Endothelin-B receptors and ventricular arrhythmogenesis in the rat model of acute myocardial infarction
Basic Research in Cardiology, ISSN: 0300-8428, Vol: 105, Issue: 2, Page: 235-245
2010
- 29Citations
- 27Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations29
- Citation Indexes29
- 29
- CrossRef22
- Captures27
- Readers27
- 27
Article Description
The arrhythmogenic effects of endothelin-1 (ET-1) are mediated via ETA-receptors, but the role of ETB-receptors is unclear. We examined the pathophysio-logic role of ETB-receptors on ventricular tachyarrhythmias (VT/VF) during myocardial infarction (MI). MI was induced by coronary ligation in two animal groups, namely in wild-type (n = 63) and in ETB-receptor-deficient (n = 61) rats. Using a telemetry recorder, VT/VF episodes were evaluated during phase I (the 1st hour) and phase H (2-24 h) post-MI, with and without prior β-blockade. Action potential duration at 90% repolarization (APD90) was measured from mono-phasic epicardial recordings and indices of sympathetic activation were assessed using fast-Fourier analysis of heart rate variability. Serum epinephrine and norepinephrine were measured with radioimmunoassay. MI size was similar in the two groups. There was a marked temporal variation in VT/VF duration; during phase I, it was higher (p = 0.0087) in ETB-deficient (1, 519 ± 421 s) than in wild-type (190 ± 34 s) rats, but tended (p = 0.086) to be lower in ETB-defi-cient (4.2 ± 2.0 s) than in wild-type (27.7 ± 8.0 s) rats during phase II. Overall, the severity of VT/VF was greater in ETB-deficient rats, evidenced by higher (p = 0.0058) mortality (72.0% vs. 32.1%). There was a temporal variation in heart rate and in the ratio of low- to high-frequency spectra, being higher (<0.001) during phase I, but lower (p < 0.05) during phase II in ETB-deficient rats. Likewise, 1 h post-MI, serum epinephrine (p = 0.025) and norepi-nephrine (p < 0.0001) were higher in ETB-deficient (4.20 ± 0.54, 14.24 ± 1.39 ng/ml) than in wild-type (2.30 ± 0.59, 5.26 ± 0.67 ng/ml) rats, respectively. After β-blockade, VT/VF episodes and mortality were similar in the two groups. The ETB-receptor decreases sympathetic activation and arrhythmogenesis during the early phase of MI, but these effects diminish during evolving MI.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=77950360102&origin=inward; http://dx.doi.org/10.1007/s00395-009-0066-7; http://www.ncbi.nlm.nih.gov/pubmed/19838761; http://link.springer.com/10.1007/s00395-009-0066-7; http://www.springerlink.com/index/10.1007/s00395-009-0066-7; http://www.springerlink.com/index/pdf/10.1007/s00395-009-0066-7; https://dx.doi.org/10.1007/s00395-009-0066-7; https://link.springer.com/article/10.1007/s00395-009-0066-7
Springer Science and Business Media LLC
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