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Cardioprotection conferred by exercise training is blunted by blockade of the opioid system.

Galvão TF, Matos KC, Brum PC, Negrão CE, Luz PL, Chagas AC - Clinics (Sao Paulo) (2011)

Bottom Line: No additional decrease in infarct size occurred in the exercise training plus morphine group.No difference in myocardial capillary density (p = 0.88) was observed in any group.The effect of chronic exercise training in decreasing infarct size seems to occur, at least in part, through the opioid receptor stimulus and not by increasing myocardial perfusion.

View Article: PubMed Central - PubMed

Affiliation: Heart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil. tatianafgg@einstein.br

ABSTRACT

Objectives: To investigate the effect of opioid receptor blockade on the myocardial protection conferred by chronic exercise and to compare exercise training with different strategies of myocardial protection (opioid infusion and brief periods of ischemia-reperfusion) preceding irreversible left anterior descending coronary ligation.

Introduction: The acute cardioprotective effects of exercise training are at least partly mediated through opioid receptor-dependent mechanisms in ischemia-reperfusion models.

Methods: Male Wistar rats (n = 76) were randomly assigned to 7 groups: (1) control; (2) exercise training; (3) morphine; (4) intermittent ischemia-reperfusion (three alternating periods of left anterior descending coronary occlusion and reperfusion); (5) exercise training+morphine; (6) naloxone (a non-selective opioid receptor blocker) plus morphine; (7) naloxone before each exercise-training session. Myocardial infarction was established in all groups by left anterior descending coronary ligation. Exercise training was performed on a treadmill for 60 minutes, 5 times/week, for 12 weeks, at 60% peak oxygen (peak VO₂). Infarct size was histologically evaluated.

Results: Exercise training significantly increased exercise capacity and ΔVO2 (VO₂ peak - VO₂ rest) (p < 0.01 vs. sedentary groups). Compared with control, all treatment groups except morphine plus naloxone and exercise training plus naloxone showed a smaller infarcted area (p < 0.05). No additional decrease in infarct size occurred in the exercise training plus morphine group. No difference in myocardial capillary density (p = 0.88) was observed in any group.

Conclusions: Exercise training, morphine, exercise training plus morphine and ischemia-reperfusion groups had a smaller infarcted area than the control group. The effect of chronic exercise training in decreasing infarct size seems to occur, at least in part, through the opioid receptor stimulus and not by increasing myocardial perfusion.

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Infarcted area (scar area /left ventricular (LV) muscle area) among groups. *p<0.05 vs. control; §p<0.05 vs. ET+N; £p<0.05 vs ET. C  =  control; ET  =  exercise training; M  =  morphine; IR  =  intermittent ischemia-reperfusion; M+N  =  morphine plus naloxone; ET+M  =  exercise training plus morphine; ET+N  =  exercise training plus naloxone.
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f3-cln_66p151: Infarcted area (scar area /left ventricular (LV) muscle area) among groups. *p<0.05 vs. control; §p<0.05 vs. ET+N; £p<0.05 vs ET. C  =  control; ET  =  exercise training; M  =  morphine; IR  =  intermittent ischemia-reperfusion; M+N  =  morphine plus naloxone; ET+M  =  exercise training plus morphine; ET+N  =  exercise training plus naloxone.

Mentions: In comparison with the control group, the treatment groups ET, M, IR and ET+M had a smaller relative scar area/LV area (0.24 vs 0.07; 0.13; 0.13; 0.12, respectively; p<0.05). This difference was not seen in the M+N and ET+N groups (relative values 0.22 and 0.37, respectively) (Figure 3). We also found that in the ET+M group there was no further decrease in infarcted area in comparison with morphine or ET alone (Figure 4). As shown in Table 3, the ET+N group had an increase in LV cross-sectional area (p<0.05) and scar area (p = 0.0001), compared with all other groups. In addition, there was an increase in IVS thickness in the ET group (compared with the control group) and in the ET+M group (compared with the control, intermittent IR and morphine groups). In the ET+N group, there was no alteration in the IVS thickness.


Cardioprotection conferred by exercise training is blunted by blockade of the opioid system.

Galvão TF, Matos KC, Brum PC, Negrão CE, Luz PL, Chagas AC - Clinics (Sao Paulo) (2011)

Infarcted area (scar area /left ventricular (LV) muscle area) among groups. *p<0.05 vs. control; §p<0.05 vs. ET+N; £p<0.05 vs ET. C  =  control; ET  =  exercise training; M  =  morphine; IR  =  intermittent ischemia-reperfusion; M+N  =  morphine plus naloxone; ET+M  =  exercise training plus morphine; ET+N  =  exercise training plus naloxone.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3044560&req=5

f3-cln_66p151: Infarcted area (scar area /left ventricular (LV) muscle area) among groups. *p<0.05 vs. control; §p<0.05 vs. ET+N; £p<0.05 vs ET. C  =  control; ET  =  exercise training; M  =  morphine; IR  =  intermittent ischemia-reperfusion; M+N  =  morphine plus naloxone; ET+M  =  exercise training plus morphine; ET+N  =  exercise training plus naloxone.
Mentions: In comparison with the control group, the treatment groups ET, M, IR and ET+M had a smaller relative scar area/LV area (0.24 vs 0.07; 0.13; 0.13; 0.12, respectively; p<0.05). This difference was not seen in the M+N and ET+N groups (relative values 0.22 and 0.37, respectively) (Figure 3). We also found that in the ET+M group there was no further decrease in infarcted area in comparison with morphine or ET alone (Figure 4). As shown in Table 3, the ET+N group had an increase in LV cross-sectional area (p<0.05) and scar area (p = 0.0001), compared with all other groups. In addition, there was an increase in IVS thickness in the ET group (compared with the control group) and in the ET+M group (compared with the control, intermittent IR and morphine groups). In the ET+N group, there was no alteration in the IVS thickness.

Bottom Line: No additional decrease in infarct size occurred in the exercise training plus morphine group.No difference in myocardial capillary density (p = 0.88) was observed in any group.The effect of chronic exercise training in decreasing infarct size seems to occur, at least in part, through the opioid receptor stimulus and not by increasing myocardial perfusion.

View Article: PubMed Central - PubMed

Affiliation: Heart Institute, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil. tatianafgg@einstein.br

ABSTRACT

Objectives: To investigate the effect of opioid receptor blockade on the myocardial protection conferred by chronic exercise and to compare exercise training with different strategies of myocardial protection (opioid infusion and brief periods of ischemia-reperfusion) preceding irreversible left anterior descending coronary ligation.

Introduction: The acute cardioprotective effects of exercise training are at least partly mediated through opioid receptor-dependent mechanisms in ischemia-reperfusion models.

Methods: Male Wistar rats (n = 76) were randomly assigned to 7 groups: (1) control; (2) exercise training; (3) morphine; (4) intermittent ischemia-reperfusion (three alternating periods of left anterior descending coronary occlusion and reperfusion); (5) exercise training+morphine; (6) naloxone (a non-selective opioid receptor blocker) plus morphine; (7) naloxone before each exercise-training session. Myocardial infarction was established in all groups by left anterior descending coronary ligation. Exercise training was performed on a treadmill for 60 minutes, 5 times/week, for 12 weeks, at 60% peak oxygen (peak VO₂). Infarct size was histologically evaluated.

Results: Exercise training significantly increased exercise capacity and ΔVO2 (VO₂ peak - VO₂ rest) (p < 0.01 vs. sedentary groups). Compared with control, all treatment groups except morphine plus naloxone and exercise training plus naloxone showed a smaller infarcted area (p < 0.05). No additional decrease in infarct size occurred in the exercise training plus morphine group. No difference in myocardial capillary density (p = 0.88) was observed in any group.

Conclusions: Exercise training, morphine, exercise training plus morphine and ischemia-reperfusion groups had a smaller infarcted area than the control group. The effect of chronic exercise training in decreasing infarct size seems to occur, at least in part, through the opioid receptor stimulus and not by increasing myocardial perfusion.

Show MeSH
Related in: MedlinePlus