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. 2009 Aug;179(6):701-10.
doi: 10.1007/s00360-009-0352-6. Epub 2009 Mar 11.

Body and brain temperature coupling: the critical role of cerebral blood flow

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Body and brain temperature coupling: the critical role of cerebral blood flow

Mingming Zhu et al. J Comp Physiol B. 2009 Aug.

Abstract

Direct measurements of deep-brain and body-core temperature were performed on rats to determine the influence of cerebral blood flow (CBF) on brain temperature regulation under static and dynamic conditions. Static changes of CBF were achieved using different anesthetics (chloral hydrate, CH; alpha-chloralose, alphaCS; and isoflurane, IF) with alphaCS causing larger decreases in CBF than CH and IF; dynamic changes were achieved by inducing transient hypercapnia (5% CO(2) in 40% O(2) and 55% N(2)). Initial deep-brain/body-core temperature differentials were anesthetic-type dependent with the largest differential observed with rats under alphaCS anesthesia (ca. 2 degrees C). Hypercapnia induction raised rat brain temperature under all three anesthesia regimes, but by different anesthetic-dependent amounts correlated with the initial differentials--alphaCS anesthesia resulted in the largest brain temperature increase (0.32 +/- 0.08 degrees C), while CH and IF anesthesia lead to smaller increases (0.12 +/- 0.03 and 0.16 +/- 0.05 degrees C, respectively). The characteristic temperature transition time for the hypercapnia-induced temperature increase was 2-3 min under CH and IF anesthesia and approximately 4 min under alphaCS anesthesia. We conclude that both, the deep-brain/body-core temperature differential and the characteristic temperature transition time correlate with CBF: a lower CBF promotes higher deep-brain/body-core temperature differentials and, upon hypercapnia challenge, longer characteristic transition times to increased temperatures.

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Figures

Fig. 1
Fig. 1
A typical time course of brain temperature changes induced by a 15-min period of hypercapnia. Data were obtained from one rat under αCS anesthesia. Hypercapnia was induced at 20 min, and was switched off at 35 min (shaded bars indicate hypercapnia period)
Fig. 2
Fig. 2
Graph showing a typical result from exponential modeling (solid line) of one of the 15 min hypercapnia induced brain temperature time courses. Data (dots) represent measurement duration of those 6 mm deep brain location during first hypercapnia period for a rat under αCS anesthesia
Fig. 3
Fig. 3
Magnitudes of brain temperature changes, ΔT, and characteristic temperature transition times, tc, during and after hypercapnia events for rats under three different anesthesia regimes. Data represent all rats (α-chloralose, αCS, n = 6; chloral hydrate, CH, n = 6; isoflurane, IF, n = 6). Error bars represent SD. Statistical significance analysis is for CH versus αCS or IF versus αCS (**P < 0.005; *P < 0.05). Differences for tc between CH and IF do not reach statistical significance
Fig. 4
Fig. 4
Example of temperature correlation between body and 6 mm deep brain location in a rat solely anesthetized by 1.2% isoflurane during a process of slow body cooling from 38 to 33°C in 3 h
Fig. 5
Fig. 5
Graph shows further decoupling of brain temperatures during a 65-min period when IF was substituted with αCS anesthesia. The rat was first anesthetized with 2.0% IF, then further administered with 40 mg/kg αCS i.p. at 10 min. The 2.0% IF anesthesia was removed after the shaded 5-min period. Note that the small decrease of body-core temperature at 10 min is due to temporary rectal temperature drop by cold αCS solution injected
Fig. 6
Fig. 6
Correlation of brain/body-core temperature differential and CBF* under three anesthesia regimes. Here CBF* values are estimated from the characteristic time constant tc obtained during both hypercapnia challenge (filled symbols) and post-hypercapnia (empty symbols) periods: CBF* = ctissue/(ρb · cb · tc), in which ctissue represents brain tissue heat capacity, cb and ρb are the same as previously defined in Eq. 2. We use the term CBF* because exact relationship between tc and CBF in the presence of heat exchange with the environment is not known. “×” and “−” are simulated data based on a previously published brain temperature distribution equation (see (Zhu et al., 2006), Eq. 2) and with heat transfer coefficient h equal to 0.005 and 0.001 (W/(cm2 °C))

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