Sertralin endotel hasarlı aortta kontraksiyonu etkiler mi?
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Dosyalar
Tarih
2023
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Necmettin Erbakan Üniversitesi Sağlık Bilimleri Enstitüsü
Erişim Hakkı
info:eu-repo/semantics/embargoedAccess
Özet
Selektif Serotonin Geri Alım İnhibitorü (SSRI) grubu antidepresan ilaçlar kardiyovasküler rahatsızlığı olan hastalarda yaygın olarak kullanılmaktadır. Ancak özellikle damar üzerindeki etkileri deneysel bir çalışmada araştırılmamıştır. Bu çalışmada sertralinin (SE) aort kontraksiyonu üzerine etkilerini hem sağlıklı hem de hasarlı sıçan aortu üzerinde araştırmayı amaçladık. Bu çalışmada 2 grup (n=24) halinde 24 Wistar albino rat kullanıldı. Grup 1; aort- sağlam endotel (n=12), grup 2 aorta- hasarlı endotel (n=12). İnen torasik aort, yetişkin Wistar albino sıçanın servikal dislokasyonundan sonra hızla izole edildi. Aort dokuları temizlendi ve 3-4 mm uzunluğunda halkalar halinde kesildi. Daha sonra halkalar, 37°C'de termoregüle edilmiş ve havalandırılmış (%95 O2 ve %5 CO2) Krebs-Henseleit solüsyonu içeren organ banyolarına yerleştirildi. Aort halkalarının izometrik gerilimindeki değişiklikler, dört kanallı bir kuvvet yer değiştirme transdüseri kullanılarak kaydedildi. Çalışmanın ilk bölümünde sağlam endotel halkaları, ikinci bölümünde ise mekanik olarak hasar görmüş endotel halkaları kullanıldı. Fenilefrin (FE 10-6M) uygulandı ve her iki grupta da kasılmalar kaydedildi. Daha sonra grup 1'e kümülatif (10-9-10-4 M) Sertralin (50 mg) verildi. Grup 2'de endoteli iğne ile yırtarak aort endotel hasarı oluşturuldu. Asetilkolin (Ach 10-6M) uygulanarak endotel hasarı kontrol edildikten sonra hasarlı stripler bir saat süreyle organ banyolarında yıkandı ve ikinci doz FE 10-6M verildi, ardından kümülatif olarak Sertralin (50 mg) verildi (10 -9-10-4 M) 2. gruba ve kasılmaları kaydedildi. Grup 1'e kümülatif (10-9-10-4 M) sertralin (50 mg) verildikten sonra ilk üç sertralin dozunda (10-9, 10-8, 10-7) spontan kasılmalarda belirgin inhibisyon saptandı. (p<0.05), geri kalan sertralin dozlarında kasılma inhibisyonu devam etti. Sertralin 10-6-5-4 de 10-9-8-7 doza göre kasılmalarda belirgin inhibisyon yaptı. Grup 2'de ikinci FE kasılmalarının inhibisyonu sertralin dozlarından sonra da devam etti ancak grup 1'e göre daha az anlamlıydı. Sertralin, sıçan izole aortunda FE kaynaklı düz kas kontraksiyonunu inhibe ettiği tespit edilmiştir. Endotel hasarlı aort dokusunda FE kaynaklı düz kas kontraksiyonları daha yavaş inhibe olmuştur. Endotel hasarı sonucunda aortta NO salınımı azalmış ve NO'ya bağlı vazodilatasyon etkinin de azaldığı düşünülmektedir. Sertralinin kardiyovasküler sistem üzerine olan etkilerinin daha iyi anlaşılması için ileri düzeyde araştırmalara ihtiyaç bulunmaktadır.
Selective Serotonin Reuptake Inhibitor (SSRI) group antidepressant drugs are widely used in patients with cardiovascular disorders. However, its effects on the veins have not been investigated in an experimental study. In this study, we aimed to investigate the effects of sertraline on aortic contraction in both healthy and damaged rat aorta. In this study we used 24 Wistar albino rats in 2 groups (n=24). Group 1; aorta- intact endothelium (n=12), group 2 aorta- damaged endothelium (n=12). The descending thoracic aorta was quickly isolated after cervical dislocation of adult Wistar albino rat. Aorta tissues were cleaned and sectioned into 3-4 mm long rings. Then the rings were placed in organ baths containing Krebs–Henseleit solution, which was thermoregulated at 370C and aerated (95 % O2 and 5% CO2). Changes in isometric tension of aorta rings were recorded using a four channel force displacement transducer. Endothelium intact rings were used in the first part of the study and mechanically damaged endothelial rings were used in the second part. Phenylephrine (PE 10-6 M) was applied and contractions were recorded in both groups. Then Sertraline (50 mg) was given cumulatively (10-9 -10-4 M) to group 1. In group 2 aorta injury was achieved by tearing the endothelium with a needle. After controlling endothelial damage by applying acetylcholine (Ach 10 -6M), all damaged strips were washed for one hour in organ baths and second dose of phenylephrine (PE 10-6 M) was administered, then Sertraline (50 mg) was given cumulatively (10-9 -10-4 M) to group 2 and contractions were recorded. After sertraline (50 mg) was given cumulatively (10-9 -10-4 M) to group 1, significant inhibition of spontaneous contractions was noticed in the first three doses of sertraline (10-9, 10-8, 10-7) (p<0.05), inhibition of contractions kept on in the rest of the sertraline doses. Sertraline 10-6 -5 -4 made also significant inhibition in contractions according to 10-9 -8 -7 doses. In group 2, inhibition of second PE contractions continued after sertraline doses, but it was less significant when compared with group 1. Sertraline was found to inhibit PE-induced smooth muscle contraction in rat isolated aorta. PE-induced smooth muscle contractions were inhibited more slowly in endothelium damaged aortic tissue. It is thought that as a result of endothelial damage, NO secretion in the aorta decreases and the vasodilation effect due to NO is also reduced. Further studies are needed to better understand the effects of sertraline on the cardiovascular system.
Selective Serotonin Reuptake Inhibitor (SSRI) group antidepressant drugs are widely used in patients with cardiovascular disorders. However, its effects on the veins have not been investigated in an experimental study. In this study, we aimed to investigate the effects of sertraline on aortic contraction in both healthy and damaged rat aorta. In this study we used 24 Wistar albino rats in 2 groups (n=24). Group 1; aorta- intact endothelium (n=12), group 2 aorta- damaged endothelium (n=12). The descending thoracic aorta was quickly isolated after cervical dislocation of adult Wistar albino rat. Aorta tissues were cleaned and sectioned into 3-4 mm long rings. Then the rings were placed in organ baths containing Krebs–Henseleit solution, which was thermoregulated at 370C and aerated (95 % O2 and 5% CO2). Changes in isometric tension of aorta rings were recorded using a four channel force displacement transducer. Endothelium intact rings were used in the first part of the study and mechanically damaged endothelial rings were used in the second part. Phenylephrine (PE 10-6 M) was applied and contractions were recorded in both groups. Then Sertraline (50 mg) was given cumulatively (10-9 -10-4 M) to group 1. In group 2 aorta injury was achieved by tearing the endothelium with a needle. After controlling endothelial damage by applying acetylcholine (Ach 10 -6M), all damaged strips were washed for one hour in organ baths and second dose of phenylephrine (PE 10-6 M) was administered, then Sertraline (50 mg) was given cumulatively (10-9 -10-4 M) to group 2 and contractions were recorded. After sertraline (50 mg) was given cumulatively (10-9 -10-4 M) to group 1, significant inhibition of spontaneous contractions was noticed in the first three doses of sertraline (10-9, 10-8, 10-7) (p<0.05), inhibition of contractions kept on in the rest of the sertraline doses. Sertraline 10-6 -5 -4 made also significant inhibition in contractions according to 10-9 -8 -7 doses. In group 2, inhibition of second PE contractions continued after sertraline doses, but it was less significant when compared with group 1. Sertraline was found to inhibit PE-induced smooth muscle contraction in rat isolated aorta. PE-induced smooth muscle contractions were inhibited more slowly in endothelium damaged aortic tissue. It is thought that as a result of endothelial damage, NO secretion in the aorta decreases and the vasodilation effect due to NO is also reduced. Further studies are needed to better understand the effects of sertraline on the cardiovascular system.
Açıklama
Yüksek Lisans Tezi
Anahtar Kelimeler
Aort, Endotel, Sertralin, Kontraksiyon, Vazorelaksasyon, Aorta, Endothelium, Sertraline, Contraction, Vasorelaxation
Kaynak
WoS Q Değeri
Scopus Q Değeri
Cilt
Sayı
Künye
Eker, C. B. (2023). Sertralin endotel hasarlı aortta kontraksiyonu etkiler mi?. (Yayımlanmamış yüksek lisans tezi). Necmettin Erbakan Üniversitesi, Sağlık Bilimleri Enstitüsü Fizyoloji Anabilim Dalı, Konya.
