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Objective: To observe the different concentrations of sufentanil contractile function of thoracic aortic rings from spontaneously hypertensive and normotensive rats. Method: male spontaneously hypertensive rats (spontaneously hypertensive rat, SHR) and male normotensive Wistar rats (normotensive rat, NTR) 8 each weighing 250-350g, free thoracic aorta were decapitated, made -4mm long vascular ring, 4 segments of each rat vascular ring. Vascular rings from male NTR 32, using a randomized block design, divided into: normal saline control group (NC group, n = 8), low concentrations of sufentanil group (NS1, 7 × 10 -1 1mol · L -1 , n = 8), the concentration of sufentanil group (NS2, 2 × 10 -1 0 mol L -1 , n = 8) and high concentration of sufentanil group (NS3, 1 × 10 -9 mol · L the -1 , n = 8 ); 32 vascular rings from male SHR were randomly divided into: normal saline control group (SC group, n = 8), low concentrations of sufentanil group (SS1, 7 × 10 -1 1mol · L -1 , n = 8), the concentration of the Sufentanil group (SS2, 2 × 10 -1 0 mol · L -1 , n = 8), and high concentrations of sufentanil group (SS3 1 × 10 to -9 mol · L -1 , n = 8). Hanging on the vascular ring the vascular tension measurement device, tension stable after adding 60 mol / L KCl contraction the vascular ring records vascular ring tension (G1). Saline and different concentrations were added after elution KCl equilibrium and stability of sufentanil 100μl pre-incubation vascular ring, are then added to the bath for 20 min 10 -6 , 10 -5 ,10-4 ,10-3 mol / L of norepinephrine (norepinephrine, NE) 100μl, so that the bath of NE in the final concentration and successively reached 10 -8 , 10 -7 , 10 -6 , 10 -5 mol / L, full contraction of the blood vessels, and record the the different NE final concentration of vascular ring tension (G2) The calculated vascular ring contraction amplitude (G 2 / G 1 100%). Vascular ring contraction amplitude changes observed after pre-incubation of different concentrations of sufentanil vascular ring contractile response to cumulative concentrations of NE. Results: 1) The SC group compared to the CC group, NE caused by vascular ring contraction amplitude was significantly higher. 2) compared with the NC NS1 arterial ring contraction amplitude was no significant change (P> 0.05), NS2, of NS3 vascular ring contraction amplitude decreased (P lt; 0.05). 3) compared with the SC, SS1, SS2, SS3 vascular ring contraction amplitude decreased (P lt; 0.05). 4) compared with NS3, SS3 group away from the vascular ring contraction amplitude was significantly reduced. (P lt; 0.01). Conclusion: SHR group thoracic aortic reactivity to NE significantly enhanced compared to the NTR group, high concentration Shufen too Nicole inhibition of NE-induced NTR contractile response of isolated thoracic aorta. The different concentrations Shufen too Nicole significantly inhibited the contractile response of NE-induced SHR thoracic aorta
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