Cold defense mechanisms in vagotomized rats

被引:30
作者
Romanovsky, AA
Kulchitsky, VA
Simons, CT
Sugimoto, N
Szekely, M
机构
关键词
thermoregulation; skin vasoconstriction; brown fat; cold exposure; ephedrine;
D O I
10.1152/ajpregu.1997.273.2.R784
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Subdiaphragmatically vagotomized rats cannot mount a febrile response to pyrogens and are believed to have severe thermoregulatory deficiencies. We addressed the issue of thermoeffector competence of vagotomized rats by asking three questions. In Expt. 1 we asked, can vagotomized rats readily recruit tail skin vasoconstriction in the course of a moderate cold exposure? In Expt. 2 the question was, can brown adipose tissue (BAT) thermogenesis readily be activated in vagotomized rats (e.g., in response to a tail pinch)? In Expt. 3, we investigated the question: can vagotomized rats elevate their body temperature in response to ephedrine (a drug of high hyperthermizing potential) to the same extent as sham-operated controls? Rats were vagotomized or sham operated and implanted with a catheter into the jugular vein and a thermocouple into the interscapular BAT. To prevent the common complications of vagotomy, special perioperative care was given. During experiments, colonic, tail skin, and BAT temperatures (T-c, T-sk, and T-BAT, respectively) were measured. The vagotomized animals were well nourished and had a body mass (325 +/- 6 g) similar to that of the controls (338 +/- 6 g). In Expt. 1, in response to external cooling (15 degrees C, 1 h), the vagotomized (n = 30) and sham-operated (n = 31) rats recruited tail skin vasoconstriction at close values of both T-c (37.84 +/- 0.08 and 37.97 +/- 0.07 degrees C) and T-sk (33.16 +/- 0.17 and 33.18 +/- 0.18 degrees C, respectively). In Expt. 2, tail pinch-associated stress in vagotomized rats resulted in a sharp rise in the T-BAT - T-c gradient by 0.3-1.0 degrees C. In Expt. 3, ephedrine administered intravenously (whether in a 5 or 35 mg/kg dose) evoked similar hyperthermic responses in the vagotomized and sham-operated rats: a moderate (similar to 2.5 degrees C) T-c rise in the low dose and a ''supramaximal'' (similar to 5.0 degrees C) rise in the high dose. In sum, the answer to all three questions asked is yes. Vagotomized rats, at least when well nourished, exhibit no signs of thermoeffector deficiency. It is, therefore, not effector incompetence but rather vagal deafferentation per se that can explain the febrile irresponsiveness of vagotomized rats.
引用
收藏
页码:R784 / R789
页数:6
相关论文
共 33 条
[1]  
[Anonymous], NEUROANATOMY PHYSL A
[2]  
Blatteis CM, 1997, NEWS PHYSIOL SCI, V12, P1
[3]   ALPHA-ADRENERGIC RECEPTOR-MEDIATED THERMOGENESIS IN BROWN ADIPOSE-TISSUE OF RAT [J].
BORST, SE ;
OLIVER, RJ ;
SEGO, RL ;
SCARPACE, PJ .
GENERAL PHARMACOLOGY-THE VASCULAR SYSTEM, 1994, 25 (08) :1703-1710
[4]   PRIOR VAGOTOMY BLOCKS VMH OBESITY IN PAIR-FED RATS [J].
COX, JE ;
POWLEY, TL .
AMERICAN JOURNAL OF PHYSIOLOGY, 1981, 240 (05) :E573-E583
[5]   RAPID BUT TRANSIENT ATROPHY OF BROWN ADIPOSE-TISSUE IN CAPSAICIN-DESENSITIZED RATS [J].
CUI, JY ;
HIMMSHAGEN, J .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (04) :R562-R567
[6]   LONG-TERM DECREASE IN BODY-FAT AND IN BROWN ADIPOSE-TISSUE IN CAPSAICIN-DESENSITIZED RATS [J].
CUI, JY ;
HIMMSHAGEN, J .
AMERICAN JOURNAL OF PHYSIOLOGY, 1992, 262 (04) :R568-R573
[7]   CAPSAICIN DESENSITIZATION INDUCES ATROPHY OF BROWN ADIPOSE-TISSUE IN RATS [J].
CUI, JY ;
ZARORBEHRENS, G ;
HIMMSHAGEN, J .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (02) :R324-R332
[8]   QUANTITATIVE CONTRIBUTION OF BROWN ADIPOSE-TISSUE THERMOGENESIS TO OVERALL METABOLISM [J].
FOSTER, DO .
CANADIAN JOURNAL OF BIOCHEMISTRY AND CELL BIOLOGY, 1984, 62 (07) :618-622
[9]   MODULATION OF BROWN ADIPOSE TISSUE-MEDIATED THERMOGENESIS BY LESIONS TO THE NUCLEUS TRACTUS SOLITARIUS IN THE RAT [J].
FYDA, DM ;
COOPER, KE ;
VEALE, WL .
BRAIN RESEARCH, 1991, 546 (02) :203-210
[10]   NUCLEUS TRACTUS SOLITARII LESIONS ALTER THE METABOLIC AND HYPERTHERMIC RESPONSE TO CENTRAL PROSTAGLANDIN-E1 IN THE RAT [J].
FYDA, DM ;
COOPER, KE ;
VEALE, WL .
JOURNAL OF PHYSIOLOGY-LONDON, 1991, 442 :337-349