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Biphasic fever: What triggers the second body temperature rise?
WS2-K-1-02 ALTERATION OF FEBRILE RESPONSE OF RATS TO INTRAPERITONEAL ENDOTOXIN ACCORDING TO METHODS OF ADMINISTRATION. N. S u g l m o t o 1, O. S h l d o 1, M. T a n a b e 1, S. I n a l s h l 2, AND T. N a g a s a k a 1. 1)Dept. o f P h y s i o l . , S c h o o l o f M e d i c i n e , K a n a z a w a Univ., K a n a z a w a 920, J a p a n . 2 ) G r a d u a t e S c h o o l o f N a t u r a l S c i e n c e a n d T e c h n o l o g y , K a n a z a w a Univ., K a n a z a w a 920, J a p a n . Male W l s t a r r a t s ( S t d : W i s t a r / S T ) , w e i g h i n g 320 - 350 g, w e r e h o u s e d i n p l a s t i c c a g e s w l t h a 12:12 h l i g h t - d a r k cycle at an ambient temperature (T a) o f 24" C. At l e a s t 10 d a y s before measurement, they were implanted lntraperltoneally with blotelemetrlc batteryoperated transmitters for measuring body core temperature (Tb) u n d e r p e n t o b a r b l t a l sodium anesthesia. Additionally, a polyethylene catheter f i l l e d w l t h s t e r i l e s a l i n e was positioned in the peritoneal cavity. The catheter was t u n n e l e d s u b c u t a n e o u s l y and exteriorized at the head. On t h e d a y o f m e a s u r e m e n t , e a c h r a t was l o o s e l y r e s t r a i n e d in a cylindrical w i r e m e s h c a g e a t T a o f 24" C. A f t e r T b h a d b e e n s t a b i l i z e d , llpopolysaccharide (LPS) d i s s o l v e d i n s t e r i l e s a l i n e was a d m i n i s t e r e d l n t r a p e r i t o n e a l l y into the rat at a dose o f 10 p g / k g t h r o u g h t h e i n t r a p e r i t o n e a l catheter or by a direct injection using a syringe with a 23-gauge needle. T b was r e c o r d e d e v e r y min b e f o r e a n d f o r 7 h o u r s a f t e r t h e LPS administration. T h e same m e a s u r e m e n t s w e r e p e r f o r m e d in u n r e s t r a i n e d animals. In t h e restrained r a t s , LPS a d m i n i s t e r e d t h r o u g h t h e l n t r a p e r l t o n e a l catheter produced monophaslc f e v e r , p e a k l n g 160 min a f t e r t h e a d m i n i s t r a t i o n . D i r e c t LPS I n j e c t i o n s , o n t h e o t h e r h a n d , c a u s e d b l p h a s l c f e v e r , p e a k i n g 160 rain a n d 270 rain a f t e r t h e LPS i n j e c t i o n . T h e TbS o f t h e r a t s i n j e c t e d d i r e c t l y w i t h LPS w e r e s i g n i f i c a n t l y higher then those of the rats a d m i n i s t e r e d w i t h LPS t h r o u g h t h e i n t r a p e r l t o n e a l catheter b e t w e e n 240 a n d 330 mln a f t e r administration. Slmilar results were obtained in the unrestrained rats. These results s u g g e s t t h a t t h e f e b r i l e r e s p o n s e o f r a t s t o LPS i s m o d i f i e d b y t h e m o d e o f i n j e c t i n g LPS, i.e., direct intraperltoneal injection enhances LPS-induced fever.
WS2-K-1-03 BIPHASIC FEVER: WHAT TRIGGERS THE SECOND BODY TEMPERATURE RISE? A. A. Romanovsky t, 2, C. M. Blatteis 2 l) Inst. of Physiology, Belarusian Academy of Sciences, Minsk, Belarus 2) Dept. of Physiology and Biophysics, Univ. of Tennessee, Memphis, Tennessee, U.S.A. Both exogenous and endogenous pyrogens, administered intravenously (i.v.), characteristically induce monophasic body temperature (Tb) rises at low doses and biphasic fevers at higher doses. The mechanism of initiation of the second T b rise of the typically biphasic lipopolysaccharide (LPS) fever is not known. This study was undertaken to test the hypothesis that the second Tb rise during fever is initiated by the first T b rise p e r se. Experiments were conducted in guinea pigs implanted with an intraperitoneal thermode, i.v. catheter, and intrahypothalamic thermocouple. Intraperitoneal cooling (IPC) was performed by perfusing water (22°C) through the thermode under afebrile conditions, during the first (0-40 min after pyrogen injection) or second (80-120 min) phase of the biphasic LPS (2 0.g/kg, i.v.) fever or during a monophasic LPS (0.5 Itg/kg, i.v.) fever. Throughout IPC, the rate of heat withdrawal was maintained at 11.6 + 1.2 mW/g. No IPC was performed in the corresponding controls. The higher dose of LPS induced a typical biphasic fever with the first peak (1.5 ± 0.1 °C) occuring at ca. 50 min and the second (1.2 ± 0.1 °C) at ca. 130 min after pyrogen administration. When started immediately after LPS injection at the higher dose, IPC completely blocked the first phase of the biphasic fever. This blockade was followed by a Tb rise, which, although similar to the rise in the second phase, might alternatively be interpreted as being a result of the delayed occurence of the first phase, previously suppressed by IPC. We excluded the latter possibility by showing the absence of overshoot in T b restoration after IPC applied during the second phase of biphasic fever, during monophasic fever, or under afebrile conditions. We conclude, therefore, that the second Tb rise of biphasic LPS fever is not induced by the first T b rise p e r s e . Although the present data do not clarify what mechanisms are responsible for triggering the second febrile phase, they allow the rejection of our initial hypothesis. (Supported by NIH grants NS 22716 and HL 47650).
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WS2-K-1-03 BIPHASIC FEVER: WHAT TRIGGERS THE SECOND BODY TEMPERATURE RISE? A. A. Romanovsky t, 2, C. M. Blatteis 2 l) Inst. of Physiology, Belarusian Academy of Sciences, Minsk, Belarus 2) Dept. of Physiology and Biophysics, Univ. of Tennessee, Memphis, Tennessee, U.S.A. Both exogenous and endogenous pyrogens, administered intravenously (i.v.), characteristically induce monophasic body temperature (Tb) rises at low doses and biphasic fevers at higher doses. The mechanism of initiation of the second T b rise of the typically biphasic lipopolysaccharide (LPS) fever is not known. This study was undertaken to test the hypothesis that the second Tb rise during fever is initiated by the first T b rise p e r se. Experiments were conducted in guinea pigs implanted with an intraperitoneal thermode, i.v. catheter, and intrahypothalamic thermocouple. Intraperitoneal cooling (IPC) was performed by perfusing water (22°C) through the thermode under afebrile conditions, during the first (0-40 min after pyrogen injection) or second (80-120 min) phase of the biphasic LPS (2 0.g/kg, i.v.) fever or during a monophasic LPS (0.5 Itg/kg, i.v.) fever. Throughout IPC, the rate of heat withdrawal was maintained at 11.6 + 1.2 mW/g. No IPC was performed in the corresponding controls. The higher dose of LPS induced a typical biphasic fever with the first peak (1.5 ± 0.1 °C) occuring at ca. 50 min and the second (1.2 ± 0.1 °C) at ca. 130 min after pyrogen administration. When started immediately after LPS injection at the higher dose, IPC completely blocked the first phase of the biphasic fever. This blockade was followed by a Tb rise, which, although similar to the rise in the second phase, might alternatively be interpreted as being a result of the delayed occurence of the first phase, previously suppressed by IPC. We excluded the latter possibility by showing the absence of overshoot in T b restoration after IPC applied during the second phase of biphasic fever, during monophasic fever, or under afebrile conditions. We conclude, therefore, that the second Tb rise of biphasic LPS fever is not induced by the first T b rise p e r s e . Although the present data do not clarify what mechanisms are responsible for triggering the second febrile phase, they allow the rejection of our initial hypothesis. (Supported by NIH grants NS 22716 and HL 47650).
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