The preparation and use of the hamster cheek pouch for studies of the microcirculation

After a certain period of time filtered ultraviolet light produces platelet aggregation in microvessels on the cerebral surface of the mouse, but only when sodium fluorescein is first injected intravascularly to provide a light-absorbing, heat-generating target. The platelet aggregates fluoresce. They occur only in the illuminated field and adhere to arteriolar and venular walls. Vasoconstriction is not detected prior to or up to 30 seconds after aggregation. Electron microscopy reveals damaged endothelium and undamaged red cells, as well as aggregates consisting almost exclusively of platelets in varying stages of aggregation, pseudopod formation, and degranulation. The time between onset of the noxious stimulus and recognition of the first aggregate can be measured as the vessels are observed microscopically. This "time of aggregation" is prolonged by pentobarbital as opposed to urethane anesthesia, and also is related to time elapsed after craniotomy. We also found that aspirin and indomethacin significantly prolong time to first aggregate, but only on the arteriolar side of the circulation. This is so even though the composition of the aggregates is the same on both the arteriolar and venular sides. Heparin has no effect.

Platelet aggregation in the cerebral microcirculation: effect of aspirin and other agents.

ADMINISTRATION of gastrin or histamine leads to the secretion of hydrochloric acid by the vertebrate stomach. The details of this process are so far largely unknown. The effects of a variety of hormones in other tissues are mediated by the intracellular level of cyclic AMP (adenosine 3′,5′-monophosphate)1. In several such examples the naturally occurring unsaturated fatty acid, prostaglandin E1 (PGE1), blocks hormonal action. Thus inhibition of epinephrine-induced lipolysis2 and vasopressin-induced changes in osmotic permeability3 by PGE1 have been attributed to interference with the accumulation of cyclic AMP induced by the respective hormone in the target organ or tissue.

Inhibition of gastric acid secretion in vitro by prostaglandin E1.

Platelet thrombus induced in vivo by filtered light and fluorescent dye in mesenteric microvessels of the rat.

The role of hemodynamics on platelet thrombus formation was studied in venules and arterioles of the rat mesentery. Thrombus formation was induced by the fluorescent dye/light method for examination of the following factors: 1) the effect of wall shear rate on thrombus initiation, 2) the effect of wall shear rate on the growth of thrombi, and 3) the relation between platelet thrombus initiation and intraluminal velocity profile. The range of wall shear rate was up to approximately 1,000 1/sec in venules and from 640 to 2,900 1/sec in arterioles. Platelet thrombus initiation occurred more rapidly at higher wall shear rate in venules and at lower wall shear rate in arterioles. Thrombus initiation time was shortest around a wall shear rate of 900 1/sec in venules and around 700 1/sec in arterioles. Thrombus growth rate in venules was greatest at a wall shear rate of 1,500-2,000 1/sec. Thrombus initiation and its relation to blood flow was also examined in branched and curved microvessels. In these vessels platelet thrombi were also first initiated at the sites of higher wall shear rate in venules and of lower wall shear rate in arterioles.

Effect of wall shear rate on thrombogenesis in microvessels of the rat mesentery.

WHEN an artery of the cerebral cortex of an anaesthetized rabbit is pinched with a pair of fine forceps so that it bleeds briefly, some platelets rapidly form a haemostatic plug outside the vessel and others adhere to its endothelial lining at the site of injury to form platelet clumps or ‘white bodies’ which embolize intermittently in the blood stream. The formation and embolization of white bodies may go on for several hours1–3.

R. B. Philp

Papers

Effect of Anaesthetics on the Duration of Embolization of Platelet Thrombi formed in Injured Blood Vessels