January 1, 2000Journal of Cardiovascular Pharmacology
Endothelin-A-Receptor Antagonist LU 135.252 Inhibits the Formation of Ventricular Arrhythmias Caused By Intrapericardial Infusion of Endothelin-1
Key result
LU 135.252 inhibits ET-1-induced arrhythmias and MAPD prolongation in dogs but not ischemic changes.
- n=12
Why the study?
Does the endothelin-A-receptor antagonist LU 135.252 prevent ventricular arrhythmias caused by intrapericardial endothelin-1 infusion in open-chest dogs?
Population
12 open-chest mongrel dogs
Comparison
Intravenous bolus of endothelin-A-receptor… vs Intrapericardial infusion of endothelin-1 for 30…
Design
Preclinical
Follow-up
30 minutes
Authors
Discussion
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Member takes
Implication
Supports ET-A blockade in ET-1 arrhythmia models; leaves open translation to human ischemic arrhythmias.
Structured PICO
Does the endothelin-A-receptor antagonist LU 135.252 prevent ventricular arrhythmias caused by intrapericardial endothelin-1 infusion in open-chest dogs?
P
Population
12 open-chest mongrel dogs subjected to intrapericardial ET-1 infusion to induce ventricular arrhythmias.
I
Intervention
Intravenous bolus of endothelin-A-receptor antagonist LU 135.252 (5 mg/kg) given 10 minutes prior to intrapericardial infusion of endothelin-1 (33 pmol/kg/min) for 30 min
C
Comparator
Intrapericardial infusion of endothelin-1 (33 pmol/kg/min) for 30 min without LU 135.252 treatment
O
Outcome
Ventricular arrhythmias and electrophysiological effects (monophasic action potential durations and early after depolarizations)surrogate
The endothelin-A-receptor antagonist LU 135.252 inhibits the arrhythmogenic and electrophysiological effects of pericardial endothelin-1 infusion in a canine model, although it does not prevent ischemic changes.
Cite This Study
Kiss et al. (2000) studied ET-1-induced ventricular arrhythmias (n=12). LU 135.252 vs. ET-1 infusion without LU treatment was evaluated on Ventricular arrhythmias and MAPD prolongation. LU 135.252 inhibited the arrhythmogenic action, MAPD prolongation, and early after depolarization formation caused by pericardial ET-1 infusion in dogs, but did not prevent ischemic changes.