Brain temperature

Globus MY, Busto R, Lin B, Schnippering H, Ginsberg MD. Detection of free radical activity during transient global ischemia and recirculation effects of intraischemic brain temperature modulation. J Neurochem 1995 65 1250-1256. 

Previously, in vitro recovery was the most commonly used method for estimating ECF concentrations of a substance (Benveniste, 1989 Stable et al., 1991). To determine in vitro recovery, the probe is immersed in a known concentration of the analyte, preferably at brain temperature, and perfused with a medium free of the analyte. Percent recovery (or relative recovery) is defined as the ratio between two measures (a) the concentration of the analyte that is recovered from the probe and (b) the known concentration. In vitro calibration is limited and no longer considered appropriate, because it fails to factor in physiological factors, such as extracellular tortuosity and neurochemical reuptake, which iirfluence in vivo but not in vitro recovery (Benveniste, 1989 Benveniste and Huttemeier, 1990 Bungay et al., 1990 Hsiao et al., 1990 Morrison et al., 1991 Parsons et al., 1991b Parsons and Justice, 1992 Stable, 2000). 

Obal F Jr, Sary G, Alfoldi P, Rubicsek G, Obal F. Vasoactive intestinal polypeptide promotes sleep without effects on brain temperature in rats at night. Neurosci Lett 1986 64 236-240. 

Kapas L, Obal F, Jr., Alfoldi P, Rubicsek G, Penke B, Obal F. Effects of nocturnal intraperitoneal administration of cholecystokinin in rats simultaneous increase in sleep, increase in EEG slow-wave activity, reduction of motor activity, suppression of eating, and decrease in brain temperature. Brain Res 1988 438 155-164. 

In 1987, however, a study by Busto et al. (5) showed that small decreases in brain temperature (as little as 2-5°C below normal brain temperature) conferred a marked protective effect against experimental global cerebral ischemia. This finding, as well as subsequent animal studies that modeled neurodegenerative diseases and CNS injury, led to a resurgence of interest in mild hypothermia as a method of cerebral protection. 

How the temperature is measured (i.e., brain vs arterial, venous, tympanic, bladder, or rectal temperature) is also critical, as the core temperature is usually 0.3-1.1°C lower than brain temperature (51). However, it is important to consider that these values may be different in patients with acute cerebral ischemia or trauma. 

Ginsberg M. D., Stemau L. L., Globus M. Y., Dietrich W. D., and Busto R. (1992) Therapeutic modulation of brain temperature relevance to ischemic brain injury. Cerebrovasc. Brain Metab. Rev. 4, 189-225. 

Schwab S., Schwarz S., Aschoff A., Keller E., and Hacke W. (1998) Moderate hypothermia and brain temperature in patients with severe middle cerebral artery infarction. Acta Neurochir. Suppl. 71, 131-134. 

Dietrich W. D., Busto R., Halley M., and Valdes I. (1990) The importance of brain temperature in alterations of the blood-brain barrier following cerebral ischemia. J. Neuropathol. Exp. Neurol. 49,486 -97. 

HenkerR. A., Brown S. D., and Marion D. W. (1998) Comparison of brain temperature with bladder and rectal temperatures in adults with severe head injury. Neurosurgery 42,1071-1075. 

Busto R. and Ginsberg M. D. (1998) The influence of altered brain temperature in cerebral ischemia. In Cerebrovascular Disease Pathophysiology, Diagnosis and Management (Ginsberg M. D. and Bogousslavsky, J., eds.), Blackwell Science, Malden, pp. 287-307. 

Nurse S. and Corbett D. (1994) Direct measurement of brain temperature during and after intraischemic hypothermia correlation with behavioral, physiological, and histological endpoints. J. Neurosci. 14,7726-7734. 

Freund T. F., Buzsaki G., Leon A., and SomogyiP. (1990) Hippocampal cell death following ischemia effects of brain temperature and anesthesia. Exp. Neurol. 108, 251-260. 

Kil H. Y., Zhang J., and Piantadosi C. A. (1996) Brain temperature alters hydroxyl radical production during cerebral ischemia/reperfusion in rats. J. Cereb. Blood... 

Busto R., Globus M. Y., Neary J. T., and Ginsberg M. D. (1994) Regional alterations of protein kinase C activity following transient cerebral ischemia effects of intraischemic brain temperature modulation. J. Neurochem. 63, 1095-1103. 

Eguchi Y., Yamashita K., Iwamoto T., and Ito H. (1997) Effects of brain temperature on calmodulin and microtubule-associated protein 2 immunoreactivity in the gerbil hippocampus following transient forebrain ischemia. J. Neurotrauma 14, 109-118. 

The mechanisms whereby brain cells die during ischemia are not fully understood. Experimental evidence points to a complex array of parallel hemodynamic, biochemical, and electrophysiological events that combine to produce neuronal damage. In experimental cerebral ischemia, the severity of this damage can be significantly reduced by treatment with mild hypothermia (2-5°C below normal brain temperature). 

Brain temperature also depends on regional cerebral blood flow (rCBF). Following vascular occlusion, deep brain tissues may suffer a transient temperature rise reflecting the failure of arterial blood to remove metabolic heat (28). As superficial tissues cool, the temperature in deep tissues also decreases. Thus, by retarding or interrupting blood flow, ischemia upsets temperature regulation. 

D. Brain temperature and blood-brain barrier permeability to hydrophilic tracers. Brain Res. 319,191-212. 

Minamisawa H., Mellergard P., Smith M. L., et al. (1990) Preservation of brain temperature during ischemia in rats. Stroke 21, 758-764. 

Hayward J. N. and Baker M. A. (1969) A comparative study of the role of the cerebral arterial blood in the regulation of brain temperature in five mammals. Brain Res. 16,417 140. 

Sick T. J., Tang R., and Perez-Pinzon M. A. (1999) Cerebral blood flow does not mediate the effect of brain temperature on recovery of extracellular potassium ion activity after transient focal ischemia in the rat. Brain Res. 821,400-406. 

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