Teimoori Ariyan, Orhan Halit Güner, Demirtaş Elif, Zeynalova Nargiz, Efe Oğuzhan Ekin, Emre Aydıngöz Selda
Department of Medical Pharmacology, Başkent University Faculty of Medicine, Ankara, Turkey.
Gen Thorac Cardiovasc Surg. 2025 Jun;73(6):420-427. doi: 10.1007/s11748-024-02089-9. Epub 2024 Sep 30.
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.
本研究的主要目的是评估牛磺酸对血管缺血再灌注（IR）模型中内皮功能障碍的保护作用。
将9只雄性Sprague-Dawley大鼠（350 - 500 g）的胸主动脉切成环，随机分为对照组（n = 7）、IR组（n = 8）、IR + 1 mM牛磺酸组（n = 7）、IR + 10 mM牛磺酸组（n = 8）、IR + 30 mM牛磺酸组（n = 8）和IR + 100 mM牛磺酸组（n = 5）。IR组的主动脉环在4℃的0.9%盐水中保存24小时，置于用95%O₂ + 5%CO₂通气的Krebs-Henseleit溶液中，在37℃下，并用次氯酸钠（200 μM）处理30分钟。记录对氯化钾（80 mM）、去氧肾上腺素（10⁻⁶ M）、乙酰胆碱（10⁻⁸ M）和硝普钠（SNP，10⁻⁸ M）的反应。计算E（最大反应）和pD₂（产生半数最大反应的浓度的负对数）。
IR降低了氯化钾收缩反应（对照组1047±176 mg，IR组682±128 mg，p = 0.0007），30 mM和100 mM牛磺酸可使其逆转（分别为960±313 mg，p = 0.02和1066±488 mg，p = 0.02）。IR损害了去氧肾上腺素、乙酰胆碱和SNP反应（p < 0.0001）。牛磺酸不影响IR损害的去氧肾上腺素收缩反应。IR降低了乙酰胆碱舒张反应的pD₂（对照组，7.1±0.1；IR组，6.0±0.2；p < 0.01）和E（对照组，83.5±2.7%；IR组，26.8±2.5%；p < 0.0001），两者均被100 mM牛磺酸逆转（pD₂ 7.2±0.1；p < 0.001；E 45.4±2.6%；p < 0.0001）。对于SNP舒张反应，IR降低了pD₂（对照组8.2±0.1，IR组7.7±0.1，p < 0.01），100 mM牛磺酸可使其逆转（8.5±0.1，p < 0.0001）。
牛磺酸可保护IR损伤后的内皮功能。进一步的研究应探索这种作用的机制以及将牛磺酸添加到血管移植物保存溶液中的潜力。
