Evaluation of a porcine model to study in vivo platelet activation.

Introduction: In order to investigate if decompression sickness involves platelet activation an animal model was evaluated.

Materials And Methods: Twenty-four thiopentone-midazolam-fentanyl-anaesthetized pigs in four groups received 5-min infusions of adenosine diphosphate (25 mg/kg) or platelet activating factor (0.4 microg/kg).

Nitrogen microbubbles induce a disappearance of single platelets (aggregation) with porcine platelets: a comparative study of the effects of anticoagulants and blood collection methods.

The pathogenesis of decompression illness (DCI) is uncertain. DCI involves all parts of the organism where gas bubbles are produced. They have both primary and secondary effects and have been classified as an agonist aggregating human platelets.

Secretion of β-thromboglobulin and Serotonin from Human Platelets Induced by Microbubbles Differs from Secretion Induced by Collagen and Polystyrene Microspheres.

The effect of nitrogen (N(2))-microbubbles on human platelets resembles that of common agonists in terms of aggregation, but displays one unusual feature in that cyclooxygenase-inhibitors (e.g. aspirin) poorly inhibit the reaction.

Microbubble-induced phospholipase C activation does not correlate with platelet aggregation.

The effect of nitrogen-(N2-)microbubbles on platelets resembles that of common platelet agonists with respect to aggregation and secretion, but is considerably slower and is poorly inhibited by aspirin. This paper reports the effect of microbubbles on platelet phospholipase C activity in gelfiltered human platelets prelabelled with [32P]Pi ([32P]-GFP). The experiments were run in the presence of an ADP scavenging system in order to rule out effects of ADP.