Influence of sleep on circulation in normal and hypertensive animals

Zanchetti, Alberto; Guazzi, Maurizio D.; Baccelli, G

doi:10.1007/978-3-642-49737-7_6

Cited by 2 publications

(1 citation statement)

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“…In contrast with our observations, Zanchetti and Guazzi and their associates (18,19) noted a larger than normal fall in pressure during desynchronized sleep in cats after sinoaortic denervation; they concluded that it was due to chemoreceptor denervation since it did not occur following selective baroreceptor denervation. These different results might depend on a species difference.…”

Section: Discussioncontrasting

confidence: 99%

Hemodynamic Characteristics of Chronic Experimental Neurogenic Hypertension in Unanesthetized Dogs

Ferrario

McCubbin

Page

1969

Circulation Research

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The hemodynamic changes accompanying experimental neurogenic hypertension due to sinoaortic denervation were measured in unanesthetized dogs for 3 weeks with chronically implanted arterial catheters and aortic flow transducers. Hypertension was modest, the average increase in mean arterial pressure being 31 ± 5 (SE) mm Hg. In about half of the dogs it was due predominantly to increase in cardiac output and in the others to increase in peripheral resistance; one factor or the other tended to maintain the hypertension in each dog throughout the experiments. Arterial pressure became extremely labile during the first few days after denervation and remained so during the entire experiment. This lability was closely correlated with environmental stimuli; rather minor distractions caused a sharp fall in pressure due variably to decrease in both cardiac output and peripheral resistance; greater distractions or physical activity caused a rise in pressure due usually to increase in peripheral resistance. Mean arterial pressures were higher when measured by transcutaneous puncture of a femoral artery, presumably because of the necessity of restraint and the discomfort associated with passage of a needle. Before sinoaortic denervation, arterial pressures fell to basal levels during sleep. After denervation, unexpectedly and for an undetermined cause, pressures rose to very high levels during sleep; the rises were consistently due to increase in peripheral resistance. Awakening was accompanied by a sharp fall in pressure and peripheral resistance. ADDITIONAL KEY WORDSelectromagnetic flowmeter cardiac output peripheral vascular resistance buffer nerve section arterial hypertension electroencephalograms hypertension during sleep• The carotid sinus and aortic baroreceptor, or "buffer," reflexes are the most important neurogenic compensatory reflexes dealing with short-term shifts in arterial pressure. In 1929, Koch and Mies (1) showed that cutting these buffer nerves causes chronic arterial hypertension, and Volhard (2) first championed the view that disturbances in baroreceptor func : tion might account for essential hypertensionFrom the Research Division, The Cleveland Clinic Foundation, Cleveland, Ohio 44106.

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Section: Discussioncontrasting

confidence: 99%