Key result
Desynchronized sleep in rabbits at low and high ambient temperatures caused peripheral vasomotor changes incompatible with thermoregulatory homeostasis, indicating impaired central nervous regulation.
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Suggests sleep-state autonomic impairment in rabbits; leaves open relevance to human cardiovascular regulation.
Regional blood flow (BF) changes during sleep were measured in rabbits at low, neutral, and high ambient temperatures (Ta) with radioactive microspheres. At both low and high Ta, peripheral vasomotor changes at the onset of desynchronized sleep (DS) were incompatible with thermoregulatory homeostasis. At low Ta, BF decreased in muscle (with the disappearance of shivering), whereas it increased in the arteriovenous anastomoses (AVA) and in the splanchnic bed. At high Ta, BF decreased in muscle (with the disappearance of panting) and in the AVA, whereas it increased in the splanchnic bed. An impaired central nervous regulation underlies the disruption of peripheral circulation patterns in this sleep stage. The lack of adaptive vasomotor adjustments in DS, which has little consequence in normal conditions, may become relevant in cardiovascular pathophysiology when BF redistribution through increased neurogenic vasomotor activity becomes a major compensating mechanism.
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Cianci et al. (1991) studied Desynchronized sleep and thermoregulation. Desynchronized sleep at low, neutral, and high ambient temperatures was evaluated on Regional blood flow changes. Desynchronized sleep in rabbits at low and high ambient temperatures caused peripheral vasomotor changes incompatible with thermoregulatory homeostasis, indicating impaired central nervous regulation.
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