|
|
||||||||
INFLAMMATION, CYTOKINES, AND TEMPERATURE REGULATION
1Systemic Inflammation Laboratory, Trauma Research, St. Joseph's Hospital and Medical Center, Phoenix, Arizona 85013; 2Thermoregulation Laboratory, Legacy Clinical Research and Technology Center, Portland, Oregon 97140; and 3Department of Physiology, Southern Illinois University, Carbondale, Illinois 62901
Submitted 16 December 2002 ; accepted in final form 16 April 2003
The organum vasculosum laminae terminalis (OVLT) has been proposed to serve
as the interface for blood-to-brain febrigenic signaling, because ablation of
this structure affects the febrile response. However, lesioning the OVLT
causes many "side effects" not fully accounted for in the fever
literature. By placing OVLT-lesioned rats on intensive rehydration therapy, we
attempted to prevent these side effects and to evaluate the febrile response
in their absence. After the OVLT of Sprague-Dawley rats was lesioned
electrolytically, the rats were given access to 5% sucrose for 1 wk to
stimulate drinking. Sucrose consumption and body mass were monitored. The
animals were examined twice a day for signs of dehydration and treated with
isotonic saline (50 ml/kg sc) when indicated. This protocol eliminated
mortality but not several acute and chronic side effects stemming from the
lesion. The acute effects included adipsia and gross (14% of body weight)
emaciation; chronic effects included hypernatremia, hyperosmolality, a
suppressed drinking response to hypertonic saline, and previously unrecognized
marked (by
2°C) and long-lasting (>3 wk) hyperthermia. Because the
hyperthermia was not accompanied by tail skin vasoconstriction, it likely
reflected increased thermogenesis. After the rats recovered from the acute
(but not chronic) side effects, their febrile response to IL-1
(500
ng/kg iv) was tested. The sham-operated rats developed typical monophasic
fevers (
0.5°C), the lesioned rats did not. However, the absence of
the febrile response in the OVLT-lesioned rats likely resulted from the
untreatable side effects. For example, hyperthermia at the time of pyrogen
injection was high enough (3940°C) to solely prevent fever from
developing. Hence, the changed febrile responsiveness of OVLT-lesioned animals
is given an alternative interpretation, unrelated to febrigenic signaling to
the brain.
fever; adipsia; third ventricle; median preoptic nucleus
This article has been cited by other articles:
![]() |
K. Nakamura and S. F. Morrison Preoptic mechanism for cold-defensive responses to skin cooling J. Physiol., May 15, 2008; 586(10): 2611 - 2620. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. Ootsuka, W. W. Blessing, A. A. Steiner, and A. A. Romanovsky Fever response to intravenous prostaglandin E2 is mediated by the brain but does not require afferent vagal signaling Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2008; 294(4): R1294 - R1303. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. A. Steiner, V. F. Turek, M. C. Almeida, J. J. Burmeister, D. L. Oliveira, J. L. Roberts, A. W. Bannon, M. H. Norman, J.-C. Louis, J. J. S. Treanor, et al. Nonthermal Activation of Transient Receptor Potential Vanilloid-1 Channels in Abdominal Viscera Tonically Inhibits Autonomic Cold-Defense Effectors J. Neurosci., July 11, 2007; 27(28): 7459 - 7468. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. G. Whyte and A. K. Johnson Lesions of the anteroventral third ventricle region exaggerate neuroendocrine and thermogenic but not behavioral responses to a novel environment Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2007; 292(1): R137 - R142. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Tavares, F. J. Minano, R. Maldonado, and M. J. Dascombe Endotoxin fever in granulocytopenic rats: evidence that brain cyclooxygenase-2 is more important than circulating prostaglandin E2 J. Leukoc. Biol., December 1, 2006; 80(6): 1375 - 1387. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. A. Steiner, S. Chakravarty, J. R. Robbins, A. S. Dragic, J. Pan, M. Herkenham, and A. A. Romanovsky Thermoregulatory responses of rats to conventional preparations of lipopolysaccharide are caused by lipopolysaccharide per se-- not by lipoprotein contaminants Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2005; 289(2): R348 - R352. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. I. Ivanov, A. A. Steiner, S. Patel, A. Y. Rudaya, and A. A. Romanovsky Albumin is not an irreplaceable carrier for amphipathic mediators of thermoregulatory responses to LPS: compensatory role of {alpha}1-acid glycoprotein Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2005; 288(4): R872 - R878. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. von Meyenburg, B. H. Hrupka, D. Arsenijevic, G. J. Schwartz, R. Landmann, and W. Langhans Role for CD14, TLR2, and TLR4 in bacterial product-induced anorexia Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2004; 287(2): R298 - R305. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. C. Almeida, A. A. Steiner, N. C. Coimbra, and L. G. S. Branco Thermoeffector neuronal pathways in fever: a study in rats showing a new role of the locus coeruleus J. Physiol., July 1, 2004; 558(1): 283 - 294. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Rummel, T. Hubschle, R. Gerstberger, and J. Roth Nuclear translocation of the transcription factor STAT3 in the guinea pig brain during systemic or localized inflammation J. Physiol., June 1, 2004; 557(2): 671 - 687. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |