MILTON AND SABINE WENDLANDT

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330 A. S. MILTON AND S. WENDLANDT tion of 0*2-10 ,tg PGE1 whether this antipyretic drug was given before or after PGE1. In fact, the hyperthermias induced by PGE1 appeared to be accentuated. For instance, in the experiment of Fig. 2, 4-Ac was injected 30 min before the intraventricular injection of 10 jug PGE1 which produced a particularly large rise of 30 C. On the other hand the prolonged U0 I- 0 41 40 Q. 39 SE u '4J 9C) 38 37 0 5 Hours 10 Fig. 2. Temperature record of an unanaesthetized cat. At the first arrow marked 4-Ac, 50 mg/kg was injected i.P. and at the arrow marked PGE1, 10 #ag PGE1 was injected into the third ventricle (same experiment as given on third line from bottom in Table 1). secondary rise observed sometimes after an injection of PGE1 was abolished by the 4-Ac injection, the temperature began to fall after a latency of about 15 min and fell even below the level recorded before the PGE1 injection. Normal temperature was either not affected by an i.P. injection of 4-Ac, 50 mg/kg, or it fell by not more than half a degree. The accentuation of the immediate and the abolition of the late hyperthermias were due to the 4-Ac and not to the solvent because these
PROSTAGLANDINS AND BODY TEMPERATURE 331 effects were not obtained with control injections of propylene glycol-O9 % NaCl solution. The aboliton of the late rise resembled the similar effect previously observed with 4-Ac on the fever produced by intraventricular injections of 5-HT or bacterial pyrogen (Milton & Wendlandt, 1968). PGE2. This prostaglandin was injected intraventricularly in doses of 1 and 5 jug only. Both doses raised temperature and produced behavioural effects similar to those observed with PGE1. The rise in temperature was of immediate onset and reached a maximum within an hour; temperature then either returned to the pre-injection level within 3-4 hr, or, after having begun to fall, rose again and this secondary rise lasted up to 10 hr. 41 UO 40- I 39 E X 4-Ac \ , 38 mG t 2 X- 0 4-Ac _ I 5 ~ 10 ~ ~ 15 ~ ~~~~~~~~ I I 20 Hours Fig. 3. Rectal temperature of the unanaesthetized cat. At the first and third arrow i.P. injections of 4-Ac, 50 mg/kg; at the second arrow intraventricular injections of 5 ,ug PGE2. As with PGE1 the initial rise was not abolished or attenuated by 4-Ac which, however, had an antagonizing effect on the secondary rise. A typical experiment is illustrated in Fig. 3, which shows that the injection of 5 #ug PGE2 given 1 hr after an i.p. injection of 50 mg/kg 4-Ac caused a rise of over 20 C. During the following 4 hr, temperature returned to nearly preinjection level, but then began to rise again. This secondary rise was suppressed by another injection of 4-Ac and temperature fell during the following 5 hr. The occurrence of the secondary rise in spite of the first 4-Ac injection is explained by the fact that the action of 4-Ac lasts for a few hours only. In the experiment of Fig. 3 the effect of the second 4-Ac injection also began to wear off after a little over 5 hr. In other experiments in which the 4-Ac was given after the prostaglandin injection, during the initial rise, the result was the same. The initial rise continued while a secondary rise when it occurred was delayed. PGFO12,. Intraventricular injections of 1 or 1O ,tg of this prostaglandin produced no immediate effect on temperature in some cats, small rises in
Page 1 and 2: J. Physiol. (1971), 218, pp. 325-33
Page 3 and 4: PROSTAGLANDINS AND BODY TEMPERATURE
Page 5: No. of expts. 3 3 2 3 PROSTAGLANDIN

MILTON AND SABINE WENDLANDT

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