Journal
BYULLETEN SIBIRSKOY MEDITSINY
Volume 19, Issue 4, Pages 138-142Publisher
SIBERIAN STATE MEDICAL UNIV
DOI: 10.20538/1682-0363-2020-4-138-142
Keywords
myocardium; ischemia; reperfusion; receptors; chronic hypoxia
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Funding
- Russian Science Foundation [16-15-10001]
- Russian Science Foundation [16-15-10001] Funding Source: Russian Science Foundation
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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% pO(2) , 0.3% pCO(2) 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 mu g/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 vanilloid receptors 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.
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