Lipopolysaccharide 에 의한 Heme Oxygenase Induction 과 Carbon Monoxide 생성이 혈관 수축력에 미치는 영향

Effects of Lipopolysaccharide-Induced Heme Oxygenase and Carbon Monoxide Production on the Aortic Contractility

Heme oxygenase is a rate-limiting enzyme in heme catabolism that cleaves heme to form biliverdin, iron, and carbon monoxide. Heme oxygenase-1 is expressed in many types of cells and tissues and is highly induced in response to oxidative stress. Carbon monxide, one of the products of heme oxygenase, can stimulate soluble guanylate cycalses and dilate the vascular smooth muscle. So, the induction of heme oxygenase by lipopoysaccharide (LPS)-induced oxydative stress and the effect of the resultant carbon monoxide on aortic contractility were examined in this study. Zinc protoporphyrine IX (ZnPP), a inhibitor of heme oxygenase, elicited weak contraction of thoracic aortic ring, and this effect was more potent in aorta of LTS-treated rats than control and was blocked by methylene blue. The hyperreactivity to ZnPP in LPS- group was bloced by co-treatment with aminoguanidine. In the aortic ring of LPS- treated rats, ZnPP didn't change the vasoreactivity to phenylephrine or acetycholine. ZnPP elicited hypertensive the hypertensive effect of ZnPP. These results indicate that LPS indused heme oxygenase in aotra, and the resultant carbon monoxide iminished the aoric reacitivity to vasoconstrictor.