Increased Expression of ATP-sensitive K+ Channels Improves the Right Ventricular Tolerance to Hypoxia in Rabbit Hearts.
10.4196/kjpp.2011.15.4.189
- Author:
Seong Woo CHOI
1
;
Jun Seok AHN
;
Hyoung Kyu KIM
;
Nari KIM
;
Tae Hoon CHOI
;
Sung Woo PARK
;
En A KO
;
Won Sun PARK
;
Dae Kyu SONG
;
Jin HAN
Author Information
1. National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 614-735, Korea. phyhanj@inje.ac.kr
- Publication Type:In Vitro ; Original Article
- Keywords:
ATP-sensitive K+ channels;
Kir6.2;
Right ventricle;
Hypoxia
- MeSH:
Anoxia;
Glyburide;
Heart;
Heart Ventricles;
In Situ Hybridization;
L-Lactate Dehydrogenase;
Reperfusion Injury;
RNA, Messenger
- From:The Korean Journal of Physiology and Pharmacology
2011;15(4):189-194
- CountryRepublic of Korea
- Language:English
-
Abstract:
ATP-sensitive K+ channels (KATP) are major component of preventing ischemia-reperfusion injury. However, there is little information regarding to the expressional difference of K(ATP) and its function between left and right ventricles. In this study, we measured the lactate dehydrogenase release of rabbit heart slices in vitro and determined the difference of the K(ATP) expression at the both ventricles by measuring the level of K(ATP)-forming Kir6.2 (OcKir6.2) mRNA using in situ hybridization. The hearts were preconditioned with 15 min hypoxia and reoxygenated for 15 min before a hypoxic period of 60 min, followed by reoxygenation for 180 min. With hypoxic preconditioning (100% N2) with 15 min, left ventricles (LV) showed higher release of LDH comparing with right ventricles (RV). Adding KATP blocker glibenclamide (10 microM) prior to a hypoxic period of 60 min, hypoxic preconditioning effect of RV was more abolished than LV. With in situ hybridization, the optical density of OcKir6.2 was higher in RV. Therefore, we suggest that different K(ATP) expression between LV and RV is responsible for the different response to hypoxia and hypoxic preconditioning of rabbit hearts.
