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J Physiol Volume 547, Number 3, 963-970, March 15, 2003 DOI: 10.1113/jphysiol.2002.033571
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J Physiol (2003), 547.3, pp. 963-970
© Copyright 2003 D 2003 The Physiological Society
DOI: 10.1113/jphysiol.2002.033571

State-dependent regulation of cortical blood flow and respiration in hamsters: response to hypercapnia during arousal from hibernation

P. G. Osborne and M. Hashimoto

Department of Physiology, Asahikawa Medical University School of Medicine, Asahikawa 078-8510, Japan

Hibernation is characterised by a global reduction of metabolism, body temperature and blood flow, while arousal from hibernation is achieved by the reversal of these processes. Our experiments were performed on Syrian hamsters that had been chronically implanted with a cortical thermocouple and an optical fibre over the contralateral cortex, and acutely implanted with thermocouples in the rectal, cheek pouch and interscapular brown adipose tissue (BAT). Measurements revealed large thermal gradients in the body of the arousing animals. Maximum whole-body metabolic rate, which was 2.4 times normal cenothermic resting metabolic rate, coincided not with rectal temperature but more closely with respiratory rate (RR) or BAT temperature. Regional cortical blood flow (rCBF), as measured by laser-Doppler flowmetry, changed in parallel with whole-body metabolic rate, peaking at 3.8 times the normal cenothermic resting levels, when rectal temperature was 15 °C. When BAT temperature was less than 25 °C, RR, rCBF and heart rate (HR) were decreased by breathing hypercapnic gas, but these parameters were unresponsive to hyperoxic gases. At cenothermia the RR and rCBF of anaesthetised hamsters was increased by exposure to hypercapnic gases. Exposure to hyperoxic gas decreased RR but had no effect on rCBF. The mechanisms regulating rCBF, HR and RR exhibit state-dependent sensitivities to hypercapnic and hyperoxic stimuli. The large increase in rCBF observed during arousal implies that cerebral autoregulation is temporarily suspended and suggests that hamsters effectively use endogenous mechanisms to minimise the pathology normally associated with dramatic increases in rCBF.



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