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SUMMARY1. The mean velocities at which granulocytes roll along the walls of small venules have been related to their mean blood flow velocities in preparations of hamster cheek pouch and mouse mesentery. In animals anaesthetized with Nembutal, 30-200 ,tm venules were observed microscopically and the movement of rolling granulocytes quantitated on films. Apparent mean blood flow velocity was determined from films of embolizing platelet thrombi.2. In four venules the velocity distribution of about 100 rolling cells was almost symmetrical about the mode, with a small proportion moving at up to three times the mode velocity. Therefore, the mean and mode velocities were very similar.3. In two mesenteric and two cheek-pouch venules, blood flow velocity was temporarily altered during and after gentle compression with a fine glass fibre; this was associated with proportional changes in mean cell velocities.4. In four different venules of a hamster cheek pouch, the mean velocity of rolling granulocytes increased in proportion to the mean blood flow velocity (r = 0.963).5. In thirty-six venules of ten mouse mesenteries, the velocities were proportional (r = 0x915) between blood velocities of about 300 and 1000 #um/sec. Above this the velocity of the cells did not increase further.6. The rolling of granulocytes is presumably governed by two forces, the shear force of the flowing blood and an adhesive force between the surfaces of granulocytes and vascular endothelium. Our results suggest that, within limits, the proportionality between the velocities of blood flow and rolling cells is due to shear force, the adhesive force being similar for all the cells. The results suggest that this adhesion force per granulocyte is of the order of 10-5 dynes.

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SUMMARY1. Blood platelets containing different amounts of 5-hydroxytryptamine (5-HT) were produced in vivo by the injection of5-hydroxytryptamine or of reserpine into normal rabbits and of 5-hydroxytryptamine into reserpinized rabbits. Before and after these injections the aggregation of platelets was measured in vitro.2. Platelets of untreated rabbits were aggregated by adenosine diphosphate (ADP) and by 5-hydroxytryptamine; (-)-adrenaline alonQ did not produce aggregation but markedly increased aggregation by 5-hydroxytryptamine.3. Platelets saturated with 5-hydroxytryptamine in vivo were no longer aggregated in vitro by 5-hydroxytryptamine or by 5-hydroxytryptamine plus adrenaline, but their aggregation by ADP was unchanged.4. Platelets from reserpinized rabbits lost about 99 % of their 5-hydroxytryptamine; the aggregation of these platelets did not differ significantly from that of platelets from control rabbits.5. Platelets from reserpinized rabbits injected with 5-hydroxytryptamine were aggregated neither by the amine alone nor by 5-hydroxytryptamine plus adrenaline, although these platelets contained much less 5-hydroxytryptamine than saturated platelets and only about one tenth as much as platelets from untreated rabbits.6. The findings support the hypothesis that the inhibitory effect of 5-hydroxytryptamine administered in vivo on platelet aggregation in vitro is due to the association of the amine with the platelet membrane.

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In normal platelets a proportionality was found between the amount of adenosine triphosphate (ATP) and amount of 5-hydroxytryptamine (5-HT) in platelets both before and after incubating them in plasma to which 5-HT had been added. In patients receiving reserpine and in others with myeloid leukaemia, the amount of 5-HT in the platelets and the uptake of 5-HT by them were depressed, while the amount of ATP was normal. The possibility that ATP is involved in the accumulation of 5-HT by platelets is discussed.Hardisty and Stacey (1957) showed that, in two substances are plotted against one another. myeloid leukaemia and some other diseases of Although there is considerable scatter, there is a the blood, the amount of 5-hydroxytryptamine rough proportionality between the amounts of (5-HT) in the platelets is reduced. In some cases 5-HT (y) and ATP (x) in the platelets which is this was associated with an impaired capacity of expressed by the equation y=0.01 +0.023x (r= the platelets to take up 5-HT when they were 0.67, P<0.01). incubated in plasma to which 5-HT had been Fig. 2 shows that after platelets from the same added. Further, it has been shown (Born, Ingram, people had been incubated with 5-HT the proand Stacey, 1956; Born and Gillson, 1957) that portionality became closer. The corresponding the amount of 5-HT in platelets is proportional equation is y=0.035+0.094x (r=0.78, P<0.001). to the amount of adenosine triphosphate (ATP) The mean ratios of the number of ATP molecules which they contain. This paper reports observa-to the number of 5-HT molecules in the platelets tions on the amounts of 5-HT and ATP in plate-before and after incubation with 5-HT are given in lets obtained from normal people, from patients Table I

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