Key result
Acute high shear stress does not cause gross endothelial injury or promote platelet adhesion.
Acute exposure to high shear stress does not cause gross endothelial injury or denudation in dog aorta samples in vitro, suggesting shear stress alone may not directly denude endothelium in atherogenesis.
Acute high shear spares dog aortic endothelium in vitro; leaves open its role in human atherogenesis.
Shear-induced injury or denudation of arterial endothelium has been implicated in atherogenesis. This study reports on an in vitro technique for imposing high, controlled shear stresses on endothelium. Samples of dog aorta were mounted in a chamber so that the endothelium was 1 mm +/- 0.03 mm from a rotating disc. The chamber was filled with a high viscosity solution (10% polyvinyl pyrrolidone in Tyrode's solution, viscosity = 1.97 +/- .07 Poise) which was sheared over the endothelium by the disc. A servo amplifier drove the motor that rotated the disc, so that motor RPM (therefore shear stress) could be made to follow either steady or pulsatile signals played into the amplifier. Acute (10 min-1 hr) exposure to steady shear stresses of up to 2000 dyne/cm2 did not cause gross endothelial injury or denudation. Exposure of endothelium to pulsatile shear stresses that followed a tape recording of physiological flow waveforms (electromagnetic flowmeter) did not cause gross injury or denudation even when peak shear exceeded 1500 dyne/cm2. Furthermore exposure to high shear stress did not degrade the nonthrombogenic nature of the endothelium because subsequent platelet adhesion was poorly and negatively correlated with shear stress.
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B. Lowell Langille (1984) studied this question. High shear stress was evaluated on Gross endothelial injury, denudation, and platelet adhesion. Acute exposure of dog aorta endothelium to steady or pulsatile high shear stresses up to 2000 dyne/cm2 did not cause gross endothelial injury, denudation, or degrade its nonthrombogenic nature.
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