Myocardial ischemia reperfusion tolerance with exercise in hypertension

The overall purpose of this dissertation was to examine whether exercise, both acute and chronic training, protects the hypertensive myocardium from ischemia/reperfusion injury and whether this protection is associated with an increased abundance of HSP72. In the acute study, 10 week old female Wistar-Kyoto (WKY) and 10 week old spontaneously hypertensive rats (SHR) were exposed to 22 min of no flow ischemia followed by 10 min of reperfusion (I/R) following exposure to one of the following conditions: (1) no exercise (2) one hour post-exercise; and (3) 24 hours post exercise. Exercise consisted of treadmill running at 25 m/min for 60 min. In the exercise training study, 4 month old female WKY and SHR were placed into a sedentary or exercise training group.{09}Training consisted of treadmill running; 25 m/min, 1 hr/d, 5 d/wk for 16 wks. Upon completion of the training protocol, hearts were exposed to hypoperfusion/reperfusion (H/R; 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion). At 10 weeks of age, the young hypertensive myocardium was less tolerant to I/R, whereas the hearts in the compensatory phase of hypertrophy demonstrated heightened tolerance to H/R. Acute exercise exacerbated I/R LV dysfunction one hour after exercise in both WKY and SHR and did not influence either LV performance 24 hours after exercise in WKY or SHR. Post-reperfusion HSP72 abundance was not altered with acute exercise. At 32 weeks of age, myocardial tolerance to H/R was heightened with hypertrophy and with training in WKY. Exercise training superimposed on hypertension failed to confer any additional protection. Post-reperfusion HSP72 abundance was enhanced in with training in WKY and with hypertension and was highly correlated with absolute functional recovery during reperfusion. These data demonstrate the variability in the tolerance of the hypertensive myocardium to ischemia/reperfusion, as well as the influence of exercise on myocardial responses to an ischemic insult and HSP72 abundance.