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2014 | 68 | 2 | 94–100
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Udział układu histaminergicznego w działaniu resuscytacyjnym wywołanym pobudzeniem ośrodkowych receptorów melanokortynowych typu 4 u szczurów we wstrząsie krwotocznym

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Involvement of the histaminergic system in the central melanocortin type 4 receptors stimulation-induced resuscitating effect in haemorrhagic shock in rats
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EN
INTRODUCTION Central cardiovascular regulation in haemorrhagic shock is influenced by many neuronal systems, including the melanocortinergic and histaminergic systems. The aim of the study was to examine the involvement of the his-taminergic system in the resuscitating effect of melanocortin type 4 (MC4) receptor agonist Ro 27-3225. MATERIALS AND METHODS Studies were carried out on male Wistar rats subjected to irreversible haemorrhagic shock with a mean arterial pressure (MAP) of 20–25 mmHg. In the 5th minute of critical hypotension, the animals were injected intracere-broventricularly (icv) with Ro 27-3225 or a 0.9% NaCl solution (control group). RESULTS Hypovolaemia was accompanied by a decrease in pulse pressure (PP), heart rate (HR) and renal blood flow (RBF). In the control group, there were no increases in the measured parameters, and a survival rate of 2 h was 0%. Ro 27-3225 (10 nmol, icv) evoked long-lasting rises in MAP, PP and RBF as well as 100% survival at 2 h. Pre-treatment with histamine H1 receptor antagonist chlorpheniramine (50 nmol, icv) inhibited Ro 27-3225-induced increases in MAP, PP and RBF, with no influence on HR and survival at 2 h (100%). In contrast, the antagonists of H2 and H3/4 receptors – ranitidine (50 nmol, icv) and thioperamide (25 nmol, icv), respectively, had no influence on the Ro 27-3225 action. In the control groups, histamine receptor antagonists given alone did not affect the measured parameters in comparison to the saline-treated group. CONCLUSIONS The histaminergic system participates in the resuscitating effect induced by the activation of central MC4 receptors in haemorrhagic shock in rats, and histamine H1 receptors are involved.
PL
WSTĘP Ośrodkowa regulacja układu krążenia we wstrząsie krwotocznym podlega wpływom wielu układów neuronalnych, w tym melanokortynergicznego i histaminergicznego. Celem pracy było zbadanie udziału układu histaminergicznego w efekcie resuscytacyjnym wywoływanym przez agonistę receptorów melano-kortynowych typu 4 (MC4) Ro 27-3225. MATERIAŁ I METODY Badania zostały przeprowadzone u szczurów samców szczepu Wistar, z wykorzystaniem modelu nieodwracalnego wstrząsu krwotocznego, polegającego na wywołaniu kontrolowanego krwawienia, aż do stabilizacji średniego ciśnienia tętniczego (mean arterial pressure – MAP) na poziomie 20–25 mmHg. W 5 min krytycznej hipotensji do komory bocznej mózgu (icv) podawano Ro 27-3225 bądź 0,9% roztwór NaCl (grupa kontrolna). WYNIKI Hipowolemii towarzyszyło zmniejszenie ciśnienia tętna (pulse pressure – PP), częstości rytmu serca (heart rate – HR) oraz nerkowego przepływu krwi (renal blood flow – RBF). W grupie kontrolnej nie stwierdzono wzrostów wartości badanych parametrów, a wskaźnik przeżycia 2 h wynosił 0%. Ro 27-3225 (10 nmol, icv) wywoływał długotrwały wzrost MAP, PP i RBF, a także zwięk-szenie do 100% wskaźnika przeżycia 2 h. Premedykacja antagonistą receptorów histaminowych H1, chlorfenyraminą (50 nmol, icv), hamowała wzrosty MAP, PP i RBF wywoływane przez Ro 27-3225, nie wpływała natomiast na HR i wskaźnik przeżycia 2 h (100%). Antagoniści receptorów histaminowych H2 i H3/4 – ranitydyna (50 nmol, icv) i tioperamid (25 nmol, icv) nie mieli wpływu na efekty działania Ro 27-3225. W grupach kontrolnych antagoniści receptorów histaminowych podawani oddzielnie nie wpływali na badane parametry układu krążenia w porównaniu z grupą kontrolną. WNIOSKI Układ histaminergiczny uczestniczy w działaniu resuscytacyjnym wynikającym z pobudzenia ośrodkowych receptorów MC4 u szczurów we wstrząsie krwotocznym, co związane jest z aktywacją receptorów histaminowych H1.
Discipline
Year
Volume
68
Issue
2
Pages
94–100
Physical description
References
  • 1. Schadt J.C., Ludbrook J. Hemodynamic and neurohumoral responses to acute hypovolemia in conscious mammals. Am. J. Physiol. 1991; 260: H305––H318.
  • 2. Bertolini A. The opioid/anti-opioid balance in shock: a new target for therapy in resuscitation. Resuscitation 1995; 30: 29–42.
  • 3. Jochem J., Jośko J., Gwóźdź B. Endogenous opioid peptides system in haemorrhagic shock – central cardiovascular regulation. Med. Sci. Monit. 2001; 7: 545–549.
  • 4. Wikberg J.E., Muceniece R., Mandrika I. i wsp. New aspects on the melanocortins and their receptors. Pharmacol. Res. 2000; 42: 393– –420.
  • 5. Giuliani D., Mioni C., Bazzani C. i wsp. Selective melanocortin MC4 receptor agonist reverse haemorrhagic shock and prevent mulitple organ damage. Br. J. Pharmacol. 2007; 150: 595–603.
  • 6. Guarini S., Altavilla D., Cainazzo M.M. i wsp. Efferent vagal fibre stimulation blunt nuclear factor-kappa B activation and protects against hypovolemic hemorrhagic shock. Circulation 2003; 107: 1189–1194.
  • 7. Giuliani D., Ottani A., Altavilla D., Bazzani C., Squadrito F., Guarini S. Melanocortins and the cholinergic anti-inflammatory pathway. Adv. Exp. Med. Biol. 2010; 681: 71–87.
  • 8. Jochem J. Cardiovascular effects of histamine administered intracere-broventricularly in critical haemorrhagic hypotension in rats. J. Physiol. Pharmacol. 2000; 51: 229–239.
  • 9. Wada H., Inagaki N., Yamatodani A., Watanabe T. Is the histaminergic neuron system a regulatory center for whole-brain activity? Trends Neurosci. 1991; 14: 415–418.
  • 10. Jochem J. Involvement of the sympathetic nervous system in the reversal of critical haemorrhagic hypotension by endogenous central histamine in rats. Naunyn-Schmiedeberg’s Arch. Pharmacol. 2004; 369: 418–427.
  • 11. Jochem J. Involvement of the renin-angiotensin system in central histamine-induced reversal of critical haemorrhagic hypotension in rats. J. Physiol. Pharmacol. 2004; 55: 39–55.
  • 12. Jochem J. Involvement of arginine vasopressin in endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats. Inflamm. Res. 2004; 53: 269–276.
  • 13. Jochem J. Involvement of proopiomelanocortin-derived peptides in endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats. J. Physiol. Pharmacol. 2004; 55: 57–71.
  • 14. Jochem J., Rybczyk R., Irman-Florjanc T., Żwirska-Korczala K., Ni-wecka A. Central serotonin-induced pressor effect in rats is mediated in part via the histaminergic system. Inflamm. Res. 2008; 57(Suppl. 1): S35–S36.
  • 15. Guarini S., Bazzani C., Cainazzo M.M. i wsp. Evidence that melano-cortin 4 receptor mediates hemorrhagic shock reversal caused by melano-cortin peptides. J. Pharmacol. Exp. Ther. 1999; 291: 1023–1027.
  • 16. Kauvar D.S., Lefering R., Wade C.E. Impact of hemorrhage on trauma outcome: an overview of epidemiology, clinical presentations, and therapeutic considerations. J. Trauma 2006; 60(6 Suppl.): S3–S11.
  • 17. Lonati C., Sordi A., Giuliani D. i wsp. Molecular changes induced in rat liver by hemorrhage and effects of melanocortin treatment. Anesthesiology 2012; 116: 692–700.
  • 18. Finch L. Hicks P.E. The cardiovascular effects of intraventricularly administered histamine in the anaesthetised rat. Naunyn-Schmiedeberg’s Arch. Pharmacol. 1976; 293: 151–157.
  • 19. Poulakos J.J., Gertner S.B. Studies on the cardiovascular actions of central histamine H1 and H2 receptors. J. Pharmacol. Exp. Ther. 1989; 250: 500–507.
  • 20. Jochem J. Central histamine-induced reversal of critical haemorrhagic hypotension in rats – haemodynamic studies. J. Physiol. Pharmacol. 2002; 53: 75–84.
  • 21. Jochem J. Haematological, blood gas and acid-base effects of central histamine-induced reversal of critical haemorrhagic hypotension in rats. J. Physiol. Pharmacol. 2001; 52: 447–458.
  • 22. Jochem J. Central histamine-induced reversal of haemorrhagic shock versus volume resuscitation in rats. Inflamm. Res. 2002; 51(Suppl. 1): S57–S58.
  • 23. Brown R.E., Stevens D.R., Haas H.L. The physiology of brain hista-mine. Prog. Neurobiol. 2001; 63: 637–672.
  • 24. Fekete C., Liposits Z. Histamine-immunoreactive neurons of the tuber-omammillary nucleus are innervated by alpha-melanocyte stimulating hor-mone-containing axons. Generation of a new histamine antiserum for ultra-structural studies. Brain Res. 2003; 969: 70–77.
  • 25. Jochem J., Savci V., Filiz N., Rybus-Kalinowska B., Fogel W.A., Yalcin M. Involvement of the histaminergic system in cytidine 5'-diphosphocholine-induced reversal of critical haemorrhagic hypotension in rats. J. Physiol. Pharmacol. 2010; 61: 37–43.
  • 26. Jochem J., Zak A., Rybczyk R., Irman-Florjanc T. Interactions between the serotonergic and histaminergic systems in the central cardiovascular regulation in haemorrhage-shocked rats: involvement of 5-HT(1A) receptors. Inflamm. Res. 2009; 58(Suppl. 1): 38–40.
  • 27. Altinbas B., Topuz B.B., Yilmaz M.S. i wsp. The mediation of the central histaminergic system in the pressor effect of intracerebroventricularly injected melittin, a phospholipase A2 activator, in normotensive rats. Prosta-glandins Leukot. Essent. Fatty Acids 2012; 87: 153–158.
  • 28. Jochem J., Zwirska-Korczala K. Interactions between the histaminergic and opioidergic systems in the central cardiovascular regulation – haemody-namic studies. Inflamm. Res. 2004; 53(Suppl. 1): S63–S64.
  • 29. Jochem J., Zwirska-Korczala K. Involvement of central noradrenergic system in the pressor effect of histamine administered intracerebroventricular-ly in rats-haemodynamic studies. Inflamm. Res. 2002; 51(Suppl. 1): S59–S60.
  • 30. Jochem J., Zwirska-Korczala K., Sowa P., Berdowska A. Interactions between the histaminergic and angiotensinergic systems in the central cardio-vascular regulation in rats. Inflamm. Res. 2006; 55(Suppl. 1): S69–S70.
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