Heat stress protects aged hypertrophied and nonhypertrophied rat hearts against ischemic damage.
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.
Cornelussen
R N
RN
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands.
Garnier
A V
AV
Vork
M M
MM
Geurten
P
P
Reneman
R S
RS
van der Vusse
G J
GJ
Snoeckx
L H
LH
D000818:Animals; D001012:Aorta, Abdominal / Q000502:physiology; D001794:Blood Pressure; D001835:Body Weight; D002302:Cardiac Output; D006332:Cardiomegaly / Q000503:physiopathology*; D003326:Coronary Circulation; D017931:DNA Primers; D003971:Diastole; D018840:HSP70 Heat-Shock Proteins / Q000032:analysis / Q000096:biosynthesis*; D006321:Heart / Q000502:physiology / Q000503:physiopathology*; D006439:Hemodynamics; D006979:Hyperthermia, Induced; D066298:In Vitro Techniques; D008297:Male; D017202:Myocardial Ischemia / Q000503:physiopathology / Q000517:prevention & control*; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000378:metabolism*; D009929:Organ Size; D016133:Polymerase Chain Reaction; D051381:Rats; D011917:Rats, Inbred Lew; D016277:Ventricular Function, Left
D017931:DNA Primers; D018840:HSP70 Heat-Shock Proteins