What question did this study set out to answer?

To investigate how platelets impair postischemic cardiac performance and evaluate whether endogenous adenosine mitigates intracoronary platelet adhesion during early reperfusion.

July 1, 1998Journal of Cardiovascular Pharmacology

Adenosine Endogenously Released During Early Reperfusion Mitigates Postischemic Myocardial Dysfunction by Inhibiting Platelet Adhesion

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Why the study?

Does endogenous adenosine prevent platelet adhesion and postischemic myocardial dysfunction in isolated guinea pig hearts?

Population

Isolated guinea pig hearts

Comparison

Homologous platelets infused into coronaries… vs Hearts without platelets, or without specific…

Design

Preclinical

Authors

CSChristian SeligmannOrthopädische Praxis CKChristian KupattStructural Heart Disease BBBernhard F. BeckerLudwig-Maximilians-Universität München

Discussion

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Implication

Platelet-induced impairment during low-flow ischemia may worsen postischemic function; leaves open adenosine's protective role pending larger-model confirmation.

Key Points

To investigate how platelets impair postischemic cardiac performance and evaluate whether endogenous adenosine mitigates intracoronary platelet adhesion during early reperfusion.
Infused homologous platelets with or without thrombin into coronary arteries of isolated guinea pig hearts during low-flow ischemia or reperfusion to measure external heart work (EHW) and platelet adhesion.
Administered adenosine uptake blockers (dipyridamole), non-selective adenosine receptor blockers (theophylline), and selective A1 (DPCPX) and A2 (DMPX) receptor antagonists.
Assessed nitric oxide and prostaglandin I2 contributions using nitro-L-arginine (NOLAG) and indomethacin, respectively.
Platelet infusion with thrombin during low-flow ischemia reduced EHW recovery to 63 ± 4% versus 89 ± 3% in platelet-free controls (p < 0.05), whereas infusion in the first minute of reperfusion caused no functional loss unless theophylline was co-administered (EHW recovery 42 ± 12%).
Thrombin-induced intracoronary platelet adhesion peaked during low-flow ischemia (35 ± 3%) and was completely absent in the first minute of reperfusion, but reappeared at minute five (20.8 ± 4%).
Theophylline increased platelet adhesion to 33 ± 6.4% in the first minute of reperfusion, an effect mirrored additively by DPCPX and DMPX, while dipyridamole enhanced adenosine release and lowered five-minute adhesion.

Structured PICO

Does endogenous adenosine prevent platelet adhesion and postischemic myocardial dysfunction in isolated guinea pig hearts?

Population

Isolated guinea pig hearts

Intervention

Homologous platelets infused into coronaries during low-flow ischemia or reperfusion, with thrombin and various pharmacological agents (dipyridamole, theophylline, DPCPX, DMPX, NOLAG, indomethacin)

Comparator

Hearts without platelets, or without specific pharmacological blockers

Outcome

External heart work (EHW) and intracoronary platelet adhesionsurrogate

Endogenous adenosine released during early reperfusion protects against postischemic myocardial dysfunction by inhibiting platelet adhesion via A1- and A2-receptor-dependent mechanisms.

Cite This Study

Seligmann et al. (1998) studied this question.

synapsesocial.com/papers/6a730ddbb053ac046a60decf https://doi.org/10.1097/00005344-199807000-00024

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Implication

Platelet-induced impairment during low-flow ischemia may worsen postischemic function; leaves open adenosine's protective role pending larger-model confirmation.

Adenosine Endogenously Released During Early Reperfusion Mitigates Postischemic Myocardial Dysfunction by Inhibiting Platelet Adhesion

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Adenosine Endogenously Released During Early Reperfusion Mitigates Postischemic Myocardial Dysfunction by Inhibiting Platelet Adhesion

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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