What question did this study set out to answer?

To evaluate whether the endothelin A receptor antagonist LU 135252 mitigates polymorphonuclear leukocyte-mediated myocardial contractile dysfunction following ischaemia and reperfusion.

September 1, 1998Cardiovascular ResearchOpen Access

The endothelin A receptor antagonist LU 135252 protects the myocardium from neutrophil injury during ischaemia/reperfusion

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Why the study?

Does the ETA receptor antagonist LU 135252 protect the myocardium from PMN-mediated contractile dysfunction following ischaemia/reperfusion in isolated rat hearts?

Population

Isolated rat hearts subjected to global ischaemia and reperfused with buffer solution only, or human…

Comparison

ETA receptor antagonist LU 135252 or ET-1 vs Vehicle

Design

Preclinical

Authors

AGA. T. GononKarolinska University Hospital

Discussion

Member takes

Implication

Hypothesis-generating for ETA blockade in reperfusion injury; should not yet change clinical practice.

Key Points

To evaluate whether the endothelin A receptor antagonist LU 135252 mitigates polymorphonuclear leukocyte-mediated myocardial contractile dysfunction following ischaemia and reperfusion.
Isolated rat hearts were perfused via the Langendorff method and exposed to global ischaemia.
Reperfusion was performed using either buffer solution alone or human polymorphonuclear leukocytes suspended in rat plasma (HNRP), co-administered with LU 135252 or endothelin-1.
During buffer-only reperfusion, neither LU 135252 (1 and 10 μmol/l) nor endothelin-1 (1 and 10 nmol/l) significantly altered left ventricular recovery parameters relative to vehicle.
In HNRP-reperfused hearts, LU 135252 (10 μmol/l) significantly improved left ventricular developed pressure, dP/dt, and rate pressure product, while lowering left ventricular end-diastolic pressure by 20 mmHg compared to vehicle (P < 0.05).
Coronary effluent PMN outflow was significantly higher with LU 135252 (41 ± 8%) than vehicle (9 ± 5%, P < 0.01), whereas endothelin-1 administration caused total contractile arrest and zero PMN outflow.

Structured PICO

Does the ETA receptor antagonist LU 135252 protect the myocardium from PMN-mediated contractile dysfunction following ischaemia/reperfusion in isolated rat hearts?

Population

Isolated rat hearts subjected to global ischaemia and reperfused with buffer solution only, or human polymorphonuclear leukocytes (PMNs) dissolved in rat plasma (HNRP)

Intervention

ETA receptor antagonist LU 135252 (1 and 10 mumol/l) or ET-1 (0.1, 1, and 10 nmol/l)

Comparator

Vehicle

Outcome

Recovery of left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), the first derivative of left ventricular pressure (dP/dt), rate pressure product (RPP), and outflow of PMNs in the coronary effluentsurrogate

The ETA receptor antagonist LU 135252 protects the myocardium from ischemia/reperfusion injury by attenuating PMN-mediated contractile dysfunction in an isolated rat heart model.

Cite This Study

A. T. Gonon (1998) studied this question.

synapsesocial.com/papers/6a70283b84cc45bb7bdfb719 https://doi.org/10.1016/s0008-6363(98)00167-9

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The endothelin A receptor antagonist LU 135252 protects the myocardium from neutrophil injury during ischaemia/reperfusion

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

The endothelin A receptor antagonist LU 135252 protects the myocardium from neutrophil injury during ischaemia/reperfusion

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

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