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Further investigation of thromboxane‐A 2 induced arrhythmias
Author(s) -
Kosloski Lisa M.,
Best Shaun R.,
Wacker Michael J.,
Porter Charles B.,
Orr James A.
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a320-d
Subject(s) - thromboxane a2 , cardiology , medicine , vasoconstriction , proarrhythmia , blood flow , myocardial infarction , anesthesia , platelet , qt interval
Thromboxane A2 (TxA2) elicits platelet aggregation, vasoconstriction, and is released during tissue trauma (e.g., during clot formation and subsequent myocardial ischemia). Characterization of arrhythmias following left atrial injections of a TxA2 mimetic, U46619 (U4) (dose 10 to 30 μg) has been carried out in the anesthetized rabbit. Data obtained from a lead‐II EKG indicated no change in the P‐P interval, but reductions in the P‐R interval and increases in the duration of the QRS complex. Arrhythmias were mainly characterized as an accelerated idioventricular rhythm. The absence of arrhythmias following TxA2 receptor blockade (SQ29548: 10 mg) support the receptor specificity of the response. Experiments were also performed to investigate whether reductions in coronary blood flow (CBF) contributed to these U4‐induced arrthythmias. Left atrial injections of fluorescent microspheres were used to measure coronary blood flow during baseline conditionsand at two time points (30 s and 5 min) following administration of U4 (30 μg). Baseline CBF (2.17 ml/min/g) was unchanged following U4 injection (2.09 and 2.22 ml/min/g at 30 s and 5 min respectively). In summary, the origin of arrhythmias following administration of U4 is a receptor mediated event that is unrelated to alterations in CBF. Kosloski was sponsored by K‐INBRE (KAN37730). Wacker was sponsored by NIH‐IRACDA grant 63651.