Key result
Carotid compression delays opacity pulse propagation more in the external carotid bed than the brain.
Why the study?
Differences in opacity pulse propagation times and responses to carotid compression between internal and external carotid arterial beds were not well characterized in experimental animals.
Does compression of the common carotid artery alter opacity pulse propagation times in the internal and external carotid vascular beds of experimental animals?
Does compression of the common carotid artery alter opacity pulse propagation times in the internal and external carotid vascular beds of experimental animals?
Carotid compression prolongs opacity pulse propagation times more markedly in the external compared to the internal carotid bed in experimental animals, suggesting differences in vascular wall properties or collateral circulation.
Animal findings on differential carotid pulse propagation should not alter clinical practice; leaves open vascular bed-specific hemodynamics for targeted investigation.
Opacity pulses and opacity pulse propagation times were recorded from the external carotid arterial bed (ear) and from the ipsilateral internal carotid arterial bed of the pial-cortical surface within the closed skull of conscious monkeys and anesthetized cats during the resting state and during carotid compression. Propagation of opacity pulses to the ear precedes those to the ipsilateral brain by 10 to 100 msec. Mean values of all pulse propagation time measurements to both brain and ear during successive cardiac cycles are stable from one minute to the next in the resting state. With compression of the common carotid artery, pulse propagation time to both beds is prolonged for the duration of compression, returning promptly to precompression levels with release of the artery, but the degree of prolongation is more marked in the external carotid bed. It is suggested that the consistent differences observed in both species between opacity pulses and pulse propagation times in the two beds, as well as the difference in responses to carotid compression, may result from inherent differences in properties of the vascular wall in the beds concerned, and/or from differences in collateral circulatory pathways subserving these beds during carotid artery obstruction.
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Albert F. Heck (1970) studied this question. Carotid compression vs. Resting state was evaluated on Opacity pulse propagation time. Propagation of opacity pulses to the ear precedes those to the ipsilateral brain by 10 to 100 msec, and carotid compression prolongs propagation time more markedly in the external carotid bed.