title: Effects of ischemic postconditioning on the hemodynamic parameters and heart nitric oxide levels of hypothyroid rats.
abstract: BACKGROUND
  Ischemic postconditioning (IPost) is a method of protecting the heart against ischemia-reperfusion (IR) injury. However, the effectiveness of IPost in cases of ischemic heart disease accompanied by co-morbidities such as hypothyroidism remains unclear.
  
  
  OBJECTIVE
  The aim of this study was to determine the effect of IPost on myocardial IR injury in hypothyroid male rats.
  
  
  METHODS
  Propylthiouracil in drinking water (500 mg/L) was administered to male rats for 21 days to induce hypothyroidism. The hearts from control and hypothyroid rats were perfused in a Langendorff apparatus and exposed to 30 min of global ischemia, followed by 120 min of reperfusion. IPost was induced immediately following ischemia.
  
  
  RESULTS
  Hypothyroidism and IPost significantly improved the left ventricular developed pressure (LVDP) and peak rates of positive and negative changes in left ventricular pressure (±dp/dt) during reperfusion in control rats (p < 0.05). However, IPost had no add-on effect on the recovery of LVDP and ±dp/dt in hypothyroid rats. Furthermore, hypothyroidism significantly decreased the basal NO metabolite (NOx) levels of the serum (72.5 ± 4.2 vs. 102.8 ± 3.7 μmol/L; p < 0.05) and heart (7.9 ± 1.6 vs. 18.8 ± 3.2 μmol/L; p < 0.05). Heart NOx concentration in the hypothyroid groups did not change after IR and IPost, whereas these were significantly (p < 0.05) higher and lower after IR and IPost, respectively, in the control groups.
  
  
  CONCLUSIONS
  Hypothyroidism protects the heart from IR injury, which may be due to a decrease in basal nitric oxide (NO) levels in the serum and heart and a decrease in NO after IR. IPost did not decrease the NO level and did not provide further cardioprotection in the hypothyroid group.
authors.affiliation: Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: Sajad
authors.initials: S
authors.lastname: Jeddi
authors.affiliation: Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: Jalal
authors.initials: J
authors.lastname: Zaman
authors.affiliation: Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: Asghar
authors.initials: A
authors.lastname: Ghasemi
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000502:physiology*; D007037:Hypothyroidism / Q000139:chemically induced / Q000503:physiopathology*; D057775:Ischemic Postconditioning / Q000379:methods*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology* / Q000517:prevention & control; D009206:Myocardium / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D017208:Rats, Wistar; D012016:Reference Values; D015203:Reproducibility of Results; D013963:Thyroid Hormones / Q000097:blood; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D013963:Thyroid Hormones; D009569:Nitric Oxide