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Chapter: Medical Physiology: Muscle Blood Flow and Cardiac Output During Exercise; the Coronary Circulation and schemic Heart Disease

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Special Features of Cardiac Muscle Metabolism

The basic principles of cellular metabolism, apply to cardiac muscle the same as for other tissues, but there are some quantita-tive differences.

Special Features of Cardiac Muscle Metabolism

The basic principles of cellular metabolism, apply to cardiac muscle the same as for other tissues, but there are some quantita-tive differences. Most important, under resting condi-tions, cardiac muscle normally consumes fatty acids to supply most of its energy instead of carbohydrates (about 70 per cent of the energy is derived from fatty acids). However, as is also true of other tissues, under anaerobic or ischemic conditions, cardiac metabolism must call on anaerobic glycolysis mechanisms for energy. Unfortunately, glycolysis consumes tremen-dous quantities of the blood glucose and at the same time forms large amounts of lactic acid in the cardiac tissue, which is probably one of the causes of cardiac pain in cardiac ischemic conditions.

As is true in other tissues, more than 95 per cent of the metabolic energy liberated from foods is used to form ATP in the mitochondria. This ATP in turn acts as the conveyer of energy for cardiac muscular con-traction and other cellular functions. In severe coro-nary ischemia, the ATP degrades first to adenosine diphosphate, then to adenosine monophosphate and adenosine. Because the cardiac muscle cell membrane is slightly permeable to adenosine, much of this can diffuse from the muscle cells into the circulating blood.

The released adenosine is believed to be one of the substances that causes dilation of the coronary arteri-oles during coronary hypoxia, as discussed earlier.

However, loss of adenosine also has a serious cellular consequence. Within as little as 30 minutes of severe coronary ischemia, as occurs after a myocardial infarct, about one half of the adenine base can be lost from the affected cardiac muscle cells. Furthermore, this loss can be replaced by new synthesis of adenine at a rate of only 2 per cent per hour. Therefore, once a serious bout of coronary ischemia has persisted for 30 or more minutes, relief of the ischemia may be too late to save the lives of the cardiac cells. This almost certainly is one of the major causes of cardiac cellular death during myocardial ischemia.


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