Acute and Chronic Pretreatment With Atenolol Attenuates Intestinal Ischemia and Reperfusion Injury in Hypercholesterolemic Rats

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dc.contributor.authorÖztürk T.
dc.contributor.authorVural K.
dc.contributor.authorTuğlu İ.
dc.contributor.authorVar A.
dc.contributor.authorKurdal T.
dc.contributor.authorAydemir I.
dc.date.accessioned2024-07-22T08:11:44Z
dc.date.available2024-07-22T08:11:44Z
dc.date.issued2016
dc.description.abstractObjective To evaluate the protective effects of preinjury atenolol (acute v chronic) on apoptosis, contractility, oxidative stress, and inflammatory markers in hypercholesterolemic rats undergoing intestinal ischemia-reperfusion (I/R) injury. Design Prospective, experimental animal study. Setting University laboratory. Participants Male Wistar rats (n = 32). Interventions Rats were divided into the following 4 groups: 1 group was fed a normal diet (ND) (group ND+NoAT [no atenolol]), and the other 3 groups were fed a high-cholesterol diet (HCD)—group HCD+NoAT, group HCD+ChAT (chronic atenolol, 3 mg/kg/day for 8 weeks), and group HCD+AcAT (acute atenolol, 1.5 mg/kg, given 5 minutes before intestinal clamping). All rats underwent I/R injury. The superior mesenteric artery was clamped for 60 minutes, then opened for 120 minutes (reperfusion). Apoptotic cells and stimulated contractions of ileal segments were examined. Tissue markers of intestinal I/R injury were examined. Intestinal malondialdehyde, superoxide dismutase, and nitrate/nitrite levels were measured. Measurements and Main Results The chronic atenolol group had fewer apoptotic cells and higher superoxide dismutase activity compared with the other groups. Intestinal contraction was higher in both atenolol pretreatment groups compared with the NoAT groups. Chronic and acute atenolol resulted in lower ileal levels of malondialdehyde and immunolabeling-positive cells (intestinal inducible nitric oxide synthase, endothelial nitric oxide synthase, interleukin-1, and interleukin-8) after I/R injury compared with the no atenolol groups. Conclusions Both chronic and acute pre-I/R injury treatment with atenolol attenuated I/R injury in this hypercholesterolemic rat model. These findings should encourage future studies of atenolol in hypercholesterolemic patients undergoing procedures with a high risk of intestinal ischemia. © 2016 Elsevier Inc.
dc.identifier.DOI-ID10.1053/j.jvca.2016.03.140
dc.identifier.issn10530770
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/15769
dc.language.isoEnglish
dc.publisherW.B. Saunders
dc.subjectAdrenergic beta-1 Receptor Antagonists
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectAtenolol
dc.subjectDisease Models, Animal
dc.subjectHypercholesterolemia
dc.subjectInflammation
dc.subjectIntestines
dc.subjectMale
dc.subjectOxidative Stress
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReperfusion Injury
dc.subjectatenolol
dc.subjectcholesterol
dc.subjectendothelial nitric oxide synthase
dc.subjectinducible nitric oxide synthase
dc.subjectinterleukin 1
dc.subjectinterleukin 8
dc.subjectmalonaldehyde
dc.subjectnitrate
dc.subjectnitrite
dc.subjectsuperoxide dismutase
dc.subjectatenolol
dc.subjectbeta 1 adrenergic receptor blocking agent
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectArticle
dc.subjectcholesterol blood level
dc.subjectcontrolled study
dc.subjectdrug efficacy
dc.subjectenzyme activity
dc.subjecthypercholesterolemia
dc.subjectintestine contraction
dc.subjectintestine ischemia
dc.subjectmale
dc.subjectnonhuman
dc.subjectoutcome assessment
dc.subjectpriority journal
dc.subjectprospective study
dc.subjectrat
dc.subjectreperfusion injury
dc.subjectanimal
dc.subjectapoptosis
dc.subjectcomplication
dc.subjectdisease model
dc.subjectdrug effects
dc.subjecthypercholesterolemia
dc.subjectinflammation
dc.subjectintestine
dc.subjectoxidative stress
dc.subjectpathophysiology
dc.subjectreperfusion injury
dc.subjectWistar rat
dc.titleAcute and Chronic Pretreatment With Atenolol Attenuates Intestinal Ischemia and Reperfusion Injury in Hypercholesterolemic Rats
dc.typeArticle

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