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1 University of New Wouth Wales
2 University of New South Wales
3 School of Medical Sciences, University of New South Wales
* To whom correspondence should be addressed. E-mail: kandur{at}email.cz.
Subjects with severe chronic spinal cord injury are prone to hypothermia when exposed to relatively low environmental temperatures that are normally well tolerated by healthy individuals. This impaired thermoregulation is presumably due to disconnection of territories below the injury from supraspinal thermoregulatory centres. However, it is not known how these territories respond to low temperatures. Using a complete transection at T11 in rats, we examined the responses of the tail to cold (6-9°C) by measuring its changes in blood flow and skin temperature weekly for 8 weeks after injury. Despite no significant change in baseline mean flow or temperature in the tail, the transection was effective in removing the sympathetically-mediated supraspinal control of the tail vasculature since the amplitude of the pulse flow was markedly increased and the natural variations of the mean flow almost abolished. As expected, the cold challenge prior to injury caused a marked drop in mean flow, pulse amplitude and temperature of the tail. Surprisingly, the drops in mean blood flow and temperature were still observed after injury although the decrease in flow was slower and no reduction in pulse amplitude occurred. The results suggest that the cutaneous vasculature of the tail is sensitive to cold and will constrict despite disconnection from supraspinal centres. This local effect is slow but may be sufficient to maintain some level of thermoregulation to cold. Without this vascular reaction, the consequences of spinal cord injury on temperature regulation to cold would probably be much worse.
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