Preconditioning reduces myocardial complement gene expression in vivo. Am J Physiol Heart Circ Physiol 2000 Sep;279(3):H1157-65
Date
09/20/2000Pubmed ID
10993779DOI
10.1152/ajpheart.2000.279.3.H1157Scopus ID
2-s2.0-0033834774 (requires institutional sign-in at Scopus site) 23 CitationsAbstract
This investigation examined the effect of preconditioning in an in vivo model of ischemia-reperfusion injury. Anesthetized New Zealand White rabbits underwent 30 min of regional myocardial ischemia followed by 2 h of reperfusion. Hearts preconditioned with two cycles of 5 min ischemia-10 min reperfusion (IPC) or with the ATP-sensitive K (K(ATP)) channel opener, diazoxide (10 mg/kg), exhibited significantly (P < 0.05) smaller infarcts compared with control. These treatments also significantly (P < 0.001 to P < 0.05) reduced C1q, C1r, C3, C8, and C9 mRNA in the areas at risk (AAR). The K(ATP) channel blocker 5-hydroxydecanoate (5-HD; 10 mg/kg) attenuated infarct size reduction elicited by IPC and diazoxide treatment. 5-HD partially reversed the decrease in complement expression caused by IPC but not diazoxide. There were no significant differences in complement gene expression in the nonrisk regions and livers of all groups. Western blot analysis revealed that IPC also reduced membrane attack complex expression in the AAR. The data demonstrate that preconditioning significantly decreases reperfusion-induced myocardial complement expression in vivo.
Author List
Tanhehco EJ, Yasojima K, McGeer PL, McGeer EG, Lucchesi BRAuthor
Elaine J. Tanhehco MD, PhD Assistant Professor in the Radiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAnti-Arrhythmia Agents
Blotting, Western
Complement System Proteins
Decanoic Acids
Diazoxide
Gene Expression
Heart
Hemodynamics
Hydroxy Acids
Ischemic Preconditioning, Myocardial
Liver
Male
Myocardium
RNA, Messenger
Rabbits
Reperfusion Injury
Reverse Transcriptase Polymerase Chain Reaction
Vasodilator Agents
