Details

Autor(en) / Beteiligte

• Reger, Patricia O
• Barbe, Mary F
• Amin, Mamta
• Renna, Brian F
• Hewston, Leigh Ann
• MacDonnell, Scott M
• Houser, Steven R
• Libonati, Joseph R

Titel

Myocardial hypoperfusion/reperfusion tolerance with exercise training in hypertension

Ist Teil von

• Journal of applied physiology (1985), 2006-02, Vol.100 (2), p.541-547

Ort / Verlag

Bethesda, MD: Am Physiological Soc

Erscheinungsjahr

2006

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

• Departments of 1 Kinesiology, 2 Physiology, 3 Cell Biology, 4 Cardiovascular Research Center, and 5 Department of Physical Therapy, Temple University, Philadelphia, Pennsylvania Submitted 25 March 2005 ; accepted in final form 20 September 2005 The purpose of this study was to examine whether exercise training, superimposed on compensated-concentric hypertrophy, could increase myocardial hypoperfusion-reperfusion (H/R) tolerance. Female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (age: 4 mo; N = 40) were placed into a sedentary (SED) or exercise training (TRD) group (treadmill running; 25 m/min, 1 h/day, 5 days/wk for 16 wk). Four groups were studied: WKY-SED ( n = 10), WKY-TRD ( n = 10), SHR-SED ( n = 10), and SHR-TRD ( n = 10). Blood pressure and heart rate were determined, and in vitro isolated heart performance was measured with a retrogradely perfused, Langendorff isovolumic preparation. The H/R protocol consisted of a 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion. Although the rate-pressure product was significantly elevated in SHR relative to WKY, training-induced bradycardia reduced the rate-pressure product in SHR-TRD ( P < 0.05) without an attenuation in systolic blood pressure. Heart-to-body weight ratio was greater in both groups of SHR vs. WKY-SED ( P < 0.001). Absolute and relative myocardial tolerance to H/R was greater in WKY-TRD and both groups of SHR relative to WKY-SED ( P < 0.05). Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. Postreperfusion 72-kDa heat shock protein abundance was enhanced in WKY-TRD and both groups of SHR relative to WKY-SED ( P < 0.05) and was highly correlated with absolute left ventricular functional recovery during reperfusion ( R 2 = 0.86, P < 0.0001). These data suggest that both compensated hypertrophy associated with short-term hypertension and endurance training individually improved H/R and that increased postreperfusion 72-kDa heat shock protein abundance was, in part, associated with the cardioprotective phenotype observed in this study. diastole; heat shock proteins; heart Address for reprint requests and other correspondence: J. R. Libonati, Temple Univ., 122 Pearson Hall, 1800 North Broad St., Philadelphia, PA 19122 (e-mail: jlibonat{at}temple.edu )