Abstract-Capillary rarefaction occurs in many tissues in patients with essential hypertension and may contribute to an increased vascular resistance and impaired muscle metabolism. Rarefaction may be caused by a structural (anatomic) absence of capillaries, functional nonperfusion, or both. The aim of this study was to assess the extent of structural versus functional capillary rarefaction in the skin of subjects with essential hypertension. We examined skin capillary density with video microscopy before and during maximization of the number of perfused capillaries by venous congestion (structural capillary number) and before and during postocclusive reactive hyperemia (capillary recruitment, which may have a structural and/or functional basis). The study group was composed of 26 patients with never-treated essential hypertension and 26 normotensive control subjects. In both groups, intermittently perfused capillaries in the resting state were an important functional reserve for recruitment during postocclusive hyperemia. Recruitment of perfused capillaries during postocclusive reactive hyperemia was decreased in the hypertensive subjects compared with normotensive control subjects (47.9Ϯ6.8 versus 55.3Ϯ8.2 capillaries/mm 2 , respectively; PϽ0.01). During venous occlusion, maximal capillary density was significantly lower in the hypertensive subjects than in the control subjects (52.5Ϯ6.6 versus 57.2Ϯ8.6 capillaries/mm 2 , respectively; PϽ0.05), suggesting structural rarefaction. However, in the hypertensive subjects compared with the normotensive subjects, a smaller proportion of the maximal number of capillaries was perfused during postocclusive hyperemia (91.6Ϯ7.5% versus 97.2Ϯ2.7%, respectively; PϽ0.05), suggesting an additional functional impairment of capillary recruitment. If the difference in capillary numbers during venous congestion (Ϸ4.6 capillaries/mm 2 ) truly reflects the structural difference between the normotensive and hypertensive subjects, then, at most, 62% (4.6/7.4ϫ100%) of the difference in capillary numbers during postocclusive hyperemia (Ϸ7.4 capillaries/mm 2 ) can be explained by structural defects, and at least 38% can be explained by functional defects. In conclusion, in patients with essential hypertension, recruitment of perfused capillaries is impaired, which can be explained by both functional and structural rarefaction.

Open repair of non-ruptured JAA using suprarenal cross-clamping can be performed with acceptable perioperative mortality; however, postoperative deterioration of renal function is a common complication. Preservation of renal function after JAA repair requires further investigation.

Velocity profiles were determined in rabbit mesenteric arterioles (diameter 17-32 /xm). A good spatial resolution was obtained by using the blood platelets as small and natural markers of flow, providing for the first time in vivo detailed, quantitative information about the shape of the velocity profiles in micro vessels. In some experiments red blood cell velocity profiles were recorded as well. Easy detection of the cells of interest could be achieved by labelling them selectively with a fluorescent dye and visualizing them by intravital fluorescence video microscopy, using flashed illumination. Pairs of flashes were given with a short, preset time interval between both flashes, yielding in one TV picture two images of the same cell displaced over a certain distance for the given time interval. Velocity and mean radial position of cells, flowing within an optical section around the median plane of the vessel, were determined. The shape of the velocity profiles of platelets and red blood cells was similar. The profiles were flattened as compared to a parabola, both in systole and diastole. Vessel diameter did not change measurably during the cardiac cycle. As an index of the degree of blunting of the profiles, the ratio of the maximal and mean velocity of the profile was used, which is 2 for a parabola and 1 for complete plug flow. The index ranged from 1.39 to 1.54 (median 1.50), and increased with vessel diameter. Calculations showed that the blunting of the profiles cannot be explained by an influence of the finite depth of the optical section. (Circulation Research 1986;59:505-514) knowledge of the velocity profile in microvessels, i.e., the velocity distribution over the cross-sectional area of these vessels, is important for several reasons. First, adequate description of blood flow through small vessels requires information about the velocity gradients or shear rates in the fluid.1 Second, transport of cellular components in the blood is determined by both their distribution over the cross-sectional area of the vessel and the velocity profile. For instance, knowledge of the distribution of blood platelets in microvessels 2 and their velocity profile allows the calculation of the rate of platelet delivery in hemostatic plug or thrombus formation in these vessels. Third, to estimate volume flow in microvessels photometric methods are widely used, 3 employing an empirical factor derived from a model in which a parabolic velocity profile is assumed. However, in this approach an error will be made if in vivo the velocity profiles are more flattened.In vitro studies in glass tubes on the velocity profiles of ghost cell suspensions 5 Until now, precise measurement of velocity profiles in small blood vessels has not been performed in vivo for technical reasons. Photometric methods cannot be used to determine a profile because the system does not provide a direct measure of the red blood cell velocity in the plane of sharp focus. 34 With high-speed cinematography, displacement of red blood cells can be followe...

The distribution of blood platelets flowing in arterioles (21-35 microns) of the mesentery of anesthetized rabbits was studied using intravital fluorescence microscopy. Sites were selected without upstream branch points within at least 10 vessel diameters. The distribution was determined by counting in flashed video frames the number of platelets present in each of six equal segments across the vessel. Only platelets were counted that could be localized objectively within a thin optical section around the median plane of the vessel. It could be shown that differences in counting volume between the six segments were negligible. Because of the use of flashed pictures (flash duration less than 0.1 ms; interval 180 ms), the method is independent of differences in velocity over the cross-sectional area of the vessel. In all measurements (15 sites in 13 vessels in 10 animals) the distribution was nonuniform, the wall segments containing the highest platelet numbers. The general distribution as calculated from all measurements (total platelet number 6,571) and expressed in percentages was found to be 23.0, 14.6, 12.5, 12.1, 13.6, and 24.2.

Velocity profiles, as determined in vivo in rabbit mesenteric arterioles with fluorescently labeled platelets as natural flow markers, were used to calculate least estimates of the actual wall shear rate in these microvessels (17-32 micron diam). The fit of the velocity data points described the profile as close to the wall as 0.5 micron. To satisfy the no-slip condition, a thin layer of fluid with a steep velocity gradient near the wall was assumed. Least estimates of wall shear rate, as calculated from the fitted platelet-velocity profiles and using the mean velocity gradient in this layer of fluid, ranged from 472 to 4,712 s-1 with a median value of 1,700 s-1. Red blood cell center-line velocities varied between 1.3 and 14.4 mm/s (median 3.4). The wall shear rates were at least 1.46-3.94 (median 2.12) times higher than expected on the basis of a parabolic velocity distribution but with the same volume flow in the vessel. Considerable spatial differences in wall shear rate might exist even within a short segment of a vessel.