Effect of Chronic Continuous Normobaric Hypoxia on Functional State of Cardiac Mitochondria and Tolerance of Isolated Rat Heart to Ischemia and Reperfusion: Role of µ and delta2 Opioid Receptors; Physiological Research; Vol. 68, iss. 6
| Parent link: | Physiological Research Vol. 68, iss. 6.— 2019.— [P. 909-920] |
|---|---|
| Institutionell upphovsman: | |
| Övriga upphovsmän: | , , , , , , , , , , , |
| Sammanfattning: | Title screen Chronic continuous normobaric hypoxia (CNH) increases cardiac tolerance to ischemia/reperfusion injury in vivo and this effect is mediated via µ and delta2 opioid receptors (ORs) activation. CNH has also been shown to be cardioprotective in isolated rat heart. In this study, we hypothesize that this cardioprotective effect of CNH is mediated by activation of µ and delta2 ORs and preservation of mitochondrial function. Hearts from rats adapted to CNH (12 % oxygen) for 3 weeks were extracted, perfused in the Langendorff mode and subjected to 45 min of global ischemia and 30 min of reperfusion. Intervention groups were pretreated for 10 min with antagonists for different OR types: naloxone (300 nmol/l), the selective delta OR antagonist TIPP(psi) (30 nmol/l), the selective delta1 OR antagonist BNTX (1 nmol/l), the selective delta2 OR antagonist naltriben (1 nmol/l), the selective peptide µ OR antagonist CTAP (100 nmol/l) and the selective delta OR antagonist nor-binaltorphimine (3 nmol/l). Creatine kinase activity in coronary effluent and cardiac contractile function were monitored to assess cardiac injury and functional impairment. Additionally, cardiac tissue was collected to measure ATP and to isolate mitochondria to measure respiration rate and calcium retention capacity. Adaptation to CNH decreased myocardial creatine kinase release during reperfusion and improved the postischemic recovery of contractile function. Additionally, CNH improved mitochondrial state 3 and uncoupled respiration rates, ADP/O, mitochondrial transmembrane potential and calcium retention capacity and myocardial ATP level during reperfusion compared to the normoxic group. These protective effects were completely abolished by naloxone, TIPP(psi), naltriben, CTAP but not BNTX or nor-binaltorphimine. These results suggest that cardioprotection associated with adaptation to CNH is mediated by µ and delta2 opioid receptors activation and preservation of mitochondrial function. |
| Språk: | engelska |
| Publicerad: |
2019
|
| Ämnen: | |
| Länkar: | https://doi.org/10.33549/physiolres.933945 |
| Materialtyp: | Elektronisk Bokavsnitt |
| KOHA link: | https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=663835 |
MARC
| LEADER | 00000naa0a2200000 4500 | ||
|---|---|---|---|
| 001 | 663835 | ||
| 005 | 20250505170012.0 | ||
| 035 | |a (RuTPU)RU\TPU\network\35005 | ||
| 090 | |a 663835 | ||
| 100 | |a 20210312d2019 k||y0rusy50 ba | ||
| 101 | 0 | |a eng | |
| 135 | |a drcn ---uucaa | ||
| 181 | 0 | |a i | |
| 182 | 0 | |a b | |
| 200 | 1 | |a Effect of Chronic Continuous Normobaric Hypoxia on Functional State of Cardiac Mitochondria and Tolerance of Isolated Rat Heart to Ischemia and Reperfusion: Role of µ and delta2 Opioid Receptors |f E. S. Prokudina, N. V. Naryzhnaya, A. V. Mukhomedzyanov [et al.] | |
| 203 | |a Text |c electronic | ||
| 300 | |a Title screen | ||
| 330 | |a Chronic continuous normobaric hypoxia (CNH) increases cardiac tolerance to ischemia/reperfusion injury in vivo and this effect is mediated via µ and delta2 opioid receptors (ORs) activation. CNH has also been shown to be cardioprotective in isolated rat heart. In this study, we hypothesize that this cardioprotective effect of CNH is mediated by activation of µ and delta2 ORs and preservation of mitochondrial function. Hearts from rats adapted to CNH (12 % oxygen) for 3 weeks were extracted, perfused in the Langendorff mode and subjected to 45 min of global ischemia and 30 min of reperfusion. Intervention groups were pretreated for 10 min with antagonists for different OR types: naloxone (300 nmol/l), the selective delta OR antagonist TIPP(psi) (30 nmol/l), the selective delta1 OR antagonist BNTX (1 nmol/l), the selective delta2 OR antagonist naltriben (1 nmol/l), the selective peptide µ OR antagonist CTAP (100 nmol/l) and the selective delta OR antagonist nor-binaltorphimine (3 nmol/l). Creatine kinase activity in coronary effluent and cardiac contractile function were monitored to assess cardiac injury and functional impairment. Additionally, cardiac tissue was collected to measure ATP and to isolate mitochondria to measure respiration rate and calcium retention capacity. Adaptation to CNH decreased myocardial creatine kinase release during reperfusion and improved the postischemic recovery of contractile function. Additionally, CNH improved mitochondrial state 3 and uncoupled respiration rates, ADP/O, mitochondrial transmembrane potential and calcium retention capacity and myocardial ATP level during reperfusion compared to the normoxic group. These protective effects were completely abolished by naloxone, TIPP(psi), naltriben, CTAP but not BNTX or nor-binaltorphimine. These results suggest that cardioprotection associated with adaptation to CNH is mediated by µ and delta2 opioid receptors activation and preservation of mitochondrial function. | ||
| 461 | |t Physiological Research | ||
| 463 | |t Vol. 68, iss. 6 |v [P. 909-920] |d 2019 | ||
| 610 | 1 | |a электронный ресурс | |
| 610 | 1 | |a труды учёных ТПУ | |
| 610 | 1 | |a continuous normobaric hypoxia | |
| 610 | 1 | |a heart | |
| 610 | 1 | |a ischemia | |
| 610 | 1 | |a reperfusion | |
| 610 | 1 | |a mitochondria | |
| 610 | 1 | |a opioid receptors | |
| 610 | 1 | |a сердце | |
| 610 | 1 | |a ишемия | |
| 610 | 1 | |a опиоиды | |
| 701 | 1 | |a Prokudina |b E. S. |g Elena Sergeevna | |
| 701 | 1 | |a Naryzhnaya |b N. V. |g Nataliya Vladimirovna | |
| 701 | 1 | |a Mukhomedzyanov |b A. V. |g Aleksandr Valerjevich | |
| 701 | 1 | |a Gorbunov |b A. S. |g Aleksandr Sergeevich | |
| 701 | 0 | |a Zhang Yu | |
| 701 | 1 | |a Yaggi |b A. S. |g Amteshwar Singh | |
| 701 | 1 | |a Tsibulnikov |b S. Yu. |c specialist in the field of medical technology |c Senior Lecturer of Tomsk Polytechnic University, Candidate of medical Sciences |f 1986- |g Sergey Yurjevich |3 (RuTPU)RU\TPU\pers\36547 | |
| 701 | 1 | |a Nesterov |b E. A. |c Physicist, Specialist in the field of nuclear power engineering |c Researcher of Tomsk Polytechnic University |f 1976- |g Evgeny Alexandrovich |3 (RuTPU)RU\TPU\pers\32657 |9 16556 | |
| 701 | 1 | |a Lishmanov |b Yu. B. |c specialist in the field of medical technology |c lead engineer aof Tomsk Polytechnic University, doctor of medical sciences |f 1951- |g Yury Borisovich |3 (RuTPU)RU\TPU\pers\34200 | |
| 701 | 1 | |a Suleiman |b M. S. | |
| 701 | 1 | |a Oeltgen |b P. R. |g Peter | |
| 701 | 1 | |a Maslov |b L. N. |g Leonid Nikolaevich | |
| 712 | 0 | 2 | |a Национальный исследовательский Томский политехнический университет |b Физико-технический институт |b Лаборатория № 31 ядерного реактора |3 (RuTPU)RU\TPU\col\20054 |
| 801 | 2 | |a RU |b 63413507 |c 20210312 |g RCR | |
| 850 | |a 63413507 | ||
| 856 | 4 | |u https://doi.org/10.33549/physiolres.933945 | |
| 942 | |c CF | ||