Effect of SWL on renal hemodynamics: could a change in renal artery contraction-relaxation responses be the cause?

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dc.contributor.authorYilmaz, Erdal
dc.contributor.authorMert, Cagatay
dc.contributor.authorKeskil, Zuhal
dc.contributor.authorTuglu, Devrim
dc.contributor.authorBatislam, Ertan
dc.date.accessioned2020-06-25T17:52:25Z
dc.date.available2020-06-25T17:52:25Z
dc.date.issued2012
dc.departmentKırıkkale Üniversitesi
dc.descriptionBatislam, Ertan/0000-0002-7493-4573;
dc.description.abstractThe aim of this study was to reveal the effect of shock wave lithotripsy (SWL) on renal artery contraction-relaxation responses and the relation of this effect with renal hemodynamics. Twenty-four rabbits are divided into six different groups. The first two groups evaluated as the control groups. After isolating the kidneys, we applied phenylephrine (Ph) and acetylcholine (Ach) in the first group and sodium nitroprusside (SNP) and histamine (H) in the second group. In the third, fourth, fifth and sixth groups, 14.5 kV shock wave (SW) was focused on the left kidneys. We adjusted the number of shocks to a total of 500, 1,500, and 3,000 SW, in the third, fourth and fifth groups, respectively. After isolating the kidneys, Ph, Ach was given in groups 3, 4 and 5. In the sixth group, to get the SNP and the H responses, 3,000 shocks modality was utilized. Marked contractile responses were obtained by phenylephrine in the control group. In kidneys that were exposed to 500 shocks SWL procedures, a decrease in contractile responses and hence, in perfusion pressures in different concentrations of phenylephrine was noted. However, a notable change in relaxation responses occurred after 3,000-shock applications. No difference in relaxation responses to nitroprusside, a direct vasodilating agent, was observed in any group, compared to the control group. Another cause of deterioration of renal hemodynamics after SWL can be attributed to the reduction in renal artery contraction-relaxation responses that result in the vascular smooth muscle and endothelial damage.en_US
dc.identifier.citationclosedAccessen_US
dc.identifier.doi10.1007/s00240-012-0504-0
dc.identifier.endpage780en_US
dc.identifier.issn0300-5623
dc.identifier.issue6en_US
dc.identifier.pmid22945811
dc.identifier.scopus2-s2.0-84874114290
dc.identifier.scopusqualityN/A
dc.identifier.startpage775en_US
dc.identifier.urihttps://doi.org/10.1007/s00240-012-0504-0
dc.identifier.urihttps://hdl.handle.net/20.500.12587/5155
dc.identifier.volume40en_US
dc.identifier.wosWOS:000310965700019
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringeren_US
dc.relation.ispartofUrological Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectSWLen_US
dc.subjectRenal arteryen_US
dc.subjectContractionen_US
dc.subjectDilatationen_US
dc.subjectResponseen_US
dc.subjectRenal damageen_US
dc.titleEffect of SWL on renal hemodynamics: could a change in renal artery contraction-relaxation responses be the cause?en_US
dc.typeArticle

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