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 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%O₂ + 5%CO₂ at 37 °C, and exposed to sodium hypochlorite (200 μM) for 30 min. Responses to KCl (80 mM), phenylephrine (10^-10-10^-4 M), acetylcholine (10^-10-10^-4 M), and sodium nitroprusside (SNP, 10^-11-10^-5 M) were recorded. E_max (maximum response) and pD₂ (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 pD₂ (control, 7.1 ± 0.1; IR, 6.0 ± 0.2; p < 0.01) and E_max (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_2, 7.2 ± 0.1; p < 0.001; E_max, 45.4 ± 2.6%; p < 0.0001). For SNP relaxation, IR decreased pD₂ (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.