Flow Decrease (flow + decrease)

Distribution by Scientific Domains


Selected Abstracts


Effects of diffuse fatty infiltration of the liver on portal vein flow hemodynamics

JOURNAL OF CLINICAL ULTRASOUND, Issue 3 2008
Ali Balci MD
Abstract Purpose To investigate the effects of various degrees of diffuse fatty infiltration of the liver on portal vein blood flow with Doppler sonography. Methods One hundred forty subjects were examined with color and spectral Doppler sonography. The subjects were divided into 4 groups of 35 subjects each according to the degree (normal, grade 1, grade 2 and grade 3) of hepatic fatty infiltration assessed on gray-scale images. The portal vein pulsatility index (VPI) and time-averaged mean flow velocity (MFV) were calculated for each subject. VPI was calculated as (peak maximum velocity , peak minimum velocity) / peak maximum velocity. Results VPI and MFV values were, respectively, 0.32 ± 0.06 and 16.8 ± 2.6 cm/second in the normal group, 0.27 ± 0.07 and 14.2 ± 2.2 cm/second in the group with grade 1 fatty infiltration, 0.22 ± 0.06 and 12.2 ± 1.8 cm/second in the group with grade 2 fatty infiltration, and 0.18 ± 0.04 and 10.8 ± 1.5 cm/second in the group with grade 3 fatty infiltration. There was a negative inverse correlation between the grade of fatty infiltration and both VPI (f = 55.3, p < 0.001) and MFV (f = 43.9, p < 0.001). Conclusion The pulsatility index and mean velocity of the portal vein blood flow decrease as the severity of fatty infiltration increases. © 2008 Wiley Periodicals, Inc. J Clin Ultrasound, 2008. [source]


Age-related macular degeneration: hemodynamic changes

ACTA OPHTHALMOLOGICA, Issue 2009
CJ POURNARAS
Purpose Metabolic changes of the RPE associated to the dysfunction of choriocapillaries(CC)/RPE complex may induces the AMD-related changes. Additional vascular changes in the choroid potentially have deleterious effects on the RPE. Methods Quantification of CC number and lumen diameters in cross sections and alkaline phosphatase (APase) flat-embedding technique, expressing high constitutive APase activity in choriocapillaris and choroidal veins on human RPE/Bruch's Membrane/CC complex, significantly contributed to the analysis of the choroidal vasculature. Laser Doppler flowmetry (LDF) data provided additional information on the assessment of hemodynamic changes in AMD. Results Choroidal vascular density reduction and significant vasoconstriction of the choriocapillaries, occurs during the evolution of AMD. In eyes with geographic atrophy, the RPE degenerates first while CC loss is secondary to RPE degeneration. In eyes with exudative AMD, degeneration of the CC layer occurs while RPE is still functional. LDF data indicated choroidal blood flow decrease according to age and the degree of severity of AMD; the decrease in flow preceding the formation of choroidal CNV, strongly suggest that these changes may have a role in the development of CNV. As a result of vascular dysfunction, the choroidal blood flow is dysregulated in patients with neovascular AMD. The choroidal watershed zone (WZ) courses through the fovea more often in patients suffering from AMD than in age-matched controls, particularly in the presence of CNV. Choroidal neovascularisation usually arises within these WZ. Conclusion The role of choroidal ischemia in the pathophysiology of AMD is supported by the observed choroidal microcirculation anatomical and fucntional abnormalities. [source]


Patency and Flow of the Internal Jugular Vein After Functional Neck Dissection,

THE LARYNGOSCOPE, Issue 1 2000
Marķa P. Prim MD
Abstract Objectives: To assess the patency and flow of the internal jugular vein after functional neck dissection. Study Design: Prospective study of 54 internal jugular veins in 29 oncologic patients undergoing functional neck dissection between September 1994 and February 1997. Methods: Patency, presence of thrombosis, characteristics of the vein wall, compressibility, area of the vein both in rest and during Valsalva maneuver, expiratory flow speed, Valsalva flow speed, jugular flow in each side, and total jugular flow were assessed in all veins before and after dissection. All patients were evaluated before and after the procedure by means of duplex Doppler ultrasonography. Results: In no case was there thrombosis before or after the operation. Although total jugular flow decreases during the early postoperative period, it recovers to normal parameters within 3 months after surgery. Conclusions: According to these results, the patency of the internal jugular vein remains unaltered after functional neck dissection. Ultrasonographically there is no thrombosis after this procedure. [source]


Heel skin hyperaemia: direct compression versus vascular occlusion

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2003
Harvey N. Mayrovitz
Summary Vulnerability of the heel to ulceration in bed-bound persons is related to direct pressure-induced blood flow decreases. Periodic pressure reduction is a clinical strategy to help prevent ulcers by allowing flow-repayment hyperaemia that has a magnitude and duration thought to be related to the duration of the prior interval of ischaemia. However, there are reasons to question whether effects of flow stoppages caused by direct tissue loading are similar to those because of ischaemia without superimposed direct pressure. This question was investigated by comparing posterior heel skin blood flow responses via laser-Doppler perfusion monitoring of 27 supine-lying subjects in whom blood flow was reduced by 5-min of direct heel loading on a support surface and by 5-min of ankle-cuff compression. Results showed that blood flow reductions were the same for both methods but the hyperaemia was significantly greater when flow reduction was produced by direct heel loading. This was true for ratio of peak hyperaemic flow to baseline (8·20 ± 1·32 s versus 4·68 ± 0·80 s, P,0·001), hyperaemic to baseline 3-min flow-time area ratios (4·70 ± 0·65 s versus 1·95 ± 0·29 s, P,0·001) and for total hyperaemia durations (352 ± 39 s versus 181 ± 14 s, P<0·001). These findings raise new questions regarding the precise physiological effects of heel and tissue loading in general, the factors that contribute to the hyperaemic response and their clinical impact and interpretation. Possible sources of the observed greater post-loading hyperaemia responses are discussed. [source]