Receptor mechanism of infarct-limiting effect of adaptation to normobaric hypoxia
| Autor: | N. V. Naryzhnaya, A. V. Mukhomedzyanov, S. Yu. Tsibulnikov, L. N. Maslov |
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| Jazyk: | English<br />Russian |
| Rok vydání: | 2021 |
| Předmět: | |
| Zdroj: | Бюллетень сибирской медицины, Vol 19, Iss 4, Pp 138-142 (2021) |
| Druh dokumentu: | article |
| ISSN: | 1682-0363 1819-3684 |
| DOI: | 10.20538/1682-0363-2020-4-138-142 |
| Popis: | The aim of the study was to investigate the involvement of bradykinin, cannabinoid and vanilloid (TRPV1 channel) receptors in the implementation of the infarct-limiting effect of chronic normobaric hypoxia (CNH).Materials and methods. The study was performed on male Wistar rats (n = 117) weighing 250–300 g. Adaptation to CNH was modeled for 21 days at 12% pO2, 0.3% pCO2 and normal atmospheric pressure. A day after adaptation of rats to CNH coronary artery occlusion (45 min) and reperfusion (2 h) was performed. In the study the following compounds were used: selective cannabinoid CB1 receptor antagonist rimonabant (1 mg/kg), selective cannabinoid CB2 receptor antagonist AM630 (2.5 mg/kg), selective bradykinin B2 receptor antagonist HOE140 (50 μg/kg), and vanilloid receptor (TRPV1 channel) antagonist capsazepine (3 mg/kg). All antagonists were administered 15 min before coronary artery occlusion.Results. Adaptation to normobaric hypoxia promoted the formation of the pronounced infarct-limiting effect.The blockade of B2 receptor eliminated the infarct-limiting effect of CNH. Blockade of cannabinoid or vanilloidreceptors did not affect the infarct-limiting effect of CNH.Conclusion. The infarct-limiting effect of CNH depends on the activation of B2 receptor, and the adaptive increase in cardiac tolerance to ischemia/reperfusion does not depend on cannabinoid or vanilloid receptors. |
| Databáze: | Directory of Open Access Journals |
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