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1
Content available remote

Blockade of nitric oxide formation in the rat brain does not disturb development of endotoxin tolerance

100%
Soszynski D., Daniluk M., Galazka M., Dmitruk K.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 6
2

Calibration of remotely collected acceleration data with behavioral observations of roe deer (Capreolus capreolus L.)

100%
Heurich M., Traube M., Stache A., Lottker P.
Acta Theriologica
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2012
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tom 57
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nr 3
Long-term, remote monitoring of animals under natural conditions is essential for obtaining information on animal activity. Advances in biotelemetry have led to the construction of low-power accelerometers placed on Global Positioning System (GPS) collars. Such acceleration data from roe deer have not yet been classified to the various behavioral categories. Here, we determined the threshold values of such data for different behavioral categories. We equipped captive roe deer with Global Positioning System–Global System for Mobile Communications/dual-axis acceleration sensor neck collars and simultaneously measured their movement and observed their behavior. The difference between feeding and slow locomotion was significant on the x- but not the y-axis, and both of these two behavioral categories differed significantly from resting and fast locomotion. Specific thresholds for the behavioral categories—resting, feeding, and slow and fast locomotion—were established by recursive partitioning. We compared the behavior determined by these threshold values with observed behavior and found that 92% of the behavioral categories were correctly assigned. A comparison of our results with those of earlier studies showed that thresholds derived for one species cannot be directly applied to another species. We provide recommendations for the further development of acceleration sensors based on the results obtained in this study.
3
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Role of prostaglandins in heme-induced fever

100%
Walentynowicz K., Szefer M., Wojtal B., Terlecki P., Wrotek S., Kozak W.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
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nr 8
73-82
Brain stroke is often accompanied by a high fever, which is insensitive to a blockade with classic antipyretic drugs known to inhibit the synthesis of prostaglandin E2 (PGE2), a proximal mediator of fever associated with infection. The molecular mechanism of fever associated with stroke is mostly unknown, and has not been thoroughly investigated. One characteristics of the stroke is an extravasation of the erythrocytes into the brain tissue followed by a release of hemoglobin and free heme. In the present study we have tested the hypothesis that free heme itself can induce fever after releasing into the brain. The study was conducted on Sprague Dawley rats instrumented with biotelemetry devices to monitor deep body temperature, and implanted with brain cannulae projected to the lateral ventricle. We demonstrate that heme-L-lysinate microinfused intraventricularly (icv) induces a dose-dependent fever lasting ca. 8 hours. Injection of heme-L-lysinate provoked a significant elevation of PGE2 in the rat cerebro-spinal fluid collected 3 hours post-injection. The fever induced by heme-L-lysinate was blocked by an icv injection of anti- PGE2 antibody. It was not affected, however, by intraperitoneal administration of indomethacin, a cyclooxygenase inhibitor. We conclude that heme-induced fever may underlie the stroke fever.
4
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Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors attenuates fever due to LPS in rats

100%
Soszynski D., Chelminiak M.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 3
Nitric oxide (NO) has been shown to be an important mediator of febrile response to lipopolisaccharide (LPS). To clarify the role of different isoforms of NO synthase (NOS) in febrile response to immune challenge, effects of selective iNOS and nNOS inhibitors on fever to LPS were examined in freely moving biotelemetered rats. Vinyl-L-NIO (N5 - (1-Imino-3-butenyl) - ornithine (vL-NIO), a neuronal nitric oxide synthase (nNOS) inhibitor, and aminoguanidine hydrochloride, an inducible nitric oxide synthase (iNOS) inhibitor, were injected intracerebroventricularly at a dose of 10 µg/rat just before intraperitoneal injection of LPS at a dose of 50 µg/kg. Both inhibitors injected at a selected doses had no effect on normal day-time body temperature (Tb) and normal night-time Tb. vinyl-L-NIO and aminoguanidine injected intracerebroventricularly at a dose of 10 µg/animal suppressed the LPS-induced fever in rats. The fever index calculated for rats pretreated with v-LNIO or with aminoguanidine and injected with LPS was reduced by 43% and 72%, respectively, compared to that calculated for water-pretreated and LPS-injected rats. Whereas vL-NIO partly attenuated both phases of febrile rise in Tb, administration of aminoguanidine into the brain completely prevented fever induced by LPS. These data indicate that activation of iNOS inside the brain is not only responsible for triggering but also for maintaining of LPS-induced fever in rats. It is, therefore, reasonable to hypothesize that, activation of iNOS inside the brain is more important in fever development than activation of nNOS.
5
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Intracerebroventricular injection of neuronal and inducible nitric oxide synthase inhibitors does not influence febrile response in rats during turpentine abscess

100%
Soszynski D., Chelminiak M.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 4
The purpose of this study was to investigate the role of neuronal nitric oxide synthase (nNOS) and inducible NOS (iNOS) in the brain during development of fever in response to localized tissue inflammation caused by injection of turpentine in freely moving biotelemetered rats. To determine the role of both NOSs in turpentine-induced fever, we injected vinyl-L-NIO (N5 – (1-Imino-3-butenyl) – ornithine (vL-NIO), a selective nNOS inhibitor, and aminoguanidine hydrochloride, a selective iNOS inhibitor, intracerebroventricularly (i.c.v.) 5 h after turpentine injection. Rats responded with fever to intramuscular injection of 20 µl of turpentine that commenced about 5 - 6 h after injection and reached peak value between 9 - 11 h post-turpentine. The inhibition of nNOS as well as iNOS in the brain did not affect fever induced by turpentine. Fevers in control rats (treated i.c.v. with pyrogen-free water) and iNOS or nNOS inhibitor-i.c.v. treated rats injected with turpentine were essentially the same. Furthermore, on the basis of these data, we concluded that iNOS and nNOS inside the brain do not participate in generation of fever to turpentine in rats.
6
Content available remote

Hypoxia-induced sickness behaviour

80%
Kozak W., Wrotek S., Walentynowicz K.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
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nr 8
35-50
Sickness behaviour (SB) consists of the set of adaptive responses of the host to severe infections and inflammation. It includes, among others, the thermoregulatory responses such as regulated increase (fever) and/or decrease (anapyrexia) of body temperature (Tb), decrease of motor activity (lethargy), and loss of appetite (hypophagia) resulting in a transient loss of body weight. It is thought that SB is partially induced by the immune-derived mediators such as cytokines and prostaglandins acting on the central nervous system. It has repeatedly been shown, on the other hand, that severe infections (pneumonia, tissue septicemia) can impair processes of the gases exchange both in the lungs and in distal tissues including brain, which may lead to hypoxia of the affected organs. Therefore, we have tested the hypothesis that hypoxia may also provoke SB. The study was conducted on freely moving biotelemetered mice kept at 28°C ambient and 12/12 h light/dark cycle. We demonstrate that mice exposed for 7 days to hypoxia (11%O2) displayed all symptoms of SB. Interleukin-6 deficient mice (IL-6 KO) revealed reduced SB symptoms under hypoxic conditions. Recovery of the hypoxia-exposed mice to a normal rhythm in Tb, motor activity and feeding was unaffected by mepacrine, a phospholipase A2 blocker. The recovery, however, was significantly impaired by indomethacin, a cyclooxygenase inhibitor. Exposure to hypoxemia resulted in significant elevation of plasma IL-6 in both untreated and treated with lipopolysaccharide (LPS) mice. It inhibited, however, a generation of blood prostaglandins (PGE2) in mice. Based on these data we conclude that IL-6 and accumulation of free arachidonic acid in biomembranes contribute to hypoxemia-induced SB.
7
Content available remote

Antipyretic activity of N-acetylcysteine

80%
Wrotek S., Jedrzejewski T., Potera-Kram E., Kozak W.
Journal of Physiology and Pharmacology
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2011
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tom 62
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nr 6
8
Content available remote

Molecular mechanism of emotional fever - the role of nitric oxide

80%
Soszynski D.
Journal of Physiology and Pharmacology. Supplement
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2006
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tom 57
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nr 8
51-59
The purpose of these studies was to assess the involvement of nNOS and iNOS inhibitors on stress fever caused by exposure to an open field in freely moving biotelemetered rats. Vinyl-L-NIO (N5 - (1-Imino-3-butenyl) - ornithine, a neural nitric oxide synthase (nNOS) inhibitor, and aminoguanidine, an inducible nitric oxide synthase (iNOS) inhibitor, were injected into the lateral ventricle (icv) at a dose of 5 µg and 10 µg, respectively, and then immediately exposed to open field for 30 min. After exposure to the open field, rats not treated with NOS inhibitors responded with a rapid rise in Tb and it was accompanied with an increase of motor activity. Both inhibitors significantly suppressed the stress fever. vL-NIO did not influence stress-induced rise in locomotor activity as well as did not change Tb in unstressed rats. Since aminoguanidine caused a transient fall in Tb below the baseline in rats exposed or not to open field and because this inhibitor suppressed stress-induced rise in locomotor activity, we concluded that nNOS expression inside the brain is critically involved in the rise in Tb due to exposure to psychological stress.
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