Quantification of the adhesion of platelets in hamster venules in vivo.

Abstract

(i) Citrated platelet-rich plasma freshly prepared from golden hamsters was mixed with fluorescein isothiocyanate (FITC) which made the platelets fluorescent. These platelets were injected intravenously into anaesthetized hamsters with exteriorized cheek pouch preparations superfused at 37 °C with Krebs-bicarbonate solution. The exposed microcirculation was observed microscopically by bright field or fluores­cent illumination. The flowing and sticking of fluorescent platelets was recorded on video tape for quantitative analysis. (ii) In four experiments 22–36%, mean 28%, of fluorescent platelets were circulating 2-3 h after their injection. In seven experiments the fluorescent platelets accounted for 0.6–3.3 %, mean 1.7 %, of circulating platelets. (iii) In venules 20–60 μm in diameter small proportions, mean 5.4%, of circulating fluorescent platelets stopped moving by sticking to the vessel walls. About 80 % of these platelets stuck for up to 1 s, a further 10-15% for up to 5 s, and only about 2% for longer than 2 min. There was an inverse relation between size of venule and proportion of platelets sticking in them. (iv) There was a direct relation between the mean velocities at which platelets flowed through the venules and the sizes of the venules. In the smaller venules the velocity distribution of the platelets had a clear maximum which was not as evident in larger venules. (v) In a few observations on arterioles, flowing platelets could not be seen, and arrested platelets only in a dilatation and at a capillary branch. (vi) Ethylenediamine tetraacetate in the superfusing fluid decreased platelet sticking in venules but did not abolish it. (vii) Adenosine diphosphate in the superfusing fluid caused the appear­ance of platelet aggregates in venules and of sticking platelets in arterioles during progressive diminution in blood flow through both types of vessel. (viii) The observations make it improbable that the release of platelet constituents affects normal venules or arterioles except, possibly, where haemodynamic conditions are affected by wall irregularities such as dilations or branching.