Although there is considerable evidence to suggest that hemodynamics play an important role in vascular disease processes, the exact mechanisms are unknown. With this in mind, we have designed a pulsatile perfusion apparatus which reproducibly delivers pulsatile hemodynamics upon freshly excised canine carotid arteries in vitro. Quantifiable simulations included normotension with normal or lowered flow rates (120/80 mmHg, 120 and 40 ml/min), normotension with lowered or elevated transmural pressures (40-170 mmHg), and elevated pulse pressure (120 and 80 mmHg) with normal (150 ml/min) or elevated rates of flow (300 and 270 ml/min). Arterial biomechanical stresses and cellular behaviors were characterized biochemically and morphologically under all these stimulations which continued for 2-24 h. We found that increased pulse pressure alone had little effect on the total amount of radiolabeled [4-14C]cholesterol present within the medial compartment. However, normotension when coupled with altered transmural pressure yielded a three- to fourfold increase. Combinations of increased pulse pressure and flow potentiated cholesterol uptake by a factor of 10 when compared with normotension control values. Simulations that enhanced carotid arterial cholesterol uptake also influenced the endothelial cytoskeletal array of actin. Stress fibers were not present within the carotid endothelial cells of either the sham controls or the normotension and increased pulse pressure (normal flow) simulations. Endothelial cells lining carotids exposed to elevations in flow or those present within vessels perfused as per simulation b above assembled stress fibers (x = 4 and 10 per cell, respectively) within the time course of these studies. When endothelial cells were subjected to hemodynamic conditions that potentiated maximally cholesterol transport, no diffuse or stress fiber staining could be seen, but the cortical array of actin was intact. These results suggest that those biomechanical stresses that alter endothelial permeability and intimal integrity may do so via cytoskeletal actin signaling.

https://rupress.org/jcb/article-pdf/105/1/291/1055324/291.pdf

Hemodynamics and the vascular endothelial cytoskeleton.

To study arterial dilatation in response to increased flow, we observed the bilateral common carotid arteries (CCAs) of 10 16-week-old rats that were maintained for 8 weeks after construction of an arteriovenous (AV) fistula between the left CCA and the jugular vein at a level 20 mm distal from the aortic orifice. The flow in the left CCA increased 11-fold and that of the right CCA increased twofold compared with values before surgery. The left CCA showed complete desquamation of endothelial cells in the distal one third of the segment proximal to the AV fistula. In the left CCA the endothelium-preserved area dilated significantly (the luminal radius was 1.34 times larger than control; p less than 0.001, n = 4) with a significant increase of the cross-sectional area of the media (p less than 0.01, n = 4) and showed high wall shear stress (70 +/- 11 dynes/cm2 near the aortic orifice). In contrast, the endothelial cell-desquamated area did not dilate but did show very high wall shear stress (231 +/- 23 dynes/cm2) without any intimal smooth muscle cell proliferation. The right CCA dilated significantly (luminal radius was 1.07 times larger than control; p less than 0.001, n = 4) with a wall shear stress of 30 dynes/cm2 near the brachiocephalic orifice. All CCAs retained their fundamental arterial structure. We conclude that in the rat CCA, arterial dilatation in response to increased flow is a gradual remodeling process related to the presence of endothelial cells that have been influenced by the level of flow increase.

Difference in dilatation between endothelium-preserved and -desquamated segments in the flow-loaded rat common carotid artery.

Differential response of arteries and vein grafts to blood flow reduction.

Endothelial cells are stable and quiet in normal animals. They arrange regularly and have a smooth lumen surface and thin endothelial wall. According to Thoma's principle (1893) and Kamiya and Togawa's principle (1980) on the relationship of the vascular diameter to flow alteration, blood flow is in equilibrium to the diameter and in a physiological state. That is to say, there is no fast flow or slow flow. To understand the nature of the endothelial cells, we should investigate endothelial cells under flow alteration to break the equilibrium state. Endothelial cells under increased flow were studied in arteries with an arteriovenous fistula or in the capillaries of myocardium with volume-overloaded hearts or of the skeletal muscle by electrical stimulation. Those under decreased flow were studied by the closure of the fistula or by ceasing the stimulation. Endothelial cells in the coarctation of the arteries were also observed. Endothelial cells were activated by increased flow in the arteries and capillaries, while they were inactivated by decreased flow. Endothelial activation is characterized as lumen protrusions, increase of cytoplasmic or- ganelles, abluminal protrusions, basement membrane degradation, internal elastic lamina degra- dation in the arteries, and sproutings in the capillaries. These are ultrastructurally comparable to angiogenesis. Endothelial inactivation is characterized by the decrease of endothelial cell number with apoptosis, which is ultrastructurally comparable to angioregression. We assume that endo- thelial cells respond to increased flow by angiogenesis and to decreased flow by angioregression. Microsc. Res. Tech. 60:2-12, 2003. © 2003 Wiley-Liss, Inc.

Ultrastructure of endothelial cells under flow alteration.

To observe cytoplasmic microfilaments in the endothelial cells of flow-loaded arteries, an arteriovenous shunt was constructed between the common carotid artery and the external jugular vein in 26 dogs. After measuring the flow rates of the arteries, the endothelial layer was examined ultrastructurally with a transmission electron microscope at three different times: 1 week (acute experiments), 2–4 weeks (subacute experiments), and 4–7 months (chronic experiments).

Cytoplasmic microfilaments in endothelial cells of flow loaded canine carotid arteries.

Ultrastructural changes in the endothelial surface of the canine carotid artery induced by wall shear stress load.

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Ultrastructural changes in the endothelial surface of the canine carotid artery induced by wall shear stress load.