Vagotomy modifies but does not eliminate the increase in body temperature following burn injury in rats

被引:2
作者
Caldwell, FT [1 ]
Graves, DB [1 ]
Wallace, BH [1 ]
机构
[1] Univ Arkansas, Dept Surg, Little Rock, AR 72205 USA
关键词
burn injury; fever; vagotomy; circadian rhythm;
D O I
10.1016/S0305-4179(99)00006-6
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Introduction: Rats with burn injury to greater than or equal to 50% of the BSA demonstrate a significant increase in body temperature (TB) during light hours, and decrease of circadian variation in T-B This study investigated the hypothesis that part or all of the signal for increased T-B in rats with burn injury is transmitted to the central nervous system by way of afferent vagal fibers. Methods: Four groups of animals were studied: Burn-Sham Vagotomy; Control-Sham Vagotomy; Burn-Vagotomy and Control-Vagotomy. Anesthetized animals had bilateral subdiaphragmatic vagotomy (VagX) or sham VagX performed, and AM radio transmitters were implanted in the peritoneal cavity for the purpose of recording T-B and activity index (AI). Following a one week recovery period, burn animals received scald burns equal to 50.3 +/- 2.5% BSA. Results: The main effect of VagX upon T-B was a Small but significant reduction in T-B during dark hours. At least 87% of this decrease in post-burn T-B was also present for the control vagotomy group. Vagotomy had no effect on the increase in T-B for the burn groups during light hours. During dark hours, VagX significantly reduced T-B in burns and controls, and burn injury significantly reduced activity. Conclusions: One may speculate that afferent vagal signals are partially responsible for maintenance of T-B, with or without burn injury, and that the major signal for increase in T-B for animals with burn injury is not a neural one via afferent vagal pathways. (C) 1999 Elsevier Science Ltd and ISBI. All rights reserved.
引用
收藏
页码:295 / 305
页数:11
相关论文
共 12 条
[1]  
BLUTHE RM, 1994, CR ACAD SCI III-VIE, V317, P499
[2]  
Caldwell F. T. Jr., 1997, Journal of Burn Care and Rehabilitation, V18, P525, DOI 10.1097/00004630-199711000-00010
[3]  
Caldwell F. T. Jr., 1994, Journal of Burn Care and Rehabilitation, V15, P121, DOI 10.1097/00004630-199403000-00004
[4]  
Caldwell FT, 1998, J BURN CARE REHABIL, V19, P501
[5]   ANATOMICAL SPECIFICITY OF NORADRENERGIC INPUTS TO THE PARAVENTRICULAR AND SUPRAOPTIC NUCLEI OF THE RAT HYPOTHALAMUS [J].
CUNNINGHAM, ET ;
SAWCHENKO, PE .
JOURNAL OF COMPARATIVE NEUROLOGY, 1988, 274 (01) :60-76
[6]   ROLE OF INTERLEUKIN-6 IN FEVER IN RATS [J].
LEMAY, LG ;
VANDER, AJ ;
KLUGER, MJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 258 (03) :R798-R803
[7]   The vagus nerve in the thermoregulatory response to systemic inflammation [J].
Romanovsky, AA ;
Simons, CT ;
Szekely, M ;
Kulchitsky, VA .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 1997, 273 (01) :R407-R413
[8]  
SAWCHENKO PE, 1992, STRESS : NEUROENDOCRINE AND MOLECULAR APPROACHES, VOLS 1 AND 2, P15
[9]  
Sehic E, 1996, BRAIN RES, V726, P160
[10]   NEURAL AND BIOCHEMICAL MEDIATORS OF ENDOTOXIN AND STRESS-INDUCED C-FOS EXPRESSION IN THE RAT-BRAIN [J].
WAN, WH ;
WETMORE, L ;
SORENSEN, CM ;
GREENBERG, AH ;
NANCE, DM .
BRAIN RESEARCH BULLETIN, 1994, 34 (01) :7-14