Effect of potassium-induced cortical spreading depression on prostaglandin-induced fever in conscious and urethane-anesthetized rats

Potassium-induced cortical spreading depression (CSD) on prostaglandin E1 (PGE1) induced fever has been investigated in a dose-responsive experimental design in both conscious and urethane-anesthetized adult male Sprague–Dawley rats. While CSD in itself had no effect on nonfebrile body temperature even under cold ambient conditions, CSD significantly suppressed small but not large fevers induced by intracerebroventricular PGE1. The increased oxygen consumption during fever was also reduced. We also explored the possible involvement of the antipyretic peptide arginine vasopressin, in the CSD-induced suppression of fever. Long term castrated rats have significantly reduced ventral septal levels of this peptide, yet CSD was effective in suppressing the initial 40 min of PGE1 fever in these animals. Thus we conclude that increased release of ventral septal arginine vasopressin is probably not involved in the action of CSD on fever.Key words: fever, cortical spreading depression, prostaglandin, potassium, cytokines, interleukin, anesthesia, urethane.

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Cerebral cortex does not modulate “regulated” decrease in core temperature during hypoxemia in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.274.4.r1158 ◽

1998 ◽

Vol 274 (4) ◽

pp. R1158-R1161

Author(s):

Evvi-Lynn M. Rollins ◽

James E. Fewell

Keyword(s):

Cerebral Cortex ◽

Core Temperature ◽

Cortical Spreading Depression ◽

Spreading Depression ◽

Temperature Response ◽

Sprague Dawley ◽

Adult Rats ◽

The Core ◽

Sprague Dawley Rats ◽

Before And After

In newborns and adults of a number of species including humans, exposure to acute hypoxemia produces a “regulated” decease in core temperature, the mechanism of which is unknown. Considering that various cortical areas participate in autonomic regulation including thermoregulation, the present experiments were carried out to test the hypothesis that the cerebral cortex plays a role in modulating the regulated decrease in core temperature during acute hypoxemia. This hypothesis was tested by determining the core temperature response to acute hypoxemia in chronically instrumented adult Sprague-Dawley rats before and after cortical spreading depression (i.e., functional decortication) was produced by the local application of potassium chloride to the dura overlying the cerebral hemispheres. There was no effect of cortical spreading depression on baseline core temperature. Core temperature decreased during acute hypoxemia in a similar fashion when the cerebral cortex was intact as well as during functional decortication. Thus our data do not support the hypothesis that the cerebral cortex modulates the regulated decrease in core temperature that occurs in adult rats during acute hypoxemia.

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RELATIONSHIP OF OXYGEN CONSUMPTION TO BODY TEMPERATURE IN THE RESTRAINED RAT

Canadian Journal of Biochemistry and Physiology ◽

10.1139/y55-081 ◽

1955 ◽

Vol 33 (1) ◽

pp. 654-657

Author(s):

Roscoe G. Bartlett Jr. ◽

Vernon C. Bohr ◽

William I. Inman

Keyword(s):

Oxygen Consumption ◽

Body Temperature ◽

Emotional Stress ◽

Room Temperature ◽

Temperature Drop ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Relationship Of

Forty adult Sprague-Dawley rats were divided into four groups: 10 control and 10 restrained animals at room temperature [Formula: see text] and 10 control and 10 restrained animals at [Formula: see text]. Continuous recordings were made on oxygen consumption and body temperature. It was learned that the restrained animals had an initially higher oxygen consumption than the control animals. This gradient was maintained throughout a three-hour exposure in the case of the animals maintained at room temperature but in the case of the animals maintained in the cold it was reversed early in the tests, i.e., the oxygen consumption of the restrained animals fell below that of the control animals. The fall in oxygen consumption was accompanied by a fall in body temperature. From the data it was not possible to state which was the cause and which was the effect. It was suggested that both decreased oxygen consumption and temperature drop may be the effect of another cause, emotionality or emotional stress.

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RELATIONSHIP OF OXYGEN CONSUMPTION TO BODY TEMPERATURE IN THE RESTRAINED RAT

Canadian Journal of Biochemistry and Physiology ◽

10.1139/o55-081 ◽

1955 ◽

Vol 33 (4) ◽

pp. 654-657 ◽

Cited By ~ 1

Author(s):

Roscoe G. Bartlett Jr. ◽

Vernon C. Bohr ◽

William I. Inman

Keyword(s):

Oxygen Consumption ◽

Body Temperature ◽

Emotional Stress ◽

Room Temperature ◽

Temperature Drop ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Relationship Of

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Cortical Spreading Depression Causes a Long-Lasting Decrease in Cerebral Blood Flow and Induces Tolerance to Permanent Focal Ischemia in Rat Brain

Journal of Cerebral Blood Flow & Metabolism ◽

10.1097/01.wcb.0000035180.38851.38 ◽

2003 ◽

Vol 23 (1) ◽

pp. 43-50 ◽

Cited By ~ 35

Author(s):

Tatsuo Otori ◽

Joel H. Greenberg ◽

Frank A. Welsh

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Cortical Spreading Depression ◽

Spreading Depression ◽

Focal Ischemia ◽

Sprague Dawley ◽

Mca Occlusion ◽

Sprague Dawley Rats ◽

Subsequent Episode ◽

Permanent Focal Ischemia

Cortical spreading depression (CSD) has previously been shown to induce tolerance to a subsequent episode of transient cerebral ischemia. The objective of the present study was to determine whether CSD also induces tolerance to permanent focal ischemia and, if so, whether tolerance may be mediated by alterations in cerebral blood flow (CBF). Sprague-Dawley rats were preconditioned by applying potassium chloride to one hemisphere for 2 hours, evoking 19 ± 5 episodes of CSD (mean ± SD, n = 19). Three days later, the middle cerebral artery (MCA) was permanently occluded using an intraluminal suture. In a subset of animals, laser Doppler blood flow (LDF) was monitored over the parietal cortex before and during the first 2 hours of MCA occlusion. Preconditioning with CSD reduced the hemispheric volume of infarction from 248 ± 115 mm3 (n = 18) in sham-conditioned animals to 161 ± 81 mm3 (n = 19, P < 0.02). Similarly, CSD reduced the neocortical volume of infarction from 126 ± 82 mm3 to 60 ± 61 mm3 ( P < 0.01). Moreover, preconditioning with CSD significantly improved LDF during MCA occlusion from 21% ± 7% (n = 9) of preischemic baseline in sham-conditioned animals to 29% ± 9% (n = 7, P < 0.02). Preconditioning with CSD therefore preserved relative levels of CBF during focal ischemia and reduced the extent of infarction resulting from permanent MCA occlusion. To determine whether CSD may have altered preischemic baseline CBF, [14C]iodoantipyrine was used in additional animals to measure CBF 3 days after CSD conditioning or sham conditioning. CSD, but not sham conditioning, significantly reduced baseline CBF in the ipsilateral neocortex to values 67% to 75% of those in the contralateral cortex. Therefore, CSD causes a long-lasting decrease in baseline CBF that is most likely related to a reduction in metabolic rate. A reduction in the rate of metabolism may contribute to the induction of tolerance to ischemia after preconditioning with CSD.

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Cortical spreading depression blocks prostaglandin E1 and endotoxin fever in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.264.2.r456 ◽

1993 ◽

Vol 264 (2) ◽

pp. R456-R459 ◽

Cited By ~ 3

Author(s):

M. Monda ◽

Q. J. Pittman

Keyword(s):

Cortical Spreading Depression ◽

Prostaglandin E1 ◽

Spreading Depression ◽

Body Temperatures ◽

Sprague Dawley ◽

E Coli ◽

Sprague Dawley Rats ◽

Thermoregulatory Function ◽

Cortical Involvement ◽

Telemetric Measurement

We have tested the hypothesis that the cortex may play a role in the development of fever. Male Sprague-Dawley rats equipped with AM transmitters for telemetric measurement of body temperature were given intracerebroventricular prostaglandin E1 (PGE1), corticotropin-releasing hormone (CRH), or intravenous E. coli endotoxin. Application of cotton pellets soaked with 3.3 M KCl to the frontal cortex (to induce spreading depression) significantly reduced fevers to PGE1 and endotoxin when compared with fever magnitude with 0.9% NaCl application to the cortex. Neither CRH-induced hyperthermia nor normal body temperatures were altered by the spreading depression. Our results reveal a novel action of spreading depression on thermoregulatory function and indicate cortical involvement in the development of fever.

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Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.2.h751 ◽

1994 ◽

Vol 267 (2) ◽

pp. H751-H756 ◽

Cited By ~ 7

Author(s):

A. W. Cowley ◽

E. Szczepanska-Sadowska ◽

K. Stepniakowski ◽

D. Mattson

Keyword(s):

Body Weight ◽

Arginine Vasopressin ◽

Plasma Catecholamines ◽

Plasma Osmolality ◽

Sprague Dawley ◽

Prolonged Administration ◽

Chronic Stimulation ◽

Sustained Hypertension ◽

Sprague Dawley Rats

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.

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Dietary conjugated linoleic acid (CLA) induces apoptosis of colonic mucosa in 1,2-dimethylhydrazine-treated rats: a possible mechanism of the anticarcinogenic effect by CLA

British Journal Of Nutrition ◽

10.1079/bjn2001445 ◽

2001 ◽

Vol 86 (5) ◽

pp. 549-555 ◽

Cited By ~ 77

Author(s):

Hyun S. Park ◽

Ji H. Ryu ◽

Yeong L. Ha ◽

Jung H. Y. Park

Keyword(s):

Linoleic Acid ◽

Conjugated Linoleic Acid ◽

Control Diet ◽

Terminal Deoxynucleotidyl Transferase ◽

Prostaglandin E ◽

Dependent Manner ◽

Sprague Dawley ◽

Tumour Incidence ◽

Sprague Dawley Rats ◽

Dietary Conjugated Linoleic Acid

One of the objectives of the present study was to investigate whether 1 % conjugated linoleic acid (CLA) in the diet reduced tumour incidence in the colon of 1,2-dimethylhydrazine (DMH)-treated rats. Colon cancer was induced by injecting 6-week-old, male, Sprague–Dawley rats with 15 mg/kg DMH twice per week for 6 weeks. They were fed either 1 % CLA or a control diet ad libitum for 30 weeks. Dietary CLA significantly decreased colon tumour incidence (P<0·05). Our second objective was to investigate whether apoptosis in the colon mucosa of DMH-treated rats was affected by the amount of dietary CLA and whether the changes in apoptosis were related to those in fatty acid-responsive biomarkers. For this purpose, rats were killed after being fed a diet containing 0 %, 0·5 %, 1 % or 1·5 % CLA for 14 weeks. CLA was undetected in the mucosa of rats fed the 0 % CLA diet and increased to 5·9 mg/g phospholipid in rats fed the 0·5 % diet. The apoptotic index estimated by the terminal deoxynucleotidyl transferase-mediated dUTP nick and labelling technique was increased by 251 % and the 1,2-diacylglycerol content was decreased by 57 % in rats fed 0·5 % CLA. No further changes in these variables were observed when CLA in the diet was raised to 1·0 % or 1·5 %. However, dietary CLA decreased mucosal levels of prostaglandin E2, thromboxane B2 and arachidonic acid in a dose-dependent manner. The present data indicate that dietary CLA can inhibit DMH-induced colon carcinogenesis by mechanisms probably involving increased apoptosis.

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