Febrile responsiveness of vagotomized rats is suppressed even in the absence of malnutrition

Andrej A. Romanovsky, Vladimir A. Kulchitsky, Christopher T. Simons, Naotoshi Sugimoto, M. Székely

Research output: Contribution to journalArticle

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Abstract

The repeatedly observed attenuation of fever in vagotomized rats has been accepted as evidence of an essential role of vagal afferents in the transduction of pyrogenic signals from the periphery to the brain. If, however the general condition of a vagotomized animal is poor (the usual case) and accompanied by malnutrition and body mass loss (common complications of vagotomy), the febrile responsiveness can be suppressed not because of the lack of regal afferentation, but rather secondarily to a malnutrition-associated thermogenic incompetence. In the present study, we addressed this dilemma. Male Wistar rats were subjected to subdiaphragmatic vagotomy (or sham surgery) and, 24 days later, catheterized in the jugular vein. Postsurgically, the rats were closely watched and fed highly palatable food. Their febrile responsiveness [colonic (T(c)) and tail skin (T(sk)) temperature responses] to Escherichia coli lipopolysaccharide (LPS; 1 μg/kg iv) was tested on day 27 postvagotomy. To verify the completeness of vagotomy, each rat was food deprived for 24 h and then euthanized; its stomach's evacuatory function was assessed by weighing the organ. One month postsurgery, both food consumption and body mass of the vagotomized rats (33 ± 2 g/day and 313 ± 4 g, respectively) were similar to the control values (30 ± 1 g/day and 315 ± 8 g). In the sham rats, LPS induced a monophasic T(c) rise of 0.5 ± 0.3°C at 70 min postinjection (peak), preceded by a fall in T(sk). Neither this T(sk) fall (tail skin vasoconstriction) nor the resultant fever occurred in the vagotomized rats; at 70 min, T(c) change was -0.1 ± 0.1°C. The gastric mass (4.1 ± 0.5 g in the vagotomized vs. 1.8 ± 0.1 g in sham rats) indicated the effectiveness of vagotomy. In sum, although the vagotomy-associated malnutrition was successfully prevented with special perioperative care, the vagotomized animals still did not respond to LPS with fever. Malnutrition is, therefore, unlikely to constitute the main reason of the febrile irresponsiveness of vagotomized rats.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume273
Issue number2 42-2
Publication statusPublished - 1997

Fingerprint

Malnutrition
Fever
Vagotomy
Food
Tail
Stomach
Perioperative Care
Skin
Jugular Veins
Vasoconstriction
Ambulatory Surgical Procedures
Lipopolysaccharides
Wistar Rats
Signal Transduction
Escherichia coli
Temperature
Brain

Keywords

  • Febrile response
  • Lipopolysaccharides
  • Perioperative care

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Febrile responsiveness of vagotomized rats is suppressed even in the absence of malnutrition. / Romanovsky, Andrej A.; Kulchitsky, Vladimir A.; Simons, Christopher T.; Sugimoto, Naotoshi; Székely, M.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 273, No. 2 42-2, 1997.

Research output: Contribution to journalArticle

Romanovsky, Andrej A. ; Kulchitsky, Vladimir A. ; Simons, Christopher T. ; Sugimoto, Naotoshi ; Székely, M. / Febrile responsiveness of vagotomized rats is suppressed even in the absence of malnutrition. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 1997 ; Vol. 273, No. 2 42-2.
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AU - Székely, M.

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N2 - The repeatedly observed attenuation of fever in vagotomized rats has been accepted as evidence of an essential role of vagal afferents in the transduction of pyrogenic signals from the periphery to the brain. If, however the general condition of a vagotomized animal is poor (the usual case) and accompanied by malnutrition and body mass loss (common complications of vagotomy), the febrile responsiveness can be suppressed not because of the lack of regal afferentation, but rather secondarily to a malnutrition-associated thermogenic incompetence. In the present study, we addressed this dilemma. Male Wistar rats were subjected to subdiaphragmatic vagotomy (or sham surgery) and, 24 days later, catheterized in the jugular vein. Postsurgically, the rats were closely watched and fed highly palatable food. Their febrile responsiveness [colonic (T(c)) and tail skin (T(sk)) temperature responses] to Escherichia coli lipopolysaccharide (LPS; 1 μg/kg iv) was tested on day 27 postvagotomy. To verify the completeness of vagotomy, each rat was food deprived for 24 h and then euthanized; its stomach's evacuatory function was assessed by weighing the organ. One month postsurgery, both food consumption and body mass of the vagotomized rats (33 ± 2 g/day and 313 ± 4 g, respectively) were similar to the control values (30 ± 1 g/day and 315 ± 8 g). In the sham rats, LPS induced a monophasic T(c) rise of 0.5 ± 0.3°C at 70 min postinjection (peak), preceded by a fall in T(sk). Neither this T(sk) fall (tail skin vasoconstriction) nor the resultant fever occurred in the vagotomized rats; at 70 min, T(c) change was -0.1 ± 0.1°C. The gastric mass (4.1 ± 0.5 g in the vagotomized vs. 1.8 ± 0.1 g in sham rats) indicated the effectiveness of vagotomy. In sum, although the vagotomy-associated malnutrition was successfully prevented with special perioperative care, the vagotomized animals still did not respond to LPS with fever. Malnutrition is, therefore, unlikely to constitute the main reason of the febrile irresponsiveness of vagotomized rats.

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