Size Of Platelet Aggregates Research Articles

Inhibition of platelet aggregation by verapamil: quantification by in vivo and in vitro techniques.

Platelet aggregation appears to play a prominent role in myocardial ischemia. Verapamil, a slow-channel blocking agent with important antiarrhythmic and vasodilating actions, has been shown to inhibit in vitro platelet aggregation. We used an electronic particle size analyzer to evaluate the effects of verapamil on platelet aggregation in vitro and in vivo in 88 rats. The intravenous injection of verapamil (0.4 mg/kg) did not change the platelet count compared to control animals receiving an equal volume of normal saline (verapamil, 1.1 +/- 0.04 x 10(6)/mm3, vs. control, 1.2 +/- 0.09 x 10(6)/mm3, (p greater than 0.05). The mean size of platelet aggregates induced by adenosine diphosphate (0.2 microM), was reduced by verapamil (verapamil, 15.3 +/- 1.2 x 10(3) micron3 vs. control 24.4 +/- 2.7 x 10(3) micron; p less than 0.01). Platelet aggregates induced in vivo, following a standardized technique of extravasation of right iliac artery blood into the peritoneal cavity, were also smaller following verapamil infusion (verapamil, 12.6 +/- 1.1 x 10(3)micron3, vs control, 17.3 +/- 0.9 x 10(3) micron3 p less than 0.001). We conclude that verapamil exerts and inhibitory effect on platelet aggregation both in vitro and in vivo. This property may add an important new dimension to its potential therapeutic usefulness in ischemic heart disease.

The effect of acute changes in arterial blood pH and pO 2 on platelet aggregation

We examined the effects of acutely induced respiratory and metabolic acidosis and alkalosis and acute hypoxemia with controlled blood pH on subsequent in vitro platelet aggregate formation in rats. The mean size and total volume of platelet aggregates were measured with an electronic particle counter within 30 sec of drawing whole blood into a syringe containing adenosine diphosphate (2 × 10 −6 M, final concentration). There were no differences in circulating platelet count, mean platelet size or total volume of aggregates formed between the experimental and control groups. Platelets from animals who were made alkalotic formed aggregates larger than those from controls. Animals with a respiratory acidosis formed smaller aggregates. Hypoxemic animals, regardless of arterial blood pH, formed aggregates larger than controls. The mean size of platelet aggregates is a sensitive means of demonstrating effects of oxygenation and acid-base balance. Abnormal platelet aggregation in response to hypoxia and acidosis may be important in the pathogenesis of respiratory distress syndromes.

Factors Affecting the Size of Platelet Aggregates in Blood

Factors affecting the size distribution of platelet aggregates formed in whole blood were measured using an electronic particle counter. Lysis of red cells after dilution of blood for analysis allows detection of smaller aggregates without altering aggregate measurement. Differences in platelet response to increasing concentrations of ADP are detected by an increase in the mean size of platelet aggregates while the total volume of aggregates varies linearly with the volume of available platelets (r = .99). The mean aggregate size varies directly with the total volume of aggregates formed (r = .99). Mean aggregate size is inversely related to the packed red cell volume. As the reactivity of platelets is reduced by incubation with aggregation inhibitors at increasing concentrations, the mean size of aggregates becomes smaller, followed by a decrease in the total volume of aggregates. The total volume and mean size of aggregates formed after incubation with collagen and epinephrine, but not ADP, increases with time after venepuncture.

Cardiopulmonary bypass. Microembolization and platelet aggregation.

Particulate microemboli and in vitro platelet aggregation were studied in blood of patients during cardiac operations with an electronic particle size analyzer. A small gradient of microemboli developed on passage of blood through a bubble oxygenator but not through a membrane oxygenator. However, with both types of oxygenators, there was a sustained increase in the volume of microemboli in cardiotomy return blood which was much greater than in aterial blood. After cardiopulmonary bypass with both oxygenators, there was a comparable reduction in the volume of circulating platelets which exceeded that of the hemoglobin concentration, indicating platelet loss exceeded that that expected from hemodilution alone. However, the total volume and mean size of platelet aggregates induced in blood of patients after membrane oxygenation was significantly greater than similar measurements after bubble oxygenation. This study shows that membrane oxygenation reduces particulate microembolization and preserves platelet function in patients undergoing cardiac operations when compared to bubble oxygenation.

The Inhibition of Platelet Aggregation by an Aorta Intima Extract

SummaryThe platelet aggregating activity of extracts of different layers of the arterial wall was compared to that of Achilles tendon. Arterial media and tendon extracts, adjusted to equivalent protein content as an index of concentration, aggregated platelets to the same extent but an arterial intima extract did not aggregate platelets. Platelet aggregation induced by collagen could be inhibited by mixing with intima extract, but only to a maximum of about 80%. Pre-mixing adenosine diphosphate (ADP) with intima extracts diminished the platelet aggregation activity of the ADP. Depending on the relationship between ADP and intima extract concentrations aggregating activity could either be completely inhibited or inhibition abolished. Incubation of ADP with intima extract and subsequent separation of degradation products by paper chromatography, demonstrated a time-dependent breakdown of ADP with AMP, adenosine, inosine and hypoxanthine as metabolic products; ADP removal was complete. Collagen, thrombin and adrenaline aggregate platelets mainly by endogenous ADP of the release reaction. Results of experiments comparing inhibition of aggregation caused by premixing aggregating agent with intima extract, before exposure to platelets, and the sequential addition of first the intima extract and then aggregating agent to platelets, suggest that the inhibitory effect of intima extract results from ADP breakdown. It is suggested that this ADP degradation by intima extract may play a protective role in vivo by limiting the size of platelet aggregates forming at the site of minimal “wear and tear” vascular trauma.

Formation and size of platelet aggregates during hypovolemic hypotension in dog.

Formation and size of platelet aggregates during hypovolemic hypotension in dog.

Screen filtration pressure of blood--an evaluation.

The relative importance of some factors in the determination of screen filtration pressure (SFP) of human blood has been examined. The physical determinants of SFP are defined and the effect of time, anticoagulant, red cells, platelets, and leucocytes are established. Changes in SFP correspond closely to the size of platelet aggregates once a size of approximately 50 μ is exceeded.