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The effects of ischemic postconditioning on myocardial function and nitric oxide metabolites following ischemia-reperfusion in hyperthyroid rats.

Zaman J, Jeddi S, Ghasemi A - Korean J. Physiol. Pharmacol. (2014)

Bottom Line: Ischemic postconditioning (IPost) could decrease ischemia-reperfusion (IR) injury.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.

View Article: PubMed Central - PubMed

Affiliation: Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran 19395-4763, Iran. ; Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran 19395-4763, Iran.

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 µmol/L vs. 102.8±3.7 µmol/L; p< 0.05) and heart (34.9±4.1 µmol/L vs. 19.9±1.94 µmol/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.

No MeSH data available.


Related in: MedlinePlus

Alterations of LVEDP during IR; left ventricular end diastolic pressure (LVEDP); control-ischemia reperfusion (C-IR), C-ischemic postconditioning (C-IPost), hyperthyroid-IR (HP-IR); hyperthyroid-IPost (HP-IPost) and hyperthyroid-IPost-aminoguanidine (HP-IPost-AG); data are mean±SE (n=8 rats); *p<0.05 significant difference between C-IR and C-IPost. #p<0.05 significant difference between C-IR and HP-IR, and between C-IPost and HP-IPost. †p<0.05 significant difference between with HP-IPost and HP-IPost-AG.
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Figure 2: Alterations of LVEDP during IR; left ventricular end diastolic pressure (LVEDP); control-ischemia reperfusion (C-IR), C-ischemic postconditioning (C-IPost), hyperthyroid-IR (HP-IR); hyperthyroid-IPost (HP-IPost) and hyperthyroid-IPost-aminoguanidine (HP-IPost-AG); data are mean±SE (n=8 rats); *p<0.05 significant difference between C-IR and C-IPost. #p<0.05 significant difference between C-IR and HP-IR, and between C-IPost and HP-IPost. †p<0.05 significant difference between with HP-IPost and HP-IPost-AG.

Mentions: During the 30 minutes ischemia, hyperthyroid group showed a significant increase in LVEDP (contracture), compared to controls. IPost significantly reduced the LVEDP during reperfusion phase in the C-IPost group; in addition, IPost in combination with AG, significantly reduced the LVEDP during reperfusion phase in the HP-IPost-AG group compared to HP-IPost (Fig. 2).


The effects of ischemic postconditioning on myocardial function and nitric oxide metabolites following ischemia-reperfusion in hyperthyroid rats.

Zaman J, Jeddi S, Ghasemi A - Korean J. Physiol. Pharmacol. (2014)

Alterations of LVEDP during IR; left ventricular end diastolic pressure (LVEDP); control-ischemia reperfusion (C-IR), C-ischemic postconditioning (C-IPost), hyperthyroid-IR (HP-IR); hyperthyroid-IPost (HP-IPost) and hyperthyroid-IPost-aminoguanidine (HP-IPost-AG); data are mean±SE (n=8 rats); *p<0.05 significant difference between C-IR and C-IPost. #p<0.05 significant difference between C-IR and HP-IR, and between C-IPost and HP-IPost. †p<0.05 significant difference between with HP-IPost and HP-IPost-AG.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4296037&req=5

Figure 2: Alterations of LVEDP during IR; left ventricular end diastolic pressure (LVEDP); control-ischemia reperfusion (C-IR), C-ischemic postconditioning (C-IPost), hyperthyroid-IR (HP-IR); hyperthyroid-IPost (HP-IPost) and hyperthyroid-IPost-aminoguanidine (HP-IPost-AG); data are mean±SE (n=8 rats); *p<0.05 significant difference between C-IR and C-IPost. #p<0.05 significant difference between C-IR and HP-IR, and between C-IPost and HP-IPost. †p<0.05 significant difference between with HP-IPost and HP-IPost-AG.
Mentions: During the 30 minutes ischemia, hyperthyroid group showed a significant increase in LVEDP (contracture), compared to controls. IPost significantly reduced the LVEDP during reperfusion phase in the C-IPost group; in addition, IPost in combination with AG, significantly reduced the LVEDP during reperfusion phase in the HP-IPost-AG group compared to HP-IPost (Fig. 2).

Bottom Line: Ischemic postconditioning (IPost) could decrease ischemia-reperfusion (IR) injury.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.

View Article: PubMed Central - PubMed

Affiliation: Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran 19395-4763, Iran. ; Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran 19395-4763, Iran.

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 µmol/L vs. 102.8±3.7 µmol/L; p< 0.05) and heart (34.9±4.1 µmol/L vs. 19.9±1.94 µmol/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.

No MeSH data available.


Related in: MedlinePlus