Antioxidant effects of methylprednisolone and hydrocortisone on the impairment of endothelium dependent relaxation induced by reactive oxygen species in rabbit abdominal aorta.
BACKGROUND
The reperfusion following ischemia produces reactive oxygen species (ROS). We studied the influences of methylprednisolone (MPD) and hydrocortisone (CRT) on ROS effects using the endothelium of rabbit abdominal aorta.


METHODS
Isolated rabbit aortic rings were suspended in an organ bath filled with Krebs-Henseleit (K-H) solution. After precontraction with norepinephrine, changes in arterial tension were recorded following the cumulative administration of acetylcholine (ACh). The percentages of ACh-induced relaxation of aortic rings before and after exposure to ROS, generated by electrolysis of K-H solution, were used as the control and experimental values, respectively. The aortic rings were pretreated with MPD or CRT at the same concentrations, and the effects of these agents were compared with the effects of ROS scavenger inhibitors: superoxide dismutase inhibitor, diethylthiocarbamate (DETCA), and the catalase inhibitor, 3-amino-1,2,4-triazole (3AT).


RESULTS
Both MPD and CRT maintained endothelium-dependent relaxation induced by ACh in a dose-related manner in spite of ROS attack. The restored ACh-induced relaxation of MPD and CRT group was not attenuated by pretreatment of 3AT and DETCA.


CONCLUSIONS
MPD and CRT preserve the endothelium-dependent vasorelaxation against the attack of ROS, in a dose-related manner. Endothelial protection mechanisms of MPD and CRT may be not associated with hydrogen peroxide and superoxide scavenging.
Department of Anesthesiology and Pain Medicine, Hanyang University Hospital, Seoul, Korea.
Hee Jong
HJ
Lee
Jung Kook
JK
Suh
Hyun Hoo
HH
Song
Mi Ae
MA
Jeong
Jong Hoon
JH
Yeom
Dong Won
DW
Kim
3-amino-1,2,4-triazole; Diethylthiocarbamate; Endothelium; Hydrocortisone; Methylprednisolone; Reactive oxygen species