Absence of endotoxin fever but not prostaglandin E2 fever in the Brattleboro rat

1982 ◽  
Vol 242 (1) ◽  
pp. R116-R120 ◽  
Author(s):  
P. C. Eagan ◽  
N. W. Kasting ◽  
W. L. Veale ◽  
K. E. Cooper
Keyword(s):  
Prostaglandin E2 ◽  
Arginine Vasopressin ◽  
Bacterial Endotoxin ◽  
Cerebral Ventricle ◽  
Intracerebroventricular Injection ◽  
Brattleboro Rat ◽  
Febrile Response ◽  
Long Evans ◽  
Colonic Temperature ◽  
Lateral Cerebral Ventricle

Changes in colonic temperature following intracerebroventricular injection (icv) of bacterial endotoxin or prostaglandin E2 (PGE2) were measured in Long-Evans (LE) and Brattleboro (DI) rats. Indwelling cannulas were implanted into the brains of rats for subsequent microinjection into a lateral cerebral ventricle. Microinjection of 1 microgram of bacterial endotoxin into a lateral cerebral ventricle produced a fever in the LE rat but not in the DI rat. Daily injections of 1 microgram of endotoxin icv in the DI rat did not result in a fever. Intraperitoneal injections of 50 micrograms of bacterial endotoxin resulted in a fever in the LE rat, but the DI rat showed no such response. Both groups of animals did produce a fever in response to icv administration of 200 ng of PGE2. The lack of arginine vasopressin in the DI rat may be related to the animal's failure to show a febrile response to endotoxin.

scholarly journals AVP mediates the attenuated febrile response to administration of PGE1 in rats near term of pregnancy

1998 ◽  
Vol 275 (3) ◽  
pp. R691-R696 ◽  
Author(s):  
Heather L. Eliason ◽  
James E. Fewell
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Receptor Antagonist ◽  
Core Temperature ◽  
Arginine Vasopressin ◽  
Intracerebroventricular Injection ◽  
Intracerebroventricular Administration ◽  
Febrile Response ◽  
The Central Nervous System ◽  
Near Term

Rats have an attenuated febrile response to intracerebroventricular injection of PGE1 near the term of pregnancy, the mechanism of which is unknown. The present experiments were carried out to test the hypothesis that arginine vasopressin (AVP), functioning as an endogenous antipyretic substance in the central nervous system, mediates this attenuated febrile response. The febrile response to intracerebroventricular injection of 0.2 μg PGE1 was determined in pregnant and nonpregnant rats after an intracerebroventricular injection of either vehicle or a vasopressin V1-receptor antagonist. After intracerebroventricular administration of vehicle, intracerebroventricular administration of 0.2 μg PGE1 produced significant increases in core temperature in both nonpregnant and pregnant animals. The increase in core temperature, however, was attenuated both in magnitude and duration in pregnant compared with nonpregnant animals. After intracerebroventricular administration of a vasopressin V1-receptor antagonist, intracerebroventricular administration of 0.2 μg PGE1 produced significant increases in core temperature that were similar in nonpregnant and pregnant animals. Our data support the hypothesis that a pregnancy-related activation of AVP as an endogenous antipyretic substance in the central nervous system attenuates the febrile response to intracerebroventricular administration of PGE1 near term of pregnancy in rats.

The effectiveness of arginine vasopressin and sodium salicylate as antipyretics in the Brattleboro rat

1990 ◽  
Vol 512 (2) ◽  
pp. 243-247 ◽  
Author(s):  
Doreen M. Fyda ◽  
W. Bruce Mathieson ◽  
Keith E. Cooper ◽  
Warren L. Veale
Keyword(s):  
Arginine Vasopressin ◽  
Sodium Salicylate ◽  
Brattleboro Rat

Contribution of vasopressin to the maintenance of blood pressure during dehydration

1983 ◽  
Vol 245 (5) ◽  
pp. F615-F621 ◽  
Author(s):  
R. L. Woods ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Systolic Blood Pressure ◽  
Arginine Vasopressin ◽  
Cardiovascular Response ◽  
Urine Volume ◽  
Brattleboro Rats ◽  
Continuous Administration ◽  
Plasma Vasopressin ◽  
Long Evans

Normal Long-Evans rats, when dehydrated for up to 72 h, have a progressive rise in plasma vasopressin that is associated with a fall in body weight and urine volume, a rise in plasma and urine osmolality, and the maintenance of normal systolic blood pressure. In contrast, Brattleboro diabetes insipidus rats, genetically deficient in vasopressin, when dehydrated to achieve an equivalent body weight loss, have a significant 15 mmHg fall in systolic blood pressure. Even when fluid balance is corrected in the Brattleboro rats by the continuous administration of 1-desamino-8-D-arginine vasopressin, a synthetic vasopressin analogue with potent antidiuretic properties but minimal pressor activity, blood pressure still falls when the animals are dehydrated. In contrast, Brattleboro rats infused with exogenous arginine vasopressin to produce a plasma vasopressin level of 18.9 +/- 3.5 pg X ml-1 are able to maintain normal blood pressure during 48 h of dehydration. This level of vasopressin is comparable to the level found endogenously in dehydrated Long-Evans rats and is nonpressor in normal rats. These results suggest that both the antidiuretic and vasoconstrictor properties of vasopressin are important in the cardiovascular response to dehydration.

The lateral cerebral ventricle in early second trimester.

Radiology ◽  
1983 ◽  
Vol 148 (2) ◽  
pp. 529-531 ◽  
Author(s):  
D H Chinn ◽  
P W Callen ◽  
R A Filly
Keyword(s):  
Cerebral Ventricle ◽  
Second Trimester ◽  
Lateral Cerebral Ventricle

Physiological changes during thermoregulation and fever in urethan-anesthetized rats

1988 ◽  
Vol 255 (1) ◽  
pp. R73-R81 ◽  
Author(s):  
T. J. Malkinson ◽  
K. E. Cooper ◽  
W. L. Veale
Keyword(s):  
Interleukin 1 ◽  
Cerebral Ventricle ◽  
Arterial Blood ◽  
Dependent Change ◽  
Male Wistar Rats ◽  
Series Of Experiments ◽  
Dose Dependent ◽  
Conscious Animals ◽  
Maintain Body Temperature ◽  
Lateral Cerebral Ventricle

Adult male Wistar rats were anesthetized with urethan (1.5 g/kg). They were unable to maintain body temperature (Tb) in a warm (32 degrees C) or cool (9 degrees C) environment or at a laboratory room temperature of 22 degrees C. Tb was allowed to fall to 35.8, 34.5, or 33.3 degrees C, and prostaglandin E1 (PGE1, 400 ng) was delivered into a lateral cerebral ventricle. An immediate feverlike rise in Tb resulted, accompanied by vigorous shivering. Animals were vasoconstricted throughout. When Tb was raised to and maintained at 38.3 or 39.5 degrees C, animals also responded with a fever; however, the magnitude of the fever diminished as the starting Tb increased. In a series of experiments in which Tb was maintained (36.8-37.4 degrees C) by means of a heating pad, PGE1 delivered into a lateral cerebral ventricle or into the anterior hypothalamus caused a dose-dependent change in Tb, which was similar in time of onset, magnitude, and duration to that observed in conscious animals. This fever was accompanied by shivering and increased O2 uptake, heart rate, arterial blood pressure, respiratory rate, and intracranial pressure during the rising phase of the fever, and vasodilation of the paws occurred during defeveresence. Animals were also able to develop a dose-dependent rise in Tb in response to purified human interleukin 1.

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