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Preserved postischemic heart function in sucrose-fed type 2 diabetic OLETF rats.
Hong Chen1, Hideaki Higashino, Zdravko A Kamenov
1Department of Pharmacology, Second Military Medical University, 800 Xiang Yin Road, Shanghai 200433, China. hchen100@hotmail.com
Life Sciences
|April 17, 2003
Summary
Diabetic hearts show impaired function and ischemia tolerance. Sucrose feeding in type 2 diabetic rats improved heart function post-ischemia, possibly due to reduced cardiac norepinephrine release.
Area of Science:
- Cardiology
- Endocrinology
- Diabetology
Background:
- Cardiovascular disease is a major complication of diabetes mellitus.
- Diabetic heart dysfunction and ischemia tolerance remain areas of debate.
- Understanding these mechanisms is crucial for managing diabetic patients.
Purpose of the Study:
- To investigate ischemic heart function in type 2 diabetic rats.
- To explore the relationship between hyperglycemia and cardiac norepinephrine release.
- To assess the impact of sucrose feeding on diabetic heart ischemia tolerance.
Main Methods:
- Utilized Otsuka Long-Evans Tokushima Fatty (OLETF) and Long-Evans Tokushima Otsuka (LETO) rats.
- Administered sucrose to a group of OLETF rats (OLETF-S) to exacerbate hyperglycemia.
- Isolated and perfused hearts using a working heart preparation, subjected to ischemia-reperfusion, and measured hemodynamics and norepinephrine overflow.
Main Results:
- OLETF rats exhibited marked hyperglycemia, further worsened by sucrose feeding.
- Baseline cardiac output was reduced in OLETF rats but preserved in OLETF-S rats.
- OLETF hearts showed poor post-ischemic function, while OLETF-S hearts were resistant to ischemia, with lower norepinephrine release.
Conclusions:
- OLETF rat hearts are vulnerable to ischemia, but sucrose feeding confers resistance.
- Reduced cardiac norepinephrine release may protect sucrose-fed diabetic hearts from post-ischemic damage.
- This study sheds light on the complex interplay between hyperglycemia, cardiac function, and ischemia in diabetes.