| 000 | 03519nlm1a2200457 4500 | ||
|---|---|---|---|
| 001 | 663259 | ||
| 005 | 20231030041848.0 | ||
| 035 | _a(RuTPU)RU\TPU\network\34428 | ||
| 035 | _aRU\TPU\network\31642 | ||
| 090 | _a663259 | ||
| 100 | _a20210203a2019 k y0engy50 ba | ||
| 101 | 0 | _aeng | |
| 135 | _adrcn ---uucaa | ||
| 181 | 0 | _ai | |
| 182 | 0 | _ab | |
| 200 | 1 |
_aCardioprotective Properties of Opioid Receptor Agonists in Rats WithStress-Induced Cardiac Injury _fE. S. Prokudina, L. N. Maslov, N. V. Naryzhnaya [et al.] |
|
| 203 |
_aText _celectronic |
||
| 300 | _aTitle screen | ||
| 330 | _aThe objectives of this study were to investigate the role of endogenous opioids in the mediation of stress-induced cardiomyopathy (SIC), and to evaluate which opioid receptors regulate heart resistance to immobilization stress. Wistar rats were subjected to 24 h immobilization stress. Stress-induced heart injury was assessed by 99mTc-pyrophosphate accumulation in the heart. The opioid receptor (OR) antagonists (naltrexone, NxMB - naltrexone methyl bromide, MR 2266, ICI 174.864) and agonists (DALDA, DAMGO, DSLET, U-50,488) were administered intraperitoneally prior to immobilization and 12 h after the start of stress. In addition, the selective µ OR agonists PL017 and DAMGO were administered intracerebroventricularly prior to stress. Finally pretreatment with guanethidine was used. Naltrexone did not alter the cardiac 99mTc-PP accumulation in stressed rats. NxMB aggravated stress-induced cardiomyopathy (P=0.005) (SIC). The selective µ OR agonist DALDA, which does not cross the blood-brain barrier, completely prevented (P=0.006) SIC. The µ OR agonist DAMGO exhibited weaker effect than DALDA. The selective δ ligand (DSLET) and κ OR ligand (U-50,488) did not alter stress-induced 99mTc-pyrophosphate accumulation in the heart. Intracerebroventricular administration of the µ OR agonists aggravated SIC. Pretreatment with guanethidine abolished this effect (P=0.01). Guanethidine alone exhibited cardioprotective properties. A stimulation of central µ OR promotes an appearance of SIC. In contrast, stimulation of peripheral µ OR contributes to an increase in cardiac tolerance to stress. | ||
| 461 | _tPhysiological Research | ||
| 463 |
_tVol. 68, iss. 3 _v[P. 375-384] _d2019 |
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| 610 | 1 | _aэлектронный ресурс | |
| 610 | 1 | _aтруды учёных ТПУ | |
| 610 | 1 | _a99mTc-pyrophosphate | |
| 610 | 1 | _aopioid receptors | |
| 610 | 1 | _atako-tsubo syndrome | |
| 610 | 1 | _astress | |
| 610 | 1 | _acardiomyopathy | |
| 610 | 1 | _aопиоиды | |
| 610 | 1 | _aстресс | |
| 701 | 1 |
_aProkudina _bE. S. _gEkaterina Sergeevna |
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| 701 | 1 |
_aMaslov _bL. N. _gLeonid Nikolaevich |
|
| 701 | 1 |
_aNaryzhnaya _bN. V. _gNataliya Vladimirovna |
|
| 701 | 1 |
_aTsybulnikov _bS. Yu. _gSergey Yurjevich |
|
| 701 | 1 |
_aLishmanov _bYu. B. _cspecialist in the field of medical technology _clead engineer aof Tomsk Polytechnic University, doctor of medical sciences _f1951- _gYury Borisovich _2stltpush _3(RuTPU)RU\TPU\pers\34200 |
|
| 701 | 1 |
_aMadias _bJ. E. _gJohn |
|
| 701 | 1 |
_aOeltgen _bP. R. _gPeter |
|
| 712 | 0 | 2 |
_aНациональный исследовательский Томский политехнический университет _bФизико-технический институт _bЛаборатория № 31 ядерного реактора _h6471 _2stltpush _3(RuTPU)RU\TPU\col\20054 |
| 801 | 2 |
_aRU _b63413507 _c20210203 _gRCR |
|
| 856 | 4 | _uhttps://doi.org/10.33549/physiolres.933946 | |
| 942 | _cCF | ||