Several blood transfusion filters designed to remove microemboli were evaluated for filtration and flow characteristics, as well as for hemolysis and for release of particulate debris from the filter. The Dacron wool filter, a depth filter, was superior at removing microemboli measured with an electronic particle size analyzer. A 25 micrometer pore mesh filter was least effective at removing microemboli from stored blood, but demonstrated the most favorable flow rates and induced no apparent red blood cell destruction during filtration. In general, filter efficiency and filter induced hemolysis correlated inversely with flow rate. No filter tested released significant quantities of particulate debris when compared with unfiltered isotonic saline.

Blood Transfusion↗

PubMedDate not supplied

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.

Adenosine Diphosphate↗

PubMedDate not supplied

Effects of ethanol and hemolysis on in vivo and in vitro platelet aggregation.

In vivo and in vitro platelet function were measured in male rats after intravenous injection of ethanol or water. There was a dose-related ethanol suppression of platelet aggregation induced by extravasation. Increased volumes of preformed microaggregates were seen in samples taken directly from the vena cava after injection of ethanol in doses that caused hemolysis. Lower doses of ethanol produced no demonstrable microaggregates or hemolysis: however, extravasation-induced aggregation was inhibited. Hemolysis was noted after intravenous injection of water, which also reduced the total volume and mean aggregate size of platelet aggregates induced by extravasation. Blood drawn from the inferior vena cava after induction of hemolysis had an increased volume of microaggregates, regardless of the agent producing hemolysis. In vitro studies revealed changes in spontaneous and ADP-induced aggregation only at very high concentrations of ethanol (greater than 3,000 mg/dl) and no effects at ethanol levels that altered in vivo aggregation. Ethanol, in doses that do not hemolyze erythrocytes, decreases platelet aggregation.

Animals↗

PubMedDate not supplied

Inhibition of platelet aggregation by oral digoxin and reversal with nifedipine.

To study the effect of cardiac glycosides on platelet function, we obtained serial blood samples from 18 normal male volunteers before and 3, 5, and 7 weeks after beginning digoxin therapy (0.375 mg daily). The combined effect of digoxin and nifedipine (mean dose, 57 mg/day) was assessed during the 5th week. Spontaneous platelet aggregation and platelet response to adenosine diphosphate (ADP) were measured in whole blood by electronic particle sizing. Digoxin (mean serum concentration, 0.9 ng/ml) caused significant reduction in total volume and mean size of platelet aggregates formed in response to ADP. However, with addition of nifedipine, the volume and mean size of aggregates returned to baseline measurements. In vitro administration of digoxin to whole blood failed to inhibit ADP-induced platelet aggregation. The volume of spontaneously induced aggregates decreased with digoxin; however, the decrease was not statistically significant. These data indicate that digoxin given in vivo for several weeks inhibits platelet response to ADP; this effect is reversed by the addition of nifedipine.

Adenosine Diphosphate↗

PubMedDate not supplied

Filtration of the microaggregates in stored blood.

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Blood Cell Count↗

PubMedDate not supplied

Microaggregates in frozen and saline washed red blood cells.

The microaggregates which accumulate in stored blood have been implicated in the development of posttraumatic pulmonary insufficiency. These particles are known to be composed of degenerated leukocytes and platelets. Because frozen and saline washed red blood cells contain small numbers of leukocytes and platelets, they were studied as a possible source of microaggregate-free red blood cells. Using a Model T Coulter Counter to quantitate all particles 13-80 microns in size, it was shown that freezing and deglycerolization, or simple saline washing (manual or automated), could reduce the number of microaggregates in stored blood by 80 to 90 per cent. These findings add to a growing list of potential advantages in the routine use of frozen red cells for patients requiring transfusion.

Erythrocyte Aggregation↗