Myocardial adenine pool depletion and recovery of mechanical function following ischemia
| Autor: | R. N. Seelye, S. M. Humphrey, D. G. Holliss |
|---|---|
| Rok vydání: | 1985 |
| Předmět: |
Male
medicine.medical_specialty Time Factors Physiology Ischemia Myocardial Infarction Hemodynamics Biology Creatine chemistry.chemical_compound Adenosine Triphosphate Physiology (medical) Internal medicine Coronary Circulation Pi medicine Animals Nucleotide chemistry.chemical_classification Adenine Myocardium Rats Inbred Strains Metabolism Phosphate medicine.disease Rats Adenosine Diphosphate Perfusion Endocrinology Biochemistry chemistry Regional Blood Flow NAD+ kinase Cardiology and Cardiovascular Medicine |
| Zdroj: | The American journal of physiology. 248(5 Pt 2) |
| ISSN: | 0002-9513 |
| Popis: | The loss of nucleotide pool precursors from the heart during ischemia and reperfusion may affect resynthesis of ATP and consequently mechanical recovery. Isolated working rat hearts were made globally ischemic for from 15 to 25 min, and the tissue content of adenine pool metabolites, creatine, creatine phosphate (CP), and inorganic phosphate (Pi), were measured after 20 min of reperfusion. In addition, the coronary effluent was assayed for nucleotides, nucleosides, and oxypurines. Hearts that recovered 75% or more of their preischemic hemodynamic function had significantly lower ATP and NAD but greater CP and Pi than controls. Complete failure of hearts was associated with severely depleted ATP but not CP. All hearts released 25% or more of their preischemic adenine pool during the 20-min reperfusion. This loss correlated more closely with a reduction in recovery from 100 to 75% than with complete failure. Thus extensive loss of adenine pool precursors is not critically related to the failure of heart muscle to recover function but may be an important limiting factor in determining the extent and time course of mechanical recovery. |
| Databáze: | OpenAIRE |
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