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.