Abstract
The postischemic recovery of hypertrophied hearts was studied 24 h after total body hyperthermia. To this end, anesthetized aortic-banded and sham-operated rats were subjected to heat shock (AoBHS and ShamHS, respectively). Cardiac hypertrophy was induced 8 wk earlier. In isolated ejecting hearts, functional recovery after 45 min of global ischemia was poor and moderate in nonheated (control) hypertrophied (AoBC) and nonheated (control) nonhypertrophied (ShamC) hearts, respectively. Heat shock significantly improved postischemic recovery in both AoBHS and ShamHS hearts. This improvement of functional recovery was associated with a significant reduction of the duration of arrhythmias. In addition, coronary flow was significantly higher in both types of heat-shocked hearts than in the corresponding control hearts during the preischemic as well as the postischemic period. Postischemic endocardial flow, assessed using radioactive microspheres, was significantly improved in AoBHS hearts. Compared with the corresponding control hearts, the native endogenous catalase activity was not changed in AoBHS hearts but was significantly increased in ShamHS hearts. The present findings suggest that the postischemic functional improvement after total body hyperthermia can be explained by increased and more homogeneous myocardial perfusion, which may also reduce the duration of postischemic arrhythmias. This effect is especially beneficial for the hypertrophied heart, which is known to be extremely vulnerable to the ischemic insult probably caused by subendocardial underperfusion.
Original language | English |
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Pages (from-to) | H1941-1947 |
Journal | American Journal of Physiology |
Volume | 267 |
Issue number | 5 Pt 2 |
Publication status | Published - 1994 |
Keywords
- *Hemodynamic Processes
- Animals
- Body Weight
- Cardiac Output
- Cardiomegaly
- Cardiomegaly/*physiopathology/therapy
- Comparative Study
- Coronary Circulation
- Creatine Kinase
- Creatine Kinase/analysis
- Diastole
- Free Radical Scavengers
- Heart
- Heart/anatomy & histology/physiopathology
- Heat/*therapeutic use
- Hemodynamics
- Hot Temperature
- In Vitro
- L-Lactate Dehydrogenase
- L-Lactate Dehydrogenase/analysis
- Male
- Myocardial Ischemia
- Myocardial Ischemia/*physiopathology/therapy
- Myocardial Reperfusion
- Organ Size
- Rats
- Rats, Inbred Lew
- Research Support, Non-U.S. Gov't
- Time Factors
- Ventricular Function, Left