Key result
Dopexamine caused a dose-dependent inhibition of agonist-induced platelet aggregation in vitro, suggesting it is unlikely to adversely affect hyperaggregability in cardiogenic shock.
Why the study?
Does dopexamine affect platelet function and aggregation under stress conditions in healthy subjects?
Does dopexamine affect platelet function and aggregation under stress conditions in healthy subjects?
Dopexamine inhibits agonist-induced platelet aggregation in vitro, suggesting it is unlikely to worsen the hyperaggregable state in patients with cardiogenic shock after myocardial infarction.
May support platelet safety in cardiogenic shock; animal data leave open human validation.
Dopexamine is a novel analogue of dopamine which is free of alpha-adrenoceptor activity and is of therapeutic value in chronic heart failure. The effects of dopexamine on the in vitro function of platelets from 10 healthy subjects at rest, after exercise and after in vitro addition of adrenaline and noradrenaline were investigated. 2. Dopexamine in a wide range of concentrations (10(-9)M-10(-3)M) did not appear to function as an agonist on platelets either in whole blood or in PRP preparations. 3. Dopexamine caused a dose-dependent inhibition of agonist-induced platelet aggregation in both whole blood and PRP. The inhibitory effect of dopexamine was significantly greater in PRP than in whole blood, and significantly greater to adrenaline than to collagen or ADP as agonists in whole blood. 4. After exercise or after in vitro addition of adrenaline and noradrenaline at concentrations commonly seen in myocardial infarction, dopexamine produced similar levels of inhibition seen with platelets from resting subjects. 5. Dopexamine did not affect plasma catecholamine levels but caused an increase in intraplatelet noradrenaline levels. 6. This study suggests that dopexamine is unlikely adversely to affect the hyperaggregable state found in patients with cardiogenic shock after myocardial infarction.
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Wagaine‐Twabwe et al. (1990) studied Healthy subjects (n=10). Dopexamine was evaluated on In vitro platelet function and agonist-induced platelet aggregation. Dopexamine caused a dose-dependent inhibition of agonist-induced platelet aggregation in vitro, suggesting it is unlikely to adversely affect hyperaggregability in cardiogenic shock.
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