Effect of taurine on vascular dysfunction in an in vitro ischemia-reperfusion model of rat thoracic aorta

Effect of taurine on vascular dysfunction in an in vitro ischemia-reperfusion model of rat thoracic aorta

The primary objective of this study was to evaluate the protective effect of taurine on endothelial dysfunction in a vascular ischemia-reperfusion (IR) model. Thoracic aortas of 9 male Sprague-Dawley rats (350-500 g) were cut into rings and randomized into control (n = 7), IR (n = 8), IR + taurine 1...

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Hauptverfasser: Teimoori, Ariyan, Orhan, Halit Güner, Demirtaş, Elif, Zeynalova, Nargiz, Efe, Oğuzhan Ekin, Emre Aydıngöz, Selda
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container_title General thoracic and cardiovascular surgery
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creator Teimoori, Ariyan
Orhan, Halit Güner
Demirtaş, Elif
Zeynalova, Nargiz
Efe, Oğuzhan Ekin
Emre Aydıngöz, Selda
description The primary objective of this study was to evaluate the protective effect of taurine on endothelial dysfunction in a vascular ischemia-reperfusion (IR) model. Thoracic aortas of 9 male Sprague-Dawley rats (350-500 g) were cut into rings and randomized into control (n = 7), IR (n = 8), IR + taurine 1 mM (n = 7), IR + taurine 10 mM (n = 8), IR + taurine 30 mM (n = 8), and IR + taurine 100 mM (n = 5) groups. Aortic rings in the IR group were stored in 0.9% saline at 4 °C for 24 h, placed in Krebs-Henseleit solution gassed with 95%O  + 5%CO at 37 °C, and exposed to sodium hypochlorite (200 μM) for 30 min. Responses to KCl (80 mM), phenylephrine (10 -10  M), acetylcholine (10 -10  M), and sodium nitroprusside (SNP, 10 -10  M) were recorded. E (maximum response) and pD (negative logarithm of concentration producing half-maximum response) were calculated. IR decreased KCl contraction (control 1047 ± 176 mg, IR 682 ± 128 mg, p = 0.0007), which was reversed by 30 and 100 mM taurine (960 ± 313 mg, p = 0.02 and 1066 ± 488 mg, p = 0.02, respectively). IR impaired phenylephrine, acetylcholine, and SNP responses (p 
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Thoracic aortas of 9 male Sprague-Dawley rats (350-500 g) were cut into rings and randomized into control (n = 7), IR (n = 8), IR + taurine 1 mM (n = 7), IR + taurine 10 mM (n = 8), IR + taurine 30 mM (n = 8), and IR + taurine 100 mM (n = 5) groups. Aortic rings in the IR group were stored in 0.9% saline at 4 °C for 24 h, placed in Krebs-Henseleit solution gassed with 95%O  + 5%CO at 37 °C, and exposed to sodium hypochlorite (200 μM) for 30 min. Responses to KCl (80 mM), phenylephrine (10 -10  M), acetylcholine (10 -10  M), and sodium nitroprusside (SNP, 10 -10  M) were recorded. E (maximum response) and pD (negative logarithm of concentration producing half-maximum response) were calculated. IR decreased KCl contraction (control 1047 ± 176 mg, IR 682 ± 128 mg, p = 0.0007), which was reversed by 30 and 100 mM taurine (960 ± 313 mg, p = 0.02 and 1066 ± 488 mg, p = 0.02, respectively). IR impaired phenylephrine, acetylcholine, and SNP responses (p < 0.0001). Taurine did not affect IR-impaired phenylephrine contractions. IR decreased both pD (control, 7.1 ± 0.1; IR, 6.0 ± 0.2; p < 0.01) and E (control, 83.5 ± 2.7%; IR, 26.8 ± 2.5%; p < 0.0001) of acetylcholine relaxation, both of which were reversed by 100 mM taurine (pD 7.2 ± 0.1; p < 0.001; E 45.4 ± 2.6%; p < 0.0001). For SNP relaxation, IR decreased pD (control 8.2 ± 0.1, IR 7.7 ± 0.1, p < 0.01), which was reversed by 100 mM taurine (8.5 ± 0.1, p < 0.0001). Taurine protects endothelial function after IR injury. 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Thoracic aortas of 9 male Sprague-Dawley rats (350-500 g) were cut into rings and randomized into control (n = 7), IR (n = 8), IR + taurine 1 mM (n = 7), IR + taurine 10 mM (n = 8), IR + taurine 30 mM (n = 8), and IR + taurine 100 mM (n = 5) groups. Aortic rings in the IR group were stored in 0.9% saline at 4 °C for 24 h, placed in Krebs-Henseleit solution gassed with 95%O  + 5%CO at 37 °C, and exposed to sodium hypochlorite (200 μM) for 30 min. Responses to KCl (80 mM), phenylephrine (10 -10  M), acetylcholine (10 -10  M), and sodium nitroprusside (SNP, 10 -10  M) were recorded. E (maximum response) and pD (negative logarithm of concentration producing half-maximum response) were calculated. IR decreased KCl contraction (control 1047 ± 176 mg, IR 682 ± 128 mg, p = 0.0007), which was reversed by 30 and 100 mM taurine (960 ± 313 mg, p = 0.02 and 1066 ± 488 mg, p = 0.02, respectively). IR impaired phenylephrine, acetylcholine, and SNP responses (p < 0.0001). Taurine did not affect IR-impaired phenylephrine contractions. IR decreased both pD (control, 7.1 ± 0.1; IR, 6.0 ± 0.2; p < 0.01) and E (control, 83.5 ± 2.7%; IR, 26.8 ± 2.5%; p < 0.0001) of acetylcholine relaxation, both of which were reversed by 100 mM taurine (pD 7.2 ± 0.1; p < 0.001; E 45.4 ± 2.6%; p < 0.0001). For SNP relaxation, IR decreased pD (control 8.2 ± 0.1, IR 7.7 ± 0.1, p < 0.01), which was reversed by 100 mM taurine (8.5 ± 0.1, p < 0.0001). Taurine protects endothelial function after IR injury. Further studies should explore the mechanism of this effect and the potential of adding taurine to vascular graft storage solutions.]]></description><issn>1863-6705</issn><issn>1863-6713</issn><issn>1863-6713</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNo9kEtLxDAUhYMojq8_4EKydFNNmjaPpQy-QHCj63AnvcFI24xJKsy_t-PoLO6DyzmHy0fIJWc3nDF1mzlXja5Y3czFtKnMATnhWopKKi4O9ztrF-Q050_GWql5e0wWwojGGK5OSLj3Hl2h0dMCUwoj0jjSb8hu6iHRbpP9NLoS5mMYKfz271BSpCG7DxwCVAnXmPyUt5ohdthvwxIUWj5iAhcchZgKnJMjD33Gi795Rt4f7t-WT9XL6-Pz8u6lclw3pTLaSae0MrVqQGPtGsmw7lZKKc-gQS29qxEk-E6uWm8YWynOHRNGNYgtiDNyvctdp_g1YS52mF_FvocR45St4JxLMYOrZ2m9k7oUc07o7TqFAdLGcma3iO0OsZ0R21_E1symq7_8aTVgt7f8MxU_nQZ4fg</recordid><startdate>20240930</startdate><enddate>20240930</enddate><creator>Teimoori, Ariyan</creator><creator>Orhan, Halit Güner</creator><creator>Demirtaş, Elif</creator><creator>Zeynalova, Nargiz</creator><creator>Efe, Oğuzhan Ekin</creator><creator>Emre Aydıngöz, Selda</creator><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7823-7620</orcidid></search><sort><creationdate>20240930</creationdate><title>Effect of taurine on vascular dysfunction in an in vitro ischemia-reperfusion model of rat thoracic aorta</title><author>Teimoori, Ariyan ; Orhan, Halit Güner ; Demirtaş, Elif ; Zeynalova, Nargiz ; Efe, Oğuzhan Ekin ; Emre Aydıngöz, Selda</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c184t-98c6c7879274a8e2c460e2db777f0a4e86fc2ea6afd6b5f900b711c03974ee5a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Teimoori, Ariyan</creatorcontrib><creatorcontrib>Orhan, Halit Güner</creatorcontrib><creatorcontrib>Demirtaş, Elif</creatorcontrib><creatorcontrib>Zeynalova, Nargiz</creatorcontrib><creatorcontrib>Efe, Oğuzhan Ekin</creatorcontrib><creatorcontrib>Emre Aydıngöz, Selda</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>General thoracic and cardiovascular surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Teimoori, Ariyan</au><au>Orhan, Halit Güner</au><au>Demirtaş, Elif</au><au>Zeynalova, Nargiz</au><au>Efe, Oğuzhan Ekin</au><au>Emre Aydıngöz, Selda</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of taurine on vascular dysfunction in an in vitro ischemia-reperfusion model of rat thoracic aorta</atitle><jtitle>General thoracic and cardiovascular surgery</jtitle><addtitle>Gen Thorac Cardiovasc Surg</addtitle><date>2024-09-30</date><risdate>2024</risdate><issn>1863-6705</issn><issn>1863-6713</issn><eissn>1863-6713</eissn><abstract><![CDATA[The primary objective of this study was to evaluate the protective effect of taurine on endothelial dysfunction in a vascular ischemia-reperfusion (IR) model. Thoracic aortas of 9 male Sprague-Dawley rats (350-500 g) were cut into rings and randomized into control (n = 7), IR (n = 8), IR + taurine 1 mM (n = 7), IR + taurine 10 mM (n = 8), IR + taurine 30 mM (n = 8), and IR + taurine 100 mM (n = 5) groups. Aortic rings in the IR group were stored in 0.9% saline at 4 °C for 24 h, placed in Krebs-Henseleit solution gassed with 95%O  + 5%CO at 37 °C, and exposed to sodium hypochlorite (200 μM) for 30 min. Responses to KCl (80 mM), phenylephrine (10 -10  M), acetylcholine (10 -10  M), and sodium nitroprusside (SNP, 10 -10  M) were recorded. E (maximum response) and pD (negative logarithm of concentration producing half-maximum response) were calculated. IR decreased KCl contraction (control 1047 ± 176 mg, IR 682 ± 128 mg, p = 0.0007), which was reversed by 30 and 100 mM taurine (960 ± 313 mg, p = 0.02 and 1066 ± 488 mg, p = 0.02, respectively). IR impaired phenylephrine, acetylcholine, and SNP responses (p < 0.0001). Taurine did not affect IR-impaired phenylephrine contractions. IR decreased both pD (control, 7.1 ± 0.1; IR, 6.0 ± 0.2; p < 0.01) and E (control, 83.5 ± 2.7%; IR, 26.8 ± 2.5%; p < 0.0001) of acetylcholine relaxation, both of which were reversed by 100 mM taurine (pD 7.2 ± 0.1; p < 0.001; E 45.4 ± 2.6%; p < 0.0001). For SNP relaxation, IR decreased pD (control 8.2 ± 0.1, IR 7.7 ± 0.1, p < 0.01), which was reversed by 100 mM taurine (8.5 ± 0.1, p < 0.0001). Taurine protects endothelial function after IR injury. Further studies should explore the mechanism of this effect and the potential of adding taurine to vascular graft storage solutions.]]></abstract><cop>Japan</cop><pmid>39349917</pmid><doi>10.1007/s11748-024-02089-9</doi><orcidid>https://orcid.org/0000-0001-7823-7620</orcidid></addata></record>
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title Effect of taurine on vascular dysfunction in an in vitro ischemia-reperfusion model of rat thoracic aorta
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