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Nitric oxide and oxygen utilization: exercise, heart failure and diabetes
G Zhao1, R D Bernstein, T H Hintze
1Department of Physiology, New York Medical College, Valhalla 10595, USA.
Coronary Artery Disease
|July 28, 1999
Summary
Nitric oxide (NO) regulates oxygen consumption in canine skeletal and cardiac muscle. Blocking NO synthesis increases oxygen use, especially during exercise, suggesting NO matches blood flow to metabolism.
Area of Science:
- Physiology
- Biochemistry
- Cardiovascular Research
Background:
- Nitric oxide (NO) is known to regulate vascular tone.
- Emerging evidence suggests NO also modulates oxygen consumption.
- The precise role of NO in cellular metabolism requires further elucidation.
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in regulating oxygen consumption in canine skeletal and cardiac muscle.
- To determine if NO influences oxygen consumption at rest and during exercise.
- To examine the impact of heart failure and diabetes on NO-mediated oxygen consumption.
Main Methods:
- In vitro studies using isolated canine skeletal and cardiac muscle.
- In vivo studies in resting and exercising conscious dogs with blocked NO synthesis.
- Measurement of total and regional oxygen consumption.
Main Results:
- Exogenous and endogenous NO reduced oxygen consumption in isolated canine muscles, likely via effects on cytochrome oxidase.
- Blockade of NO synthesis increased total oxygen consumption in resting conscious dogs.
- During exercise, blocking NO synthesis led to greater increases in total, skeletal, and cardiac oxygen consumption.
Conclusions:
- Nitric oxide (NO) plays a crucial role in matching tissue metabolism to blood flow at rest and during exercise.
- The modulatory effect of NO on oxygen consumption is impaired in conditions like heart failure and diabetes.
- NO may also influence metabolic substrate utilization in the heart, particularly in heart failure.