyclic monophosphate (CAMP), and guanosine 3’,5’cyclic monophosphate (cGMP). The aim of the present study was, therefore, to examine cerebrovascular effects of a major inflammatory cytokine, IL-1p. To investigate the involvement of in the dilation observed, we measured 6-ketoprostaglandin (PG) F1, and PGEZ in cortical CSF and inhibited their production with indomethacin (Indo). We also measured cortical CSF cyclic nucleotides to assess the potential involvement of these second messengers in the mechanism of the vascular response. METHODS Shibata, Masaaki, http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Regulatory, Integrative and Comparative Physiology The American Physiological Society

Interleukin-1 beta peptides induce cerebral pial arteriolar dilation in anesthetized newborn pigs

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Publisher
The American Physiological Society
Copyright
Copyright © 1996 the American Physiological Society
ISSN
0363-6119
eISSN
1522-1490
Publisher site
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Abstract

pial arteriolar SHIBATA, HELENA PARFENOVA, SAMUEL L. ZUCKERMAN, M. SEYER, JAMES M. KRUEGER, AND CHARLES W. LEFFLER for Research in Neonatal Physiology, Department of Physiology and Biophysics, of Tennessee, Memphis 38163; Division of Critical Care Medicine, St. Jude Research Hospital, Memphis 38101; and Veterans Affairs Medical Center, Tennessee 38163 induced by the secondary release of inflammatory cytokines, such as interleukin (IL)-lcx, p, IL-6, and tumor necrosis factor-a (TNF-cw). To investigate potential individual components of the pathogenesis of bacterial meningitis in a neonatal model, we previously infused IL-b and TNF-(x onto the exposed cortex of piglets using a closed cranial window technique (33-35). The results suggested that these inflammatory cytokines dilate pial arterioles by mechanisms that involve , nitric oxide, adenosine 3’,5’cyclic monophosphate (CAMP), and guanosine 3’,5’cyclic monophosphate (cGMP). The aim of the present study was, therefore, to examine cerebrovascular effects of a major inflammatory cytokine, IL-1p. To investigate the involvement of in the dilation observed, we measured 6-ketoprostaglandin (PG) F1, and PGEZ in cortical CSF and inhibited their production with indomethacin (Indo). We also measured cortical CSF cyclic nucleotides to assess the potential involvement of these second messengers in the mechanism of the vascular response. METHODS Shibata, Masaaki,

Journal

AJP - Regulatory, Integrative and Comparative Physiology – The American Physiological Society

Published: May 1, 1996

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