The Effects of Ischemic Postconditioning on Myocardial Function and Nitric Oxide Metabolites Following Ischemia-Reperfusion in Hyperthyroid Rats.
10.4196/kjpp.2014.18.6.481
- Author:
Jalal ZAMAN
1
;
Sajjad JEDDI
;
Asghar GHASEMI
Author Information
1. Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran 19395-4763, Iran. Ghasemi@endocrine.ac.ir
- Publication Type:Original Article
- Keywords:
Hyperthyroidism;
Ischemia;
Nitric oxidem;
Postconditioning;
Reperfusion
- MeSH:
Animals;
Drinking Water;
Heart;
Humans;
Hyperthyroidism;
Ischemia;
Ischemic Postconditioning*;
Male;
Myocardial Ischemia;
Nitric Oxide*;
Rats*;
Reperfusion;
Thoracotomy;
Thyroxine
- From:The Korean Journal of Physiology and Pharmacology
2014;18(6):481-487
- CountryRepublic of Korea
- Language:English
-
Abstract:
Ischemic postconditioning (IPost) could decrease ischemia-reperfusion (IR) injury. It has not yet reported whether IPost is useful when ischemic heart disease is accompanied with co-morbidities like hyperthyroidism. The aim of this study was to examine the effect of IPost on myocardial IR injury in hyperthyroid male rats. Hyperthyroidism was induced with administration of thyroxine in drinking water (12 mg/L) over a period of 21 days. After thoracotomy, the hearts of control and hyperthyroid rats were perfused in the Langendorff apparatus and subjected to 30 minutes global ischemia, followed by 120 minutes reperfusion; IPost, intermittent early reperfusion, was induced instantly following ischemia. In control rats, IPost significantly improved the left ventricular developed pressure (LVDP) and +/-dp/dt during reperfusion (p<0.05); however it had no effect in hyperthyroid rats. In addition, hyperthyroidism significantly increased basal NOx (nitrate+nitrite) content in serum (125.5+/-5.4 micromol/L vs. 102.8+/-3.7 micromol/L; p< 0.05) and heart (34.9+/-4.1 micromol/L vs. 19.9+/-1.94 micromol/L; p<0.05). In hyperthyroid groups, heart NOx concentration significantly increased after IR and IPost, whereas in the control groups, heart NOx were significantly higher after IR and lower after IPost (p< 0.05). IPost reduced infarct size (p<0.05) only in control groups. In hyperthyroid group subjected to IPost, aminoguanidine, an inducible nitric oxide (NO) inhibitor, significantly reduced both the infarct size and heart NOx concentrations. In conclusion, unlike normal rats, IPost cycles following reperfusion does not provide cardioprotection against IR injury in hyperthyroid rats; an effect that may be due to NO overproduction because it is restored by iNOS inhibition.
