Heat stress protects aged hypertrophied and nonhypertrophied rat hearts against ischemic damage
Autor: | G. J. Van Der Vusse, M. M. Vork, R. S. Reneman, A. V. Garnier, Richard Cornelussen, P. Geurten, L. H. E. H. Snoeckx |
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Rok vydání: | 1997 |
Předmět: |
Male
Hyperthermia medicine.medical_specialty Cardiac output Physiology Myocardial Ischemia Ischemia Blood Pressure Cardiomegaly Myocardial Reperfusion In Vitro Techniques Polymerase Chain Reaction Ventricular Function Left Muscle hypertrophy Diastole Coronary Circulation Physiology (medical) Internal medicine medicine Animals HSP70 Heat-Shock Proteins Aorta Abdominal Cardiac Output DNA Primers Cardioprotection biology business.industry Myocardium Body Weight Hemodynamics Heart Hyperthermia Induced Organ Size medicine.disease Rats Hsp70 Endocrinology Rats Inbred Lew Anesthesia Ventricular pressure biology.protein Creatine kinase Cardiology and Cardiovascular Medicine business |
Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 273:H1333-H1341 |
ISSN: | 1522-1539 0363-6135 |
DOI: | 10.1152/ajpheart.1997.273.3.h1333 |
Popis: | To explore the effects of heat stress (HS) in aged hypertrophied and nonhypertrophied rat hearts, postischemic recovery was investigated 15 mo after aortic constriction (AoB) or sham operation (Sham). Twenty-four hours after HS (42 degrees C; 15 min) or control treatment (normothermia), global ischemia was induced for 20 min in isolated AoB hearts and for 20 or 30 min in Sham hearts. After HS, postischemic recovery after 20-min ischemia in AoB hearts and 30-min ischemia in Sham hearts, respectively, was significantly better than in corresponding controls. In AoB hearts, cardiac output (CO), left ventricular developed pressure (LVDP), and the positive maximal first derivative of left ventricular pressure (+dP/dtmax) recovered to 33 +/- 26 (means +/- SD), 87 +/- 5, and 72 +/- 12%, respectively, after HS and to 5 +/- 8, 22 +/- 39, and 17 +/- 29% of preischemic values, respectively, in controls. Postischemic arrhythmias were significantly reduced in HS hypertrophied hearts, but creatine kinase (CK) loss was not reduced. In Sham hearts subjected to 30 min ischemia, CO, LVDP, and +dP/dtmax recovered to 20 +/- 20, 75 +/- 8, and 59 +/- 15%, respectively, after HS and to 3 +/- 8, 21 +/- 32, and 16 +/- 32% of preischemic values, respectively, in controls. Duration of arrhythmias and CK loss were not reduced in the heated hearts. When Sham hearts were subjected to only 20-min ischemia, functional recovery was not different in HS and control hearts, indicating that HS pretreatment extends the ischemic interval before irreversible injury occurs in the heart. In all HS Sham hearts, the myocardial 72-kDa HS protein (HSP 70) content was significantly increased. However, in HS AoB hearts, HSP 70 levels were not significantly different from the values in the control hearts. These results indicate that HS pretreatment induces cardioprotection in aged hypertrophied and nonhypertrophied rat hearts, which, however, cannot be unequivocally related to increased HSP 70 tissue contents. |
Databáze: | OpenAIRE |
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