Regional blood flow (BF) changes during sleep were measured in rabbits at low, neutral, and high ambient temperatures (T(a)) with radioactive microspheres. At both low and high T(a), peripheral vasomotor changes at the onset of desynchronized sleep (DS) were incompatible with thermoregulatory homeostasis. At low T(a), BF decreased in muscle (with the disappearance of shivering), whereas it increased in the arteriovenous anastomoses (AVA) and in the splanchnic bed. At high T(a), 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.
Cianci, T., Zoccoli, G., Lenzi, P., Franzini, C. (1991). Loss of integrative control of peripheral circulation during desynchronized sleep. AMERICAN JOURNAL OF PHYSIOLOGY, 261(2), 373-377 [10.1152/ajpregu.1991.261.2.r373].
Loss of integrative control of peripheral circulation during desynchronized sleep
Cianci T.;Zoccoli G.;Lenzi P.;Franzini C.
1991
Abstract
Regional blood flow (BF) changes during sleep were measured in rabbits at low, neutral, and high ambient temperatures (T(a)) with radioactive microspheres. At both low and high T(a), peripheral vasomotor changes at the onset of desynchronized sleep (DS) were incompatible with thermoregulatory homeostasis. At low T(a), BF decreased in muscle (with the disappearance of shivering), whereas it increased in the arteriovenous anastomoses (AVA) and in the splanchnic bed. At high T(a), 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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.