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Korean Journal of Anesthesiology 2006;50(6):698-705.
DOI: https://doi.org/10.4097/kjae.2006.50.6.698   
Vascular Response of Isolated Rat Thoracic Aorta after Chemical Hypoxia/Reoxygenation.
Byong Soo Jang, In Kyeom Kim, Dong Gun Lim
1Department of Anesthesiology and Pain Medicine, School of Medicine, Kyungpook National University, Daegu, Korea. dglim@mail.knu.ac.kr
2Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu, Korea.
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.
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.
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.
NO plays a key role in endothelial-dependent relaxation and the recovery of the augmented contractility by vasoconstrictors after chemically-induced H/R.
Key Words: chemical hypoxia; hypoxia/reoxygenation; nitric oxide; N(G)-nitro-L-arginine methyl ester; reactive oxygen species; superoxide dismutase


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