Domenico Bottecchia

Effect of nucleus accumbens destruction in rat.

The paper presents the effects of nucleus accumbens destruction in rats. There are certain behavioral correlates (e.g., avoidance learning and dominance) which are influenced by the destruction of the nucleus accumbens, while other specific correlates are not significantly affected (namely, open field movements and competition for food). The results are discussed.

Ionophore A 23187: Some Effects on Platelet Aggregation and Clot Retraction

The ionophore for divalent cations, A 23187, induces plate aggregation and clot retraction. Acetylsalicyclic acid has a potentiating effect on the aggregation induced by A 23187 in platelet-rich plasma, while it inhibits the aggregation of washed platelets. Acetylation of plasma proteins could be the reason of the increased platelet aggregation induced by A 23187 in the presence of acetylsalicyclic acid. Platelet aggregation by A 23187 is probably activated by the passage of Ca2+ through the platelet membrane(s); the aggation, clot retraction by A 23187 requires increased availability in the intracellular space of both Ca2+ and Mg2+.

What’s Provoking Different Aggregation between Arterial and Venous Platelets in the Rat?

The present study was designed to clarify the reason why rat platelets obtained from arterial blood show a less marked aggregation than those obtained from venous blood, and to investigate the contribution of the vessel wall to this phenomenon. Incubation of arterial or venous platelet-rich plasma (PRP) with papaverine, a phosphodiesterase blocker, resulted in a more marked inhibition of the aggregation parameters for arterial than for venous PRP, indicating that a cAMP-dependent mechanism is involved. Incubation of PRP in vitro with adenosine deaminase did not significantly modify aggregation. Rats treated in vivo with different doses of acetylsalicylic acid or of tranylcypromine, two cyclo-oxygenase inhibitors, abolished the aggregation differences between arterial and venous PRP. It is suggested that this difference in platelet behavior may be due to a mechanism dependent on a PGI2-like, probably cAMP-related activity in which the heart and/or the lungs may play an important role.

Platelet aggregation following electrical stimulation

It was demonstrated that the previous in vitro electrical stimulation of human and rat platelet-rich plasma does not modify the subsequent response of platelets to the aggregating activity of ADP, thrombin, thrombofax or adrenaline. This is interesting in view of the fact that the electrical stimulation can induce clot retraction.

Electrical stimulation induces clot retraction after previous in vitro platelet aggregation.

the spontaneous clot retraction of platelet-rich plasma is inhibited by previous in vitro ADP-induced platelet aggregation. The electrical stimulation of the clot always restores a maximal clot retraction, even after a prolonged previous in vitro platelet aggregation.