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2007 | 63 | 08 |

Tytuł artykułu

Influence of bradykinin on the course of ischemia-reperfusion syndrome

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Acute ischemia and the subsequent reperfusion caused by temporary closure of blood flow in the main arteries, which activate generalized inflammatory response, lead to endothelial injury. The aim of the study was to examine the injury of tissues in the ischemia reperfusion syndrome. Additionally, we tried to estimate the role of B1 and B2 bradykinin-receptor antagonists. In our study we histologically assessed specimens of lungs, kidney, liver, small and large intestine and skeletal muscle from the thigh. We compared the samples obtained from the groups of animals that were exposed to 4 hours of complete ischemia and 120 minutes of reperfusion. We divided animals into 4 groups. Rats in the first group were the control group, animals from the second received bradykinin. In the third and fourth group respectively bradykinin along with B2 and B1 bradykinin-receptor antagonist were administered. The results of microscopic examination revealed that bradykinin exerts a protective effect on the function and structure of distant organs as well as the skeletal muscle which was subjected to ischemia and reperfusion. The most visible effects of bradykinin were found in the samples of the lung, skeletal muscle, and the large and small intestines. Administration of bradykinin receptor antagonists, especially B2 receptor blocker, reduces the advantageous effects of bradykinin. The conclusion of our study is that administration of bradykinin may be beneficial in diseases accompanied by limb ischemia where tissue blood flow and oxygen metabolism are dependent upon kinin release, which in turn will condition tissue repair.

Wydawca

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Rocznik

Tom

63

Numer

08

Opis fizyczny

p.914-918,fig.,ref.

Twórcy

autor
  • K.Marcinkowski University of Medical Sciences, Swiecickiego 6, 60-781 Poznan, Poland
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Bibliografia

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  • 9. Li Y., Sato T.: Dual signaling via protein kinase C and phosphatidyl-inositol 3-kinase/Akt contributes to bradykinin B2 receptor-induced cardioprotection in guinea pig hearts. J. Mol. Cell. Cardiol. 2001, 33, 2047-2048.
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Typ dokumentu

Bibliografia

Identyfikatory

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