PubMed · 7189338
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D E Lees, W Schuette. 1980. Microwave rewarming.. https://doi.org/10.1213/00000539-198002000-00016
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Platelet aggregation contributes to arresting bleeding at wound sites, but may cause occlusion of atherosclerotic vessels, thus curtailing blood flow to vital organs. According to current dogma, the integrin alphaIIbbeta3 plays an exclusive role in linking platelets to one another through interactions with fibrinogen or vWf. We demonstrate here that, depending on shearing flow conditions, this process may require vWf binding to glycoprotein Ibalpha, even when alphaIIbbeta3 is competent to bind adhesive ligands. Platelet activation induced solely by high shear stress is initiated by glycoprotein Ibalpha interaction with vWf, but results in aggregation only if the latter can bind concurrently to alphaIIbbeta3. In contrast, platelets exposed to high shear rate after activation by exogenous agonists such as ADP and epinephrine can aggregate when fibrinogen is the alphaIIbbeta3 adhesive ligand, yet only if vWf binding to glycoprotein Ibalpha can also occur. Thus, the latter interaction appears to provide a bond with biomechanical properties necessary to overcome the effects of high shear rate and initiate interplatelet cohesion. These findings highlight the distinct function of two adhesive receptors mediating platelet aggregation under varying fluid dynamic conditions, and modify the current interpretation of a crucial event in hemostasis and thrombosis.
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PURPOSE: To investigate whether lower blood flow velocities and higher resistive indices in the retrobulbar arteries are associated with progression of visual field defects in eyes with open-angle glaucoma with or without increased intraocular pressure. METHODS: Color Doppler imaging was performed in 16 eyes with progressive visual field defects in patients with normal-tension glaucoma, 15 eyes with practically stable visual field defects in patients with normal-tension glaucoma, 14 eyes with progressive visual field defects in glaucomatous patients with increased intraocular pressure, and 14 eyes with practically stable visual field defects in glaucomatous patients with increased intraocular pressure. Peak systolic velocity and end-diastolic velocity were measured, and resistive index was calculated in the central retinal artery, short posterior ciliary arteries, and the ophthalmic artery. RESULTS: Eyes with progressive visual field defects in patients with normal-tension glaucoma had statistically significantly lower blood flow velocities and higher resistive index in the central retinal artery and the short posterior ciliary arteries than did those with practically stable visual field defects, whereas, in the glaucomatous patients with increased intraocular pressure, such differences were not found. CONCLUSIONS: Eyes of patients with normal-tension glaucoma and progressive visual field defects have decreased blood flow velocities and increased resistive indices in their retrobulbar arteries, suggesting that these circulatory factors may be associated with the deterioration of visual field defects in patients with normal-tension glaucoma but may be less involved in the deterioration in glaucomatous patients with increased intraocular pressure.