September 30, 2009; doi:10.1152 doi:10. /ajpregu.00551.2009 show that the vestibular system contributes to blood pressure regulation. Prior studies reported that lesions that eliminate inputs from the inner ears attenuate the vasoconstriction that ordinarily occurs in the hindlimbs of conscious cats during head-up rotations. These data led to the hypothesis that labyrinthine-deficient animals would experience considerable lower body blood pooling during head-up postural alterations. The present study tested this hypothesis by comparing blood flow though the femoral artery and vein of conscious cats during 20 -60°head-up tilts from the prone position before and after removal of vestibular inputs. In vestibular-intact animals, venous return from the hindlimb dropped considerably at the onset of head-up tilts and, at 5 s after the initiation of 60°rotations, was 66% lower than when the animals were prone. However, after the animals were maintained in the head-up position for another 15 s, venous return was just 33% lower than before the tilt commenced. At the same time point, arterial inflow to the limb had decreased 32% from baseline, such that the decrease in blood flow out of the limb due to the force of gravity was precisely matched by a reduction in blood reaching the limb. After vestibular lesions, the decline in femoral artery blood flow that ordinarily occurs during head-up tilts was attenuated, such that more blood flowed into the leg. Contrary to expectations, in most animals, venous return was facilitated, such that no more blood accumulated in the hindlimb than when labyrinthine signals were present. These data show that peripheral blood pooling is unlikely to account for the fluctuations in blood pressure that can occur during postural changes of animals lacking inputs from the inner ear. Instead, alterations in total peripheral resistance following vestibular dysfunction could affect the regulation of blood pressure.blood flow patterning; venous return; cardiac output; orthostatic hypotension HEAD-UP BODY ROTATIONS in humans or animals typically result in some pooling of blood in the periphery and a resulting reduction in return of blood to the heart. Because cardiac output is directly related to cardiac preload (Starling's law of the heart) (27), cardiac output tends to decrease during head-up movements (25). Furthermore, cardiac output and peripheral vascular resistance determine systemic blood pressure, such that the sympathetic nervous system must produce a rapid net increase in peripheral resistance by inducing vasoconstriction at the onset of head-up body rotations to maintain stable blood pressure (7). Arterial baroreceptor mechanisms play an important role in regulating peripheral vasoconstriction during postural alterations (23). In addition, there is considerable evidence from studies in animals (6,8,10,11,21,22,32) and humans (1,4,12,23,26,28,30) that the vestibular system also participates in triggering increases in vasomotor activity during movements that promote peripheral blood pooling...
It is routinely assumed that the force of gravity can cause blood pooling in the dependent limbs, as venous return from the body region is reduced. However, the effects of postural alterations on blood flow to and from the limbs have not been directly compared or quantified. In the present study, blood flow in the femoral artery and vein of conscious cats were measured using transit‐time ultrasound technology as the animals were rotated head‐up by amplitudes up to 60°. 60° head‐up rotations produced significant (ANOVA, p<0.05) decreases in venous blood flow beginning ≈3 sec following tilt onset, which became maximal at ≈5 sec, with an alteration of 55‐65% from pre‐tilt values. As the animals were maintained head‐up, venous blood flow began to increase, and was 18‐29% lower than pre‐tilt values by 40 sec following rotation initiation. This recovery of venous flow was accompanied by a 17‐34% decrease in arterial blood flow that peaked ≈9 sec after tilt onset. These data confirm that venous return from the dependent limb is greatly attenuated during postural alterations, and the magnitude may be larger than expected. However, the largest perturbation in venous return is transient, and this combined with accompanying decreases in arterial blood flow limits peripheral pooling.
Prior studies showed that vestibular signals influence cardiovascular regulation by eliciting vasoconstriction in the dependent limbs during postural changes. These findings led to the hypothesis that loss of vestibular inputs would exacerbate blood pooling in the body regions below the heart during alterations of body position. We tested this hypothesis by comparing blood flow measured using transit‐time ultrasound technology from the femoral vein and artery in conscious cats subjected to head‐up tilt (HUT) at amplitudes up to 60°. Responses were recorded before and after bilateral ablation of vestibular afferents. Before vestibular lesions, blood flow decreased 24‐35% in the femoral artery by ≈9 sec following 60° HUT, presumably due to vasoconstriction, while venous blood flow decreased 55‐65%. After lesions, arterial blood flow dropped only 0‐14% at the time maximal vasoconstriction previously occurred, while venous blood flow decreased 57‐87%. The alterations were shown to be significant by ANOVA (P<0.05). Because vestibular lesions resulted in more blood flow to the leg in the femoral artery and less venous return in the femoral vein, we concluded that the lesions resulted in hindlimb blood pooling during HUT.
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