Українська Русский English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2012; 58(6): 57-66


Effect of hydrogen sulfide on isolated rat heart reaction under volume load and ischemia-reperfusion

Shymans'ka TV, Hoshovs'ka IuV, Semenikhina OM, Sahach VF.

    O.O. Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
DOI: https://doi.org/10.15407/fz58.06.057

Abstract

The present study was aimed to investigate the effect of H2S donor (NaHS) on heart function in conditions of functional loads and ischemia-reperfusion (I/R) injury by using Lan-gendorf isolated heart perfusion. NaHS (“Sigma”, 7,4 mg per kg) was dissolved in physiological solution and injected intraperitoneally 30 min before experiment. Rat isolated hearts were Langendorf-perfused and subjected to 20-minute non-fow ischemia followed by 40-minute reperfusion. The heart function was assessed by measuring the LVDP, dP/dt, coronary fow, heart rate. The opening of mitochondria permeability transition (MPT) pore was estimated by releasing of a stable factor with UV absorbance (lambda-max 250 nm) into the coronary out-fow probes during the initial phase of reperfusion. The results showed that NaHS pretreated hearts developed greater LVDP without decreasing of dP/dt min in response to an increase of left ventricle volume indicating greater functional reserves and effectiveness of Frank-Starling low realization. NaHS increased cardiac mitochondrial membrane potential but did not changed UCP3 gene expression. Signifcant post-ischemic recover of heart function in NaHS group was accompanied with tiny quantity of mitochondrial factor releasing comparing to I/R group (p<0.001). Thus, NaHS do provides cardioprotec-tive effect by inhibition of MPT pore opening.

Keywords: hydrogen sulfide, isolated heart, Frank-Starlinglow, ischemia-reperfusion, mitochondrial permeability transitionpore, uncoupling proteins, mitochondrial membranepotential.

References

  1. Abramochkin DV, Moiseenko LS, Kuzmin VS. Influence of hydrogen sulfide on the electrical activity of the atrial myocardium of a rat . Bul.Experim. biology and medicine. 2009. 147, N 6. pp. 617-620. CrossRef PubMed
  2.  
  3. Goshovskaya Yu.V., Shimanska TV, Sagach VF. The use of genipin, an inhibitor of cleavage proteins, suppresses the effect of ischemic preconditioning . Physiol. . 2011. 56, N 6. P. 38-45.
  4.  
  5. Sagach VF, Shimanska TV, Nadtochy SM. The factor released during reperfusion of the ischemic heart may be a marker of mitochondrial pore opening . Ibid. 2003. 49, N 4. P. 6-12.
  6.  
  7. Strutinskaya NA, Semenikhina OM, Chorna SV, Vavilova GL, Sagach VF. Hydrogen sulfide suppresses calcium-induced opening of the mitochondrial pore in the heart of adults and old rats . Ibid. 2011. 57, N 6. P. 3-13.
  8.  
  9. Al-Magableh M. R., Hart J. L. Mechanism of vasorelaxa-tion and role of endogenous hydrogen sulfde production in mouse aorta . Naunyn Schmiedebergs Arch. Pharmacol. 2011. 383. P. 403-413. CrossRef PubMed
  10.  
  11. Bian J.S., Yong Q.C., Pan T.T., Feng Z.N., Ali M.Y., Zhou S., Moore P.K. Role of hydrogen sulfde in the cardiopro-tection caused by ischemic preconditioning in the rat heart and cardiac myocytes . J. Pharmacol. Exp. Ther. 2006 316. P. 670-678. CrossRef PubMed
  12.  
  13. Borutaite V. , Mildaziene V. , Brown G.C., Brand M.D. Control and kinetic analysis of ischemia-damaged heart mitochondria: which parts of the oxidative phosphoryla-tion system are affected by ischemia? . Biochim. and Biophys. Acta 1995. 1272. R.154-158. CrossRef  
  14. Brand M.D. in Brown G.C., Cooper C.E., Editors, Bio-energetics: a practical approach. Oxford.: IRL Press. 1995. P. 39-62.
  15.  
  16. Chai W., Y. Wang, J.Y. Lin, X.D. Sun, L.N. Yao, Y.H. Yang, H. Zhao, W. Jiang, C.J. Gao, Q. Ding. Exogenous hydrogen sulfde protects against traumatic hemorrhagic shock via attenuation of oxidative stress . J. Surg. Res. 2011. 176, N 1. R. 210-219. CrossRef PubMed
  17.  
  18. Cheang W.S., Wong W.T., Shen B., Lau C.W., Tian X.Y., Tsang S.Y., Yao X., Chen Z.Y., Huang Y. 4-aminopyridine-sensitive K+ channels contributes to NaHS-induced mem­brane hyperpolarization and relaxation in the rat coronary artery . Vascul. Pharmacol. 2010. 53, N 3-4. P. 94-98. CrossRef PubMed
  19.  
  20. Elrod J.W., Calvert J.W., Morrison J., Doeller J.E., Kraus D.W.,Tao L, Jiao X, Scalia R., Kiss L., Szabo C. Hydrogen sulfde attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function . Proc. Natl. Acad. Sci. USA 2007. 104, N 39. P. 15560-15565. CrossRef PubMed PubMedCentral
  21.  
  22. Elrod J.W., Wong R., Mishra S., Vagnozzi R.J., Sakthievel B., Goonasekera S.A., Karch J., Gabel S., Farber J., Force T., Brown J.H., Murphy E., Molkentin J.D. Cyclophilin D controls mitochondrial pore-dependent Ca(2+) exchange, metabolic fexibility, and propensity for heart failure in mice.. J Clin Invest. 2010. 120, N 10. P.3680-3687. CrossRef PubMed PubMedCentral
  23.  
  24. Entman M.L., Michael L., Rossen R.D., Dreyer W.J., Anderson D.C., Taylor A.A., Smith C.W. Infammation in the course of early myocardial ischemia.FASEB J. 1991. 5. P. 2529-2537. CrossRef PubMed
  25.  
  26. Hausenloy DJ, Yellon DM. New directions for protecting the heart against ischaemia. reperfusion injury: targeting the reperfusion injury salvage kinase (RISK) pathway. Cardiovasc Res. 2004. 61. R.448-460. CrossRef PubMed
  27.  
  28. Hill B.C., Woon T.C., Nicholls P., Peterson J., Greenwood C., Thomson A.J. Interactions of sulphide other ligands with cytochrome c oxidase. An electron-paramagnetic-resonance study. .Biochem J. 1984. 24. R. 591-600. CrossRef PubMed PubMedCentral
  29.  
  30. Hosoki R., Matsuki N., Kimura H. The possible role of hydrogen sulfde as an endogenous smooth muscle relax­ant in synergy with nitric oxide . Biochem. and Biophys. Res. Commun. 1997. 237, N 3. P. 527-531. CrossRef PubMed
  31.  
  32. Gadalla M.M., Snyder S.H. Hydrogen sulfde as a gas-otransmitter . J. Neurochem. 2010. 113. R. 14-26. CrossRef PubMed PubMedCentral
  33.  
  34. Geng B., Chang L., Pan C., Qi Y., Zhao J., Pang Y., Du J., Tang C. Endogenous hydrogen sulfde regulation of myocardial injury induced by isoproterenol . Biochem. and Biophys. Res. Commun. 2004. 318. P. 756-763. CrossRef PubMed
  35.  
  36. Geng B., Yang J., Qi Y., Zhao J., Pang Y., Du J., Tang C. H2S generated by heart in rat and its effects on cardiac function . Ibid. 313, N 2. P. 362-368. CrossRef PubMed
  37.  
  38. Kamoun P. Endogenous production of hydrogen sulfde in mammals . Amino Acids. 2004. 26. P. 243-254. CrossRef PubMed
  39.  
  40. Lowicka E., Beltowski J. Hydrogen sulfde the third gas of interest for pharmacologists . Pharmacol. Reports. 2007. 59. P. 4-24.
  41.  
  42. Nadtochiy S.M., Tompkins A., Brookes P.S. Different mechanisms of mitochondrial proton leak in ischemia. reperfusion injury and precondition: implications for pathology and cardioprotection . Biochem. J. 2006. 395. R. 611-618. CrossRef PubMed PubMedCentral
  43.  
  44. Pan T.-T., Neo K. L., Hu L.-F., Yong Q. C., Bian J.-S. H2S preconditioning-induced PKC activation regulates intra-cellular calcium handling in rat cardiomyocytes .Amer. J. Physiol. Cell Physiol. 2008. 294, N 1. R. C169-C177. CrossRef PubMed
  45.  
  46. Sivarajah A., Collino M., Yasin M., Benetti E., Gallicchio M., Mazzon E., Cuzzocrea S., Fantozzi R., Thiemermann C. Anti-apoptotic and anti-infammatory effects of hy­drogen sulfde in a rat model of regional myocardial i. r . Shock. 2009. 31. P. 267-274. CrossRef PubMed
  47.  
  48. Sun Y., Tang C.S., Du J.B, Jin H.F. Hydrogen sulfde and vascular relaxation . Chin. Med. J. 2011. 124, N 22. P. 3816-3819.
  49.  
  50. Sun W.-H., Liu F., Chen Y., Zhu Y.-Ch. Hydrogen sulfde decreases the levels of ROS by inhibiting mitochondrial complex IV and increasing SOD activities in cardiomyo-cytes under ischemia. reperfusion.Biochem. and Biophys. Res. Commun. 2012. 421, N 2. R. 164-169. CrossRef PubMed
  51.  
  52. Van Zwieten P.A. Hydrogen sulphide: Not only foul smell­ing, but also pathophysiologically relevant . J. Hyperten. 2003. 21, N 10. P. 1819-1820. CrossRef PubMed
  53.  
  54. Wang, R. Signal transduction and the gasotransmitters. NO, CO and H2S in biology and medicine. Totowa: Humana press, 2004. 377 r.
  55.  
  56. Yong Q.C., Hu L-F., Wang S., Huang D., Bian J.S. Hydro­gen sulfde interacts with nitric oxide in the heart: possible involvement of nitroxyl . Cardiovascular. Res. 2010. 88, N 3. P.482-491. CrossRef PubMed
  57.  
  58. Zhao W., Zhang J., Lu Y., Wang R. The vasorelaxant ef­fect of H2S as a novel endogenous gaseous KAT P channel opener .EMBO J. 2001. 20. P. 6008-6016. CrossRef PubMed PubMedCentral
  59.  
  60. Zhao W., Wang R. H2S-induced vasorelaxation and underly­ing cellular and molecular mechanisms . Amer. J. Physiol. Heart. Circul. Physiol. 2002. 283. R. 474-480. CrossRef PubMed
  61.  
  62. Lu M., Zhao F.F., Tang J.J., Su C.J., Fan Y. , Ding J.H., Bian J.S., Hu G. The neuroprotection of hydrogen sulfde against MPTP-induced dopaminergic neuron degeneration involves uncoupling protein 2 rather than ATP-sensitive potassium channels . Antioxid. Redox. Signal. 2012. 17, N 6. R. 849-859. CrossRef PubMed PubMedCentral

© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2020.