Showing papers by "Giuseppe Mancia published in 1969"

Neural and non-neural mechanisms influencing circulation during sleep.

Abstract: IN the past few years there has been increasing interest in cardiovascular changes during sleep, on the assumption that they might provide some insight into the neural control of circulation in a natural condition. The hypothesis that all cardiovascular events that occur during sleep are neurally mediated has never been crucially proved, however. Furthermore, sleep is accompanied by various haemodynamic phenomena which may well have different mechanisms. In the cat the greatest cardiovascular changes occur during desynchronized sleep (DS)1,2, a stage of sleep characterized by a desynchronized electroencephalogram and bursts of rapid eye movements, and in man associated with dreaming. We have shown recently that the arterial hypotension occurring during DS is dependent chiefly on a decreased peripheral resistance, change in cardiac output being small3. This is particularly true for animals subjected to sino-aortic deafferentation3, whose hypotension during DS is greatly exaggerated because of the removal of a buffer action exerted by arterial chemoceptors4. But in the few DS episodes during which hypotension is so profound as to cause electroencephalographic signs of cerebral anoxia (a phenomenon observed in deafferented animals only), the very large decrease in arterial pressure seems to be exclusively a consequence of a dramatic fall in cardiac output3. It has been suggested3, though not demonstrated, that the decrease in peripheral resistance might result from a reduction of sympathetic vasoconstrictor activity. The decrease in cardiac output, which is independent of cardiac innervation3,5, may also be a consequence of a reduction of sympathetic activity resulting in a dilatation of capacitance vessels and a decreased venous return, although non-neural mechanisms may well be involved.

Hemodynamic Patterns during Desynchronized Sleep in Intact Cats and in Cats with Sinoaortic Deafferentation

Abstract: In unanesthetized, unrestrained cats, placed in a sound-attenuated cage, stroke volume and cardiac output were continuously monitored by an electromagnetic flow transducer chronically implanted around the ascending aorta, arterial pressure was measured by means of a femoral catheter connected to a strain-gauge transducer, and heart rate by a cardiotachograph. Total resistance was computed by dividing arterial pressure by cardiac output. Electroencephalograms, cervical electromyogram, and ocular movements were also monitored to obtain evidence of naturally occurring sleep. In animals with intact sinoaortic reflexes the fall in arterial pressure occurring during desynchronized sleep was associated with a small decrease in cardiac output and a relatively greater reduction in total resistance. After sinoaortic deafferentation, the conspicuously exaggerated fall in arterial pressure occurring during the same type of sleep was almost entirely due to a parallel exaggeration of the reduction in total resistance; changes in cardiac output were only slightly greater than before deafferentation. Only in the few episodes of desynchronized sleep in which extreme hypotension was accompanied by signs of cerebral anoxia, did cardiac output greatly decrease; in these cases, calculated resistance was found to increase. Both small and large changes in cardiac output were independent of heart innervation.

Regional blood flows during desynchronized sleep in the cat.

Abstract: Durante il sonno desincronizzato del gatto, non si ha una vasodilatazione generalizzata a tutti i letti vascolari. Mentre il distretto mesenterico si dilata, quello muscolare si costringe. La vasodilatazione viscrale dipende da una diminuita attivita simpatica; per la vasocostrizione muscolare, invece, bisogna pensare, oltre che a meccanismi nervosi, anche a fattori meccanici e metabolici.