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Methods in Enzymology 02/2001; 335:369-80. · 2.04 Impact Factor
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ABSTRACT: Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) was employed to characterize the polygalloyl polyflavan-3-ols (PGPF) in grape seed extracts. Masses corresponding to a series of PGPF units inclusive of nonamers were observed in the positive-ion reflectron mode. Masses of PGPF inclusive of undecamers were observed in the positive-ion linear mode, providing the first known evidence of PGPF of this size. Soluble PGPF of grape seed extracts were precipitated by complexation with Yb(3+). The PGPF were then recovered by dissolving the precipitate in water and removing the Yb(3+) by a weakly acidic cation-exchange resin (Amberlite IRP-64). Comparisons of HPLC chromatograms of the crude grape seed extract prior to precipitation with Yb(3+) and after recovery of the PGPF indicated that 96% of the phenolic compounds were precipitated and 99% of the precipitated PGPF were recovered by cation-exchange resin. These results indicate that MALDI-TOF MS is able to determine the mass distribution of complex mixtures of oligomeric PGPF and that precipitation of PGPF by Yb(3+) is useful for isolation and quantification.
Journal of Agricultural and Food Chemistry 06/2000; 48(5):1663-7. · 2.82 Impact Factor
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ABSTRACT: Inotropic drugs are often used to treat acute, severe heart failure resulting from acute myocardial infarction and other unstable coronary artery syndromes. However, catecholamine inotropic agents may potentiate coronary thrombosis via a platelet alpha2-adrenergic mechanism, thus exacerbating the original problem. The present studies were designed to determine whether the nonadrenergic inotropic and vasodilator drug amrinone, which elevates platelet cAMP levels, would both inhibit human platelet Ca2+ mobilization and adhesion molecule expression ex vivo and protect against experimental coronary thrombosis in vivo in dogs.
Human platelets in suspension were preincubated with amrinone 2.5 to 15 microg/mL; stimulated with the agonists thrombin 0.1 U/mL, ADP 10(-6) mol/L, or arginine vasopressin 10(7) mol/L; and studied for Ca2+ mobilization, glycoprotein IIb/IIIa activation, and P-selectin expression by fluorescent flow cytometry methods. Experimental coronary thrombosis in vivo was studied in an open-chest dog model with critical coronary artery stenosis and deep vessel wall injury. Results showed that at the cellular level, amrinone inhibited agonist-induced Ca2+ mobilization and had modest inhibitory effects on adhesion molecule expression. In vivo in dogs, intravenous amrinone 2 mg/kg plus infusion at 20 microg x kg(1) x min(-1) completely abolished coronary thrombosis.
The fact that amrinone inhibited human platelet activation at the cellular level and protected against experimental coronary thrombosis in vivo in dogs suggests a potentially advantageous antithrombotic action for this inotropic and vasodilator drug.
Circulation 10/1997; 96(5):1647-53. · 14.74 Impact Factor
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J Folts
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ABSTRACT: Coronary artery bypass grafts, angioplasty, and thrombolysis are beneficial procedures for patients with coronary artery disease. However, these procedures can fail by mechanisms related to interactions between platelets and the damaged arterial wall. An experimental model for studying some of the mechanisms of platelet interaction with endothelial- and medial-damaged stenosed arteries is described. Dogs or pigs are anesthetized, and the chest opened. The heart is exposed, the circumflex or left anterior descending coronary artery is dissected out, and an EMF or Doppler flow probe is placed on it. Distal to the flow probe, the artery is clamped with a vascular clamp to produce endothelial and/or medial injury. Then, an encircling plastic cylinder is placed around the outside of the injured artery, producing a "critical stenosis." Acute platelet thrombus formation begins to occur in the stenosed lumen, gradually increasing the amount of stenosis. This causes the coronary flow to decline and reach zero flow when the artery is completely occluded. Then, the thrombus is embolized into the distal circulation, and flow is restored to normal levels. This occurs repeatedly causing cyclic flow reductions (CFRs). These CFRs can be made larger and to occur more frequently by increasing in vivo platelet activity, by raising the plasma catecholamine levels, or by increasing the collagen exposed in the stenosed lumen by increased medial damage. If an effective dose of an antiplatelet agent is given, the CFRs will be decreased in size and frequency or abolished entirely. Aspirin and other agents abolish the CFRs in this model; however, CFRs can be renewed by infusions of catecholamines or platelet activating factor. Thus, the model may be useful for studying mechanisms that enhance or inhibit arterial thrombosis in stenosed arteries with endothelial and medial injury.
Circulation 07/1991; 83(6 Suppl):IV3-14. · 14.74 Impact Factor
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ABSTRACT: High-intensity short-duration lifting is frequently performed by athletes and laborers. Little is known about the magnitude and pattern of blood pressure response and resultant effects on left ventricular (LV) function during this form of intense isometric exercise. We monitored brachial intra-arterial pressure and LV ejection fraction (LVEF) during upright isometric dead lifting performed on a force platform. Fourteen healthy male subjects (age 27 yr) maintained maximal sustained isometric dead lift (140 +/- 34 kg) for 32 s. LVEF was measured by 99mTc first-pass radionuclide ventriculography. Mean arterial pressure increased from 107 +/- 15 mmHg at rest to a peak of 174 +/- 28 mmHg and fell precipitously to 88 +/- 13 mmHg within 10 s after release of the dead lift. LVEF decreased from 63 +/- 8 to 51 +/- 14% (P less than 0.02) in seven subjects with technically acceptable ventriculograms. We conclude that maximal upright isometric dead-lift exercise produces a marked increase in arterial pressure and corresponding LV afterload that is associated with a transient reduction in LVEF in normal men.
Journal of Applied Physiology 01/1991; 69(6):2062-6. · 3.75 Impact Factor
