Neointimal hyperplasia influenced by intravascular hemodynamics is considered partly responsible for restenosis after endovascular stenting. To evaluate the effect of stent configuration on fluid flow behavior, we visualized flow near stents, and measured the proliferation of cultured endothelial cells (ECs). A single-coil stent (coil pitch, CP = 2.5, 5, or 10 mm) was inserted into a glass tube and per-fused at 30-90 mL/min, while the flow pattern was determined by particle imaging velocimetry. The reduction of the flow velocity near the wall was correlated with the decrease in the coil interval of the stent. In perfusion cultures with stents, the proliferation of ECs was influenced by the local flow velocity distribution. When a stent with a CP value of 10mm was used, the doubling time of ECs was 30.7 h, while the doubling time was 38.5 h when the CP was 5mm. The doubling time of ECs was shorter at sites upstream of the stent wire where the velocity was higher than downstream of the wire. In conclusion, a single-coil stent can be used to modify hemodynamic factors, suggesting that improved stent design may facilitate rapid endothelialization after stent implantation.

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We investigated the effect of exogenous nitric oxide (NO) on the flow-induced endothelium-derived NO production and possible underlying mechanisms including changes in intracellular concentration of tetrahydrobiopterin (BH₄; a cofactor of NO synthase: NOS). Isolated canine femoral arteries were perfused with 100 μM S-nitroso-N-acetylpenicillamine (SNAP; an NO donor) and/or 64 μM BH₄. Perfusion of SNAP suppressed flow-induced NO production (p<0.02 vs control; n=7). Subsequent BH₄ perfusion restored the control-level NO production. Concomitant perfusion of SNAP and BH₄ retained the control-level NO production. Concomitant perfusion of SNAP and 4,5- dihydroxy-1,3-benzene disulfonic acid (Tiron; 1 mM; a membrane-permeable superoxide scavenger) also retained the control-level NO production, while perfusion of Tiron after SNAP could not restore the control-level NO production (p<0.02 vs control; n=7). We also found a significant decrease in BH₄ concentration in the endothelial cells after SNAP perfusion. In conclusion, these results indicate that exogenous NO decreases intracellular BH₄ concentration, resulting in superox-ide release from uncoupled NOS and suppresses the flow-induced endothelium-derived NO produc-tion.

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We examined the effects of short-term heavy and light exercise on coagulation activity to clarify the relationship between myocardial ischemia or sudden cardiac death and exercise. Nine healthy sedentary male volunteers performed 10 minutes of heavy (over 95% of maximum oxygen consumption) or light (60% to 65% of maximum oxygen consumption) exercise. Blood samples were obtained, blood pressure was measured and the participants were weighed before, immediately after, and 1 hour after exercise. Coagulation activity was determined by measuring rates of changes in blood viscosity using an oscillation-type viscometer without addition of anticoagulants.Hematocrit and systolic blood pressure were significantly and similarly higher immediately after heavy or light exercise. Coagulation activity increased immediately after exercise and returned to the baseline one hour later, but the magnitude of the increase was higher immediately after heavy, than after light exercise.
We concluded that general practitioners have to care for the rehabilitation training, especially in the acute heavy exercise, of the patients with atherosclerotic diseases.

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