Fever

Fever, also known as pyrexia, or a febrile response, is a medical symptom which describes an increase in internal body temperature to levels which are above normal (37 degrees Celsius, 98.6 degrees Fahrenheit). Fever should not be confused with Hyperthermia, which is an increase in body temperature over the body?s thermoregulatory set-point (approximately 37 degrees Celsius). A fever is most accurately characterized as a temporary elevation in the body?s thermoregulatory set-point, which is usually by about 1-2 degrees Celsius. This elevation in thermoregulatory set-point means that the previous "normal body temperature" would be considered hypothermic. Effector mechanisms, such as increased blood pressure, increased heart rate, activation of brown adipose tissue and muscular shivering attempt to counteract the perceived hypothermia, thereby reaching the new thermoregulatory set-point.

References

Primary Sources

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• Cao, C., Matsumura, K., Yamagata, K., and Watanabe, Y., (1996) Endothelial cells of the rat brain vasculature express cyclooxygenase-2 mRNA in response to systemic interleukin-1B: a possible site of prostaglandin synthesis responsible for fever. Brain Res 733, 263-272.
• Castellani JW, Young AJ, Sawka MN, Pandolf KB.(1998) Human thermoregulatory responses during serial cold-water immersions. J Appl Physiol, 85(1), 204-209.
• Feng, JD, Price M, Cohen J, and Satinoff E. (1989) Prostaglandin fevers in rats: regulated change in body temperature or change in regulated body temperature? Am J Physiol Regulatory Integrative Comp Physiol 257: R695-R699.
• Jakobsson, P. J., Thoren, S, Morgenstern, R., and Samuelsson B. (1999) Identification of human prostaglandin E synthase: A microsomal, glutathione-dependent, inducible enzyme, constituting a potential novel drug target. Proc Natl Acad Sci U S A. 96, 7220-7225
• Milton, A. S. & Wendlandt, S. (1970). A possible role for prostaglandin E1 as a modulator for temperature regulation in the central nervous system. J Physiol, 207(2), 76P-77P.
• Milton, A. S. & Wendlandt, S. (1971) Effects on body temperature of prostaglandins of the A, E and F series on injection into the third ventricle of unanaesthetized cats and rabbits. J Physiol, 218, 325-336.
• Opp M. R. & Krueger J. M. (1991) Interleukin 1-receptor antagonist blocks interleukin 1-induced sleep and fever. Am J Physiol, 260(2), R453-R457.
• Scammell, T. E., Elmquist, J. K., Griffin, J. D., & Saper, C. B., (1996) Ventromedial preoptic prostaglandin E2 activates fever-producing autonomic pathways. J Neurosci, 16(19), 6246-6254.
• Scammel., T. E., Griffin, J. D., Elquist, J. K. and Saper C. B. (1998) Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever. Am J Physiol Regulatory Integrative Comp Physiol. 274 (3), R783-R789.
• Vane, J. R. & Flower, R. J. (1972) Inhibition of prostaglandin synthetase in brain explains the anti-pyretic activity of paracetamol (4-Acetamidophenol). Nature, 240, 410-411.

Secondary Sources

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• Engblom, D., Ek, M., Saha, Sipra, S., Ericsson-Dahistrand, A., Jakobsson P.J., Blomqvist, A (2002) Prostaglandins as inflammatory messengers across the blood-brain barrier. J Mol Med, 80, 5-15.
• Moltz, H. (1993). Fever: causes and consequences. Neurosci Biobehav Rev. 17(3), 237-69
• Waag T, Hesselberg O, Reinertsen RE. (1995) Heat production during cold water immersion: the role of shivering and exercise in the development of hypothermia. Arctic Med Res. 54(2), 60-64.