Portland State University. Department of Biology
Larry I. Crawshaw
Term of Graduation
Date of Publication
Master of Science (M.S.) in Biology
Vagus nerve, Fever
1 online resource (v, 54 pages)
Recent evidence has suggested a role of vagal afferents in the pathogenesis of fever. Although bilateral truncal subdiaphragmatic vagotomy has been shown to attenuate the febrile response to lipopolysaccharide (LPS) and interleukin-1, no study has yet been able to verify which of the five subdiaphragmatic vagal branches (viz., the anterior and posterior celiac branches, the anterior and posterior gastric branches, and the hepatic branch) is responsible for communicating this signal. The present study tested the hypothesis that the hepatic vagal branch mediates pyrogenic signals from the periphery to the brain. Male Wistar rats underwent one of four selective vagotomiesceliac branch vagotomy (CBV), gastric branch vagotomy (GBV), hepatic branch vagotomy (HBV), or sham vagotomy (SV). On day 26-29 postvagotomy, a catheter was implanted into the right jugular vein. On day 29-32, the thermal responsiveness of each rat to LPS (0 or 1 μg/kg; iv) was tested at 30°C. Colonic temperatures (Tc) were measured in lightly restrained animals using thermocouples. Three days later, the animals were subjected to a 24 h food and water deprivation, and the effectiveness of CBV, GBV, HBV, and SV to increase gastric mass, induce pancreatic hypertrophy, and to block the porto-renal osmotic reflex was assessed by weighing the stomach and pancreas and measuring the specific gravity of bladder urine, respectively. Stomach mass, pancreatic hypertrophy and urine specific gravity separated the four treatment groups into four different clusters (P = 0.020), thus confirming that each type of vagotomy had its own effect on these parameters. The responses of the SV, CBV, and GBVrats to LPS were different from that of the HBV group (P = 0.022). After a latency of ca. 40 min, Ll Tc rose, reaching a peak of 0.7 ± 0.1°C, 0.6 ± 0.1°C, and 0.9 ± 0.2°C, in the SV, CBV, and GBV groups, respectively. HBV rats, however, responded with an attenuated fever that reached a peak of 0.1 ± 0.2°C. Similarly, the fever index of the HBV group was smaller than that of the other groups (P = 0.022). These findings suggest the hepatic vagal branch mediates peripheral pyrogenic signals to the brain.
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Simons, Christopher Todd, "The Role of the Hepatic Vagus in the Pathogenesis of Fever" (1997). Dissertations and Theses. Paper 5697.