Vascular Response of Isolated Rat Thoracic Aorta after Chemical Hypoxia/Reoxygenation.
10.4097/kjae.2006.50.6.698
- Author:
Byong Soo JANG
1
;
In Kyeom KIM
;
Dong Gun LIM
Author Information
1. Department of Anesthesiology and Pain Medicine, School of Medicine, Kyungpook National University, Daegu, Korea. dglim@mail.knu.ac.kr
- Publication Type:Original Article
- Keywords:
chemical hypoxia;
hypoxia/reoxygenation;
nitric oxide;
N(G)-nitro-L-arginine methyl ester;
reactive oxygen species;
superoxide dismutase
- MeSH:
Acetylcholine;
Animals;
Anoxia;
Aorta, Thoracic*;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Nitroprusside;
Pathologic Processes;
Phenylephrine;
Rats*;
Reactive Oxygen Species;
Relaxation;
Superoxide Dismutase;
Vasoconstrictor Agents
- From:Korean Journal of Anesthesiology
2006;50(6):698-705
- CountryRepublic of Korea
- Language:Korean
-
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.
