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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

The alterations of NOx in heart of control and hyperthyroid groups; 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 as mean±SE (n=8 rats); *p<0.05 compared with control group. **p<0.05 compared with C-IR group. #p<0.05 compared with hyperthyroid group. †p<0.05 compared with HP-IPost group.
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Figure 3: The alterations of NOx in heart of control and hyperthyroid groups; 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 as mean±SE (n=8 rats); *p<0.05 compared with control group. **p<0.05 compared with C-IR group. #p<0.05 compared with hyperthyroid group. †p<0.05 compared with HP-IPost group.

Mentions: Heart and serum NOx levels were significantly higher in the hyperthyroid group, compared to the controls. The level of NOx was enhanced significantly in both groups of HP-IR and HP-IPost. IPost had no significant effect on reduction of heart NOx level in the HP-IPost group, although, IPost significantly reduced the IR-induced enhancement in heart NOx of the control group. AG significantly reduced heart NOx levels in hyperthyroid rats subjected to IPost (Fig. 3). There was significant difference in the IS between groups of C-IR and HP-IR animals (47.5±1.9% vs. 64±2.3%). IPost significantly reduced the IS in control group, while it had no effect in the hyperthyroid group; IPost in presence of AG significantly reduced the IS in HP-IPost-AG group (60.5±2.04 vs. 47.60±1.72) (Fig. 4).


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)

The alterations of NOx in heart of control and hyperthyroid groups; 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 as mean±SE (n=8 rats); *p<0.05 compared with control group. **p<0.05 compared with C-IR group. #p<0.05 compared with hyperthyroid group. †p<0.05 compared with HP-IPost group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 3: The alterations of NOx in heart of control and hyperthyroid groups; 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 as mean±SE (n=8 rats); *p<0.05 compared with control group. **p<0.05 compared with C-IR group. #p<0.05 compared with hyperthyroid group. †p<0.05 compared with HP-IPost group.
Mentions: Heart and serum NOx levels were significantly higher in the hyperthyroid group, compared to the controls. The level of NOx was enhanced significantly in both groups of HP-IR and HP-IPost. IPost had no significant effect on reduction of heart NOx level in the HP-IPost group, although, IPost significantly reduced the IR-induced enhancement in heart NOx of the control group. AG significantly reduced heart NOx levels in hyperthyroid rats subjected to IPost (Fig. 3). There was significant difference in the IS between groups of C-IR and HP-IR animals (47.5±1.9% vs. 64±2.3%). IPost significantly reduced the IS in control group, while it had no effect in the hyperthyroid group; IPost in presence of AG significantly reduced the IS in HP-IPost-AG group (60.5±2.04 vs. 47.60±1.72) (Fig. 4).

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