The Role of NO Synthase in the Infarct-Limiting Effect of Urgent and Chronic Adaptation to Normobaric Hypoxia
We studied the role of NO synthase in the infarct-limiting effect of short-term (SNH) and chronic continuous normobaric hypoxia (CNH). In male Wistar rats, SNH (6 sessions of 10-min hypoxia 8% O2 and 10-min reoxygenation) or CNH (12% O2 for 21 days) was modeled. In 30 min after SNH or 24 h after CNH...
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| Veröffentlicht in: | Bulletin of experimental biology and medicine 2023, Vol.174 (3), p.304-307 |
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| description | We studied the role of NO synthase in the infarct-limiting effect of short-term (SNH) and chronic continuous normobaric hypoxia (CNH). In male Wistar rats, SNH (6 sessions of 10-min hypoxia 8% O2 and 10-min reoxygenation) or CNH (12% O2 for 21 days) was modeled. In 30 min after SNH or 24 h after CNH, the rats were subjected to coronary artery occlusion (45 min) and reperfusion (2 h). The following drugs were administered to rats: non-selective NO synthase inhibitor L-NAME (10 mg/kg), inhibitor of inducible NO synthase S-methylthiourea (3 mg/kg), and inhibitor of neuronal NO-synthase 7-nitroindazole (50 mg/kg). NO donor diethylenetriamine was administered intravenously in a dose 2 mg/kg. It was found that L-NAME and S-methylthiourea abolished the infarct-limiting effect of SNH and CNH. Diethylenetriamine increased cardiac tolerance to ischemia/reperfusion. It is believed that inducible NO synthase plays an important role in the cardioprotective effect of normobaric hypoxia. |
| doi_str_mv | 10.1007/s10517-023-05696-3 |
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V. ; Sementsov, A. S. ; Maslov, L. N. ; Derkachev, I. A.</creator><creatorcontrib>Naryzhnaya, N. V. ; Sementsov, A. S. ; Maslov, L. N. ; Derkachev, I. A.</creatorcontrib><description>We studied the role of NO synthase in the infarct-limiting effect of short-term (SNH) and chronic continuous normobaric hypoxia (CNH). In male Wistar rats, SNH (6 sessions of 10-min hypoxia 8% O2 and 10-min reoxygenation) or CNH (12% O2 for 21 days) was modeled. In 30 min after SNH or 24 h after CNH, the rats were subjected to coronary artery occlusion (45 min) and reperfusion (2 h). The following drugs were administered to rats: non-selective NO synthase inhibitor L-NAME (10 mg/kg), inhibitor of inducible NO synthase S-methylthiourea (3 mg/kg), and inhibitor of neuronal NO-synthase 7-nitroindazole (50 mg/kg). NO donor diethylenetriamine was administered intravenously in a dose 2 mg/kg. It was found that L-NAME and S-methylthiourea abolished the infarct-limiting effect of SNH and CNH. Diethylenetriamine increased cardiac tolerance to ischemia/reperfusion. It is believed that inducible NO synthase plays an important role in the cardioprotective effect of normobaric hypoxia.</description><identifier>ISSN: 0007-4888</identifier><identifier>EISSN: 1573-8221</identifier><identifier>DOI: 10.1007/s10517-023-05696-3</identifier><identifier>PMID: 36723734</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Analysis ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Coronary artery ; General Pathology and Pathological Physiology ; Heart ; Hemoglobin ; Hypoxia ; Internal Medicine ; Ischemia ; Laboratory Medicine ; Male ; Myocardial Infarction ; Myocardial Reperfusion Injury - drug therapy ; NG-Nitroarginine methyl ester ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide Synthase ; Pathology ; Physiology ; Rats ; Rats, Wistar ; Reperfusion</subject><ispartof>Bulletin of experimental biology and medicine, 2023, Vol.174 (3), p.304-307</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2023. 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S.</creatorcontrib><creatorcontrib>Maslov, L. N.</creatorcontrib><creatorcontrib>Derkachev, I. A.</creatorcontrib><title>The Role of NO Synthase in the Infarct-Limiting Effect of Urgent and Chronic Adaptation to Normobaric Hypoxia</title><title>Bulletin of experimental biology and medicine</title><addtitle>Bull Exp Biol Med</addtitle><addtitle>Bull Exp Biol Med</addtitle><description>We studied the role of NO synthase in the infarct-limiting effect of short-term (SNH) and chronic continuous normobaric hypoxia (CNH). In male Wistar rats, SNH (6 sessions of 10-min hypoxia 8% O2 and 10-min reoxygenation) or CNH (12% O2 for 21 days) was modeled. In 30 min after SNH or 24 h after CNH, the rats were subjected to coronary artery occlusion (45 min) and reperfusion (2 h). The following drugs were administered to rats: non-selective NO synthase inhibitor L-NAME (10 mg/kg), inhibitor of inducible NO synthase S-methylthiourea (3 mg/kg), and inhibitor of neuronal NO-synthase 7-nitroindazole (50 mg/kg). NO donor diethylenetriamine was administered intravenously in a dose 2 mg/kg. It was found that L-NAME and S-methylthiourea abolished the infarct-limiting effect of SNH and CNH. Diethylenetriamine increased cardiac tolerance to ischemia/reperfusion. 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The following drugs were administered to rats: non-selective NO synthase inhibitor L-NAME (10 mg/kg), inhibitor of inducible NO synthase S-methylthiourea (3 mg/kg), and inhibitor of neuronal NO-synthase 7-nitroindazole (50 mg/kg). NO donor diethylenetriamine was administered intravenously in a dose 2 mg/kg. It was found that L-NAME and S-methylthiourea abolished the infarct-limiting effect of SNH and CNH. Diethylenetriamine increased cardiac tolerance to ischemia/reperfusion. It is believed that inducible NO synthase plays an important role in the cardioprotective effect of normobaric hypoxia.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36723734</pmid><doi>10.1007/s10517-023-05696-3</doi><tpages>4</tpages></addata></record> |
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| subjects | Analysis Animals Biomedical and Life Sciences Biomedicine Cell Biology Coronary artery General Pathology and Pathological Physiology Heart Hemoglobin Hypoxia Internal Medicine Ischemia Laboratory Medicine Male Myocardial Infarction Myocardial Reperfusion Injury - drug therapy NG-Nitroarginine methyl ester NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide Synthase Pathology Physiology Rats Rats, Wistar Reperfusion |
| title | The Role of NO Synthase in the Infarct-Limiting Effect of Urgent and Chronic Adaptation to Normobaric Hypoxia |
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