Vascular Response of Isolated Rat Thoracic Aorta after Chemical Hypoxia/Reoxygenation / 대한마취과학회지

ABSTRACT

BACKGROUND: Hypoxia/reoxygenation (H/R) results in formation of toxic reactive oxygen species (ROS), which can impair the vascular pathophysiology. Nitric oxide (NO) is an important free radical in many physiological or pathological processes including H/R injury. The loss of NO after H/R might be one of the major causes of an impaired vascular response. METHODS: Isolated rat aortic rings were prepared and NaCN was used to induce chemical hypoxia. The NaCN concentration and the hypoxia/reoxygenation time were determined by the responsiveness of phenylephrine (Phe), sodium nitroprusside (SNP) and acetylcholine (Ach). A cumulative doses of Phe and SNP (10(-9)-10(-5.5) M) were added to construct the vascular contraction and relaxation curves. The cumulative doses of Ach (10(-9)-10(-5) M) were added to construct the relaxation after precontraction with Phe (10(-6) M). The effects of the N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) and the superoxide dismutase (SOD, 50 unit) pretreatment during chemical H/R were evaluated. RESULTS: The NaCN concentration and H/R time were 1 mM, 30 minutes/5 minutes, respectively. Chemical hypoxia reduced the Phe-induced vascular contraction significantly. However chemical H/R increased the Phe-induced contraction significantly, and impaired the relaxation by SNP and Ach. A pretreatment with L-NAME increased the Phe-induced contraction and impaired the relaxation by SNP as well as Ach. The SOD pretreatment reduced the Phe-induced increased vascular contraction after NaCN-induced chemical H/R. CONCLUSIONS: NO plays a key role in endothelial-dependent relaxation and the recovery of the augmented contractility by vasoconstrictors after chemically-induced H/R.