Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The applicability of the adenosine triphosphate (ATP) catabolites, inosine and hypoxanthine as markers of myocardial ischemia in humans with coronary artery disease has been investigated. Inosine and hypoxanthine were assayed enzymatically after separation by a new column chromatographic method. The myocardial lactate extraction at rest (17 +/- 13%) changed to production values (-23 +/- 28%) during pacing-induced angina (P less than 0.0005). Coronary venous inosine values increased from 535 +/- 185 nmol/l at rest to 1030 +/- 740 nmol/l during angina (P less than 0.005), the arterial values amounted to 770 +/- 325 nmol/l and 805 +/- 515 nmol/l respectively (P, NS). The calculated myocardial uptake of inosine at rest (27 +/- 16%) changed to production values (-25 +/- 29%) during angina (P less than 0.0005). Coronary venous hypoxanthine increased from 1000 +/- 760 nmol/l at rest to 1235 +/- 800 nmol/l during angina (P, NS), the arterial values amounted to 1300 +/- 1040 nmol/l and 1235 +/- 800 nmol/l respectively (P, NS). The myocardial extraction changed from 20 +/- 18% at rest to -5.4 +/- 29% during angina (P less than 0.0025). The significant positive correlation (r = 0.61, P less than 0.0025) between myocardial release and uptake of inosine and lactate during severe angina demonstrates that anaerobic glycolysis is accompanied by ATP breakdown. During a second pacing period at less increased pressure--rate product after nitroglycerin, lactate production (-1.7 +/- 22%) already occurred whereas extraction of inosine (19 +/- 19%) and hypoxanthine (24 +/- 15%) did not change. In conclusion, lactate functions as a sensitive marker of myocardial ischemia and inosine is useful in detecting ischemic myocardial energy deficiency by the indication of insufficient glycolytic ATP supply.
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PMID:Myocardial release of inosine, hypoxanthine and lactate during pacing-induced angina in humans with coronary artery disease. 42 23

The coronary venous efflux of lactate, inosine and hypoxanthine during pacing-induced angina has been compared with myocardial extraction of the catabolites during exercise-induced angina. Inosine and hypoxanthine were analyzed by enzyme assay after separation by column chromatography. Myocardial lactate extraction at rest (15 +/- 9%, mean +/- SD) was converted to production levels (-34 +/- 26%) during pacing-induced angina (p less than 0.0005) and increased (24 +/- 13%) during exercise (p less than 0.05). The arterial values at rest (850 +/- 330 mumol/1) were unchanged during pacing and increased five-fold during exercise (4380 +/- 1860 mumol/1). The mean myocardial inosine extraction at rest (33 +/- 10%) was transformed to release values (-41 +/- 30%) during pacing (p less than 0.0005) as well as during exercise (-20 +/- 27%) (p less than 0.0005). The hypoxanthine extraction at rest (25 +/- 11%) decreased during pacing (-7.8 +/- 29%) (p less than 0.0025) and exercise (10 +/- 25%) (NS). The slight increase of arterial inosine and hypoxanthine values was not significant. Myocardially produced lactate, a sensitive marker of pacing-induced ischemia, was obscured by elevated arterial concentrations during exercise. However, inosine significantly correlated with lactate during pacing, and was useful in detecting ischemic myocardial energy deficiency during exercise-induced angina.
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PMID:Myocardial release of lactate, inosine and hypoxanthine during atrial pacing and exercise-induced angina. 75 23

Inosine at the dose of 200 mg was administered via central vein to 16 cases of various cardiac diseases, including effort angina pectoris, myocardial infarction, valvular disease, idiopathic cardiomyopathy, and congenital heart disease. Left ventricular performance was assessed by the time-course of various hemodynamic parameters (pulmonary wedge pressure, heart rate, LVP, LVEDP, max dp/dt, dp/dt/P, and cardiac output) including ejection fraction in some cases. Inosine caused significant decrease in pulmonary wedge pressure ranged from-7% to -47% during 5 min period following injection. Significant decrease in LVEDP ranged from -4% to -67% was also observed. Meanwhile significant decrease in systolic left ventricular pressure (LVP) was observed. In patients with relatively low value of max dp/dt (less than 1,500 mmHg/sec), the increase ranged from 100 to 300 mmHg/sec (6% to 38%) except 1 case with hypertrophic obstructive cardiomyopathy. In all cases, increase in dp/dt/P ranged from 4% to 44% during 5 min period following injection. In addition, the ejection fraction increased slightly in 2 out of the 3 cases studied. Cardiac output increased in all cases except a normal case by 1% to 31% during the period of 5 to 10 min following injection. Change in the heart rate was not significant. Quantitative evaluation disclosed the beneficial effects of inosine on the left ventricular function through the remarkable load-reducing effect and the unequivocal positive inotropic effect, particularly in the cases of disturbed functions. In addition, mild coronary vasodilation action was also noted.
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PMID:Effect of Inosie on left ventricular performance and its clinical significance. 720 Jan 56