Serial pulsatility index measurements in renal grafts before, during, and after episodes of urinary obstruction. (49/1458)

The usefulness of pulsatility index determinations for the diagnosis of obstructive collecting system dilatation was investigated in 10 renal transplant patients whose grafts developed urinary obstruction from different causes. For this purpose we compared pulsatility index values obtained (1) before the ultrasonographic detection of obstruction or baseline study, (2) 1 day before surgical repair, and (3) within 2 weeks after surgery. In 7 of 10 obstructed grafts, the pulsatility index values were increased only mildly to moderately preoperatively. In the remaining three grafts, a mild decrease in pulsatility index was observed in spite of severe collecting system dilatation. Changes in pulsatility index were not statistically significant. Impedance measurements appeared not to be useful for diagnosing obstructive collecting system dilatation.  (+info)

Assessment of Doppler velocimetry of the fetal umbilical artery by multigate spectral Doppler scanning and traditional pulsed Doppler ultrasonography plus color flow mapping. (50/1458)

The Doppler signal of blood flow originates from the sonographic scattering from the circulating red blood cells. However, the physics of blood flow is complex as expressed by the Bernoulli equation, and the flow velocity at different positions in the laminar flow of the same vessel is variable. Using multigate spectral Doppler scanning, we recorded multiple Doppler flow signals over a segment of the umbilical artery and compared the results with traditional pulsed Doppler ultrasonography. The intraobserver variations of the pulsatility index, the resistive index, and the systolic-to-diastolic ratio were evaluated in 30 human fetuses between 29 and 42 weeks of gestation. The correlation coefficient was calculated to establish the relationship between the results of multigate spectral Doppler scanning and the traditional pulsed Doppler ultrasonographic method. The Doppler indices of these two measurements are all significantly correlated. However, since a significant difference exists between the Doppler flow measurements of multigate spectral Doppler scanning and the traditional pulsed Doppler ultrasonographic method, the range of measurement agreement for these two methods suggests that this difference should be taken into account in the interpretation of Doppler flow velocity measurements.  (+info)

Maternal ophthalmic artery doppler velocimetry in type 1 diabetes during pregnancy. (51/1458)

Our purpose was to evaluate whether maternal ophthalmic artery pulsatility index (PI) in normotensive pregnancies with type 1 diabetes is different from that in normal normotensive pregnancies. The ophthalmic artery in 15 normal normotensive pregnant women, and 13 normotensive pregnant women with type 1 diabetes was studied once with colour Doppler flow imaging and pulsed Doppler ultrasonography after 16 weeks gestation. The heart rate, mean arterial blood pressure, and ophthalmic artery PI were calculated in each group. The PI (1.94 +/- 0.45) in normotensive pregnant women with type 1 diabetes was significantly lower than that (2.73 +/- 0.32) in normal normotensive pregnant women (P < 0.0001). There was no significant difference in maternal heart rate or mean arterial blood pressure between the two groups. These results suggest that vascular resistance in the maternal orbital circulation is reduced in pregnancies with type 1 diabetes that are normotensive. The lower PI in pregnant women with type 1 diabetes should be interpreted as orbital vascular vasodilatation, indicating orbital hyperperfusion or hyperaemia.  (+info)

Abdominal aortic aneurysm wall mechanics and their relation to risk of rupture. (52/1458)

PURPOSE: to see whether aneurysmal aortic wall mechanics can be used as a predictor of abdominal aortic aneurysm (AAA) rupture. METHOD: among 285 individuals, followed conservatively for AAA and monitored for aneurysm growth and wall mechanics on at least one occasion at our institution between January 1991 and January 1998, eleven subsequently ruptured. Wall mechanics were estimated as stiffness (beta). This was calculated from diameter and pulsatile diameter change, determined non-invasively by an ultrasonic echo-tracking system and blood pressure obtained by the auscultatory method. The results were compared with those of 121 individuals electively operated on for AAA. RESULTS: no difference in aortic stiffness was found between those that subsequently ruptured (beta=35, median) compared to those non-ruptured (beta=38, median) AAAs (p=0.855). There was no difference in diameter in ruptured (58.8 mm) compared with non-ruptured (54.1 mm) AAAs (p=0.129). All ruptured AAAs showed an expansion of diameter over time. CONCLUSION: this study shows no difference in aneurysmal aortic wall mechanics in those AAAs that subsequently ruptured compared with electively operated AAAs. The results indicate that it is not possible to use aneurysmal aortic wall stiffness as a predictor of rupture.  (+info)

Isolation of endothelial cells and their progenitor cells from human peripheral blood. (53/1458)

PURPOSE: We have developed techniques to isolate endothelial cell (EC) progenitors from human peripheral and umbilical cord blood. METHODS: Human adult peripheral and umbilical cord blood monocytes were isolated by centrifugation, and progenitor cells were separated with the use of magnetic polystyrene beads that were coated with a monoclonal antibody specific for the CD34 cell-membrane antigen. Cells were propagated in selective media, and developing cultures were immunostained for CD31, CD34, factor VIII, and vascular endothelial growth factor cell receptors. ECs that developed were transfected with a gene for prourokinase and used to line ePTFE grafts, which were evaluated in vitro in a pulsatile flow system. RESULTS: Umbilical cord monocyte cultures demonstrated colonies that resembled ECs at approximately 2 weeks, with growth being best supported by EC growth media plus 20% calf serum with iron. Immunostaining of colonies was positive for CD31 and factor VIII. After 18 days in culture, CD34(+) cells from adult peripheral blood were noted, which had the typical cobblestone appearance of ECs and immunostained positively for CD31 and factor VIII-related antigens. Cultures of umbilical cord-derived cells and adult peripheral blood-derived cells developed complex line formations within 1 week in culture that stained positively for vascular endothelial growth factor receptor-2. Urokinase-transfected ECs were shown to overexpress urokinase. Prosthetic grafts lined with transfected cells showed 87.33% +/- 4.97% cell adherence after 2 hours in a pulsatile flow system at clinically relevant shear stress. CONCLUSION: We conclude that endothelial progenitor cells can be isolated from human adult peripheral and umbilical cord blood and developed into EC cultures as a source of cells for vascular graft seeding and gene therapy.  (+info)

Concordant induction of rapid in vivo pulsatile insulin secretion by recurrent punctuated glucose infusions. (54/1458)

Insulin is largely secreted as serial secretory bursts superimposed on basal release, insulin secretion is regulated through changes of pulse mass and frequency, and the insulin release pattern affects insulin action. Coordinate insulin release is preserved in the isolated perfused pancreas, suggesting intrapancreatic coordination. However, occurrence of glucose concentration oscillations may influence the process in vivo, as it does for ultradian oscillations. To determine if rapid pulsatile insulin release may be induced by minimal glucose infusions and to define the necessary glucose quantity, we studied six healthy individuals during brief repetitive glucose infusions of 6 and 2 mg x kg(-1) x min(-1) for 1 min every 10 min. The higher dose completely synchronized pulsatile insulin release at modest plasma glucose changes ( approximately 0.3 mM = approximately 5%), with large ( approximately 100%) amplitude insulin pulses at every single glucose induction (n = 54) at a lag time of 2 min (P < 0.05), compared with small (10%) and rare (n = 3) uninduced insulin excursions. The smaller glucose dose induced insulin pulses at lower significance levels and with considerable breakthrough insulin release. Periodicity shift from either 7- to 12-min or from 12- to 7-min intervals between consecutive glucose (6 mg x kg(-1) x min(-1)) infusions in six volunteers revealed rapid frequency changes. The orderliness of insulin release as estimated by approximate entropy (1.459 +/- 0.009 vs. 1.549 +/- 0.027, P = 0.016) was significantly improved by glucose pulse induction (n = 6; 6 mg x kg(-1) x min(-1)) compared with unstimulated insulin profiles (n = 7). We conclude that rapid in vivo oscillations in glucose may be an important regulator of pulsatile insulin secretion in humans and that the use of an intermittent pulsed glucose induction to evoke defined and recurrent insulin secretory signals may be a useful tool to unveil more subtle defects in beta-cell glucose sensitivity.  (+info)

Heritability of central systolic pressure augmentation: a twin study. (55/1458)

Less than 50% of the variance in left ventricular mass is explained by conventional factors such as age, blood pressure, and body size. Genetic influences may account for part of the unexplained variance. The central (aortic) pressure augmentation index has been suggested as a noninvasive measure of pulsatile load, which is a likely determinant of left ventricular mass. We quantified the genetic influence on augmentation index and determined the extent to which this influence is dependent on the effects of age, height, heart rate, and blood pressure. We performed a classical twin study composed of 225 monozygotic and 594 dizygotic female white twin pairs aged 18 to 73 years. Augmentation index and mean arterial pressure were based on the central pressure wave derived from the radial waveform as measured by applanation tonometry. Quantitative genetic modeling techniques were used to analyze the data. The heritability of augmentation index was 37%, whereas heritabilities for blood pressure traits varied between 13% and 25%. Most of the variance in augmentation index could be explained by genetic and environmental factors specifically influencing augmentation index. Only a relatively small part of the total variance in augmentation index could be attributed to genes in common with height (3.1%), heart rate (4.6%), and mean arterial pressure (5.6%). Age explained 19% of the total variation in augmentation index. In conclusion, augmentation index has a significant heritable component, which is largely independent of the influence of blood pressure, heart rate, height, and age. Finding genes for the augmentation index could help to unravel pathophysiological mechanisms causing left ventricular hypertrophy and lead to improvements in prevention, diagnosis, and treatment of at-risk populations.  (+info)

Altered flow-induced arterial remodeling in vimentin-deficient mice. (56/1458)

The endothelial cytoskeleton plays a key role in arterial responses to acute changes in shear stress. We evaluated whether the intermediate filament protein vimentin is involved in the structural responses of arteries to chronic changes in blood flow (BF). In wild-type mice (V+/+) and in vimentin-deficient mice (V-/-), the left common carotid artery (LCA) was ligated near its bifurcation, and 4 weeks later, the structures of the occluded and of the contralateral arteries were evaluated and compared with the structures of arteries from sham-operated mice. Body weight and mean carotid artery BF did not differ between the strains, but LCA and right carotid artery (RCA) diameter (737+/-14 microm [LCA] and 723+/-14 microm [RCA] for V-/- versus 808+/-20 microm [LCA] and 796+/-20 microm [RCA] for V+/+) and medial cross-sectional area (CSAm) were significantly smaller in V-/- (21+/-1 and 22+/-2 x 10(3) microm(2) for LCA and RCA, respectively) than in V+/+ (28+/-2 and 28+/-3 x 10(3) microm(2) for LCA and RCA, respectively). In V+/+, LCA ligation eliminated BF in the occluded vessel (before ligation, 0. 35+/-0.02 mL/min) and increased BF from 0.34+/-0.02 to 0.68+/-0.04 mL/min in the RCA. In V-/-, the BF change in the occluded LCA was comparable (from 0.38+/-0.05 mL/min to zero-flow rates), but the BF increase in the RCA was less pronounced (from 0.33+/-0.02 to 0. 50+/-0.05 mL/min). In the occluded LCA of V+/+, arterial diameter was markedly reduced (-162 microm), and CSAm was significantly increased (5 x 10(3) microm(2)), whereas in the high-flow RCA of V+/+, carotid artery diameter and CSAm were not significantly modified. In the occluded LCA of V-/-, arterial diameter was reduced to a lesser extent (-77 microm) and CSAm was increased to a larger extent (10 x 10(3) microm(2)) than in V+/+. In contrast to V+/+, the high-flow RCA of V-/- displayed a significant increase in diameter (52 microm) and a significant increase in CSAm (5 x 10(3) microm(2)). These observations provide the first direct evidence for a role of the cytoskeleton in flow-induced arterial remodeling. Furthermore, they dissociate (1) between acute and chronic arterial responses to altered BF, (2) between alterations of lumen diameter and wall mass during arterial remodeling, and (3) between developmental and imposed flow-induced arterial remodeling.  (+info)