Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Analysis of data obtained in the study of the blood enzymatic and isoenzymatic spectra (creatine phosphokinase and lactate dehydrogenase with simulatenous study of aspartate and alanine transaminases) in patients with various forms of ischemic heart disease showed the close correlation of the studied tests with the clinical picture of the disease, the degree and depth of myocardial involvement. The enzymatic tests studied are of diagnostic and prognostic importance and may be used in the differential diagnosis of various forms of ischemic heart disease.
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PMID:[Aspects of a study of the blood enzymatic and isoenzymatic spectrum in different forms of ischemic heart disease]. 67 6

In nine patients with ischaemic heart disease at rest and during pacing differences of free plasma amino acids, lactate, ammonia and uric acid between arterial blood and blood in the coronary sinus (a-cs differences) were investigated. At rest one single significant difference was found, i.e. a positive a-cs difference in aspartate. During pacing significant positive differences were recorded in aspartate, glutamate, leucine and isoleucine and significant negative a-cs differences in cystine-cysteine, glutamine and aspartic acid and in alanine. Among the correlations between a-cs differences the negative relationship between lactate and alanine and the negative correlation between cystine-cysteine and leucine, isoleucine and glutamine is significant. There is a positive relationship between the a-cs difference of alanine and glutamine and between the differences of leucine, isoleucine and glutamate. The a-cs differences of ammonia and uric acid correlate negatively.
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PMID:Amino acid metabolism in the heart muscle in subjects with ischaemic heart disease at rest and during pacing. 69 15

Coronary artery disease causes an increase in glutamate uptake and alanine output by the heart. We assessed the effects of acute myocardial ischemia on alanine and glutamate exchange and ammonia production in 10 anesthetized open-chest domestic swine (46.9 +/- 0.7 kg). Coronary blood flow was controlled through an extracorporal perfusion circuit. After a nonischemic control period (aerobic) the blood flow in the left anterior descending coronary artery was reduced by 60%. Arterial and anterior interventricular venous samples where drawn before and during 35 min of ischemia. Subendocardial blood flow, measured using radiolabeled microspheres, decreased from 1.27 +/- 0.16 to 0.25 +/- 0.09 (ml/g)/min, and left-ventricular wall-thickening fell to 47% of aerobic values. Ischemia resulted in a significant increase in the rate of glucose uptake (p less than 0.05) and a switch to net lactate production (p less than 0.01). Ischemia did not affect the rates of alanine output (-0.9 +/- 1.0 vs. -0.3 +/- 0.3 mumol/min) or glutamate uptake (-0.4 +/- 1.1 vs. 0.3 +/- 0.6 mumol/min), but did increase the venous-arterial difference for ammonia (-4.1 +/- 4.1 to 52.7 +/- 5.5 microM, p less than 0.0001) and the ammonia output (-0.33 +/- 0.24 to 1.34 +/- 0.14 mumol/min, p less than 0.0001). In conclusion, acute ischemia did not stimulate greater alanine output or glutamate uptake. However, acute ischemia did cause an increase in anaerobic glycolysis rate and ammonia output, which reflects a profound disruption in myocardial energy metabolism.
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PMID:Alanine, glutamate, and ammonia exchanges in acutely ischemic swine myocardium. 159 Jul 40

1 We studied the effects of a form of interleukin-8 (i.e., [Ala-IL8]77) on endothelial dysfunction and myocardial injury in rabbits. Pentobarbitone-anaesthetized rabbits were subjected to 1.5 h occlusion of the marginal coronary artery and 3.5 h reperfusion. [Ala-IL8]77 (50 micrograms or its vehicle) was given i.v. as a bolus 10 min prior to reperfusion. [Ala-IL8]77 was also studied in isolated perfused hearts of rabbits. 2 Myocardial ischaemia plus reperfusion in untreated rabbits produced severe endothelial dysfunction and myocardial injury, including marked myocardial necrosis, elevated cardiac myeloperoxidase (MPO) activity in ischaemic cardiac tissue, and loss of response of marginal coronary rings to the endothelium-dependent vasodilators, acetylcholine (ACh) and A23187. 3 Administration of [Ala-IL8]77 10 min prior to reperfusion resulted in significant protective effects in post-ischaemic reperfusion. Compared with untreated rabbits, [Ala-IL8]77 caused a reduced necrotic zone (P less than 0.01), lower MPO activity in the necrotic zone (P less than 0.05), and significantly preserved vasorelaxant responses of marginal coronary artery rings to endothelium-dependent vasodilators, ACh (P less than 0.001) and A23187 (P less than 0.001). 4 These results indicate that myocardial ischaemia and reperfusion result in a severe endothelial dysfunction and myocardial injury which involved the interaction of neutrophils and endothelial cells. However, [Ala-IL8]77 did not appear to exert a direct endothelial protective effect in the absence of neutrophils in rabbit isolated perfused hearts. 5 Inhibition of neutrophil accumulation in the myocardium, perhaps by prevention of endothelial dysfunction resulting from [Ala-IL8]77, leads to significant protective effects in ischaemia and reperfusion in rabbits.
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PMID:Cardioprotective and endothelial protective effects of [Ala-IL8]77 in a rabbit model of myocardial ischaemia and reperfusion. 165 42

We studied the effects of heparin, given as 12,500 units intravenously, on cardiac metabolism during catheterization of the coronary sinus at rest and during repeated rapid atrial pacing in 8 patients with stable angina pectoris, positive stress tests and coronary arterial disease and in 8 patients with normal coronary arteries without objective signs of ischemic heart disease. Heparin did not influence angina, ST-segment depression or myocardial lactate production induced by pacing in the group with diseased coronary arteries. In both groups, heparin increased the arterial levels (70%) and the myocardial uptake (40-50%) of free fatty acids, the latter only during non-ischemic conditions. Myocardial net uptakes of glucose, lactate and glutamate and the release of alanine were reduced by heparin in the subjects with normal coronary arteries but not in those with ischemic heart disease. Myocardial oxygen consumption was unchanged. In the patients with normal coronary arteries, the levels of free fatty acid in the arteries were positively related to myocardial uptake of fatty acids and the release of citrate but inversely related to cardiac uptake of lactate and glucose. These relations were lacking in the patients with diseased coronary arteries. The metabolic effects of heparin on the heart, therefore, were diminished in patients with ischemic heart disease when compared to controls. This is probably due to an altered regulation of substrate preference in ischemic hearts.
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PMID:Cardiac metabolic effects of heparin differentiate between patients with normal and stenotic coronary arteries. 197 Aug 7

This study reports the results of a retrospective review of the case records of 28 seriously ill patients who received intravenous cimetidine (generally 300 mg q8h) for the treatment of gastric discomfort and/or hemorrhage or for prophylaxis against stress-induced ulcers. Most of these patients presented with complex symptoms arising from a variety of pathological conditions including ischemic heart disease, myocardial infarction, cerebrovascular accident, pneumonia, and trauma. A number of patients also had acute gastrointestinal hemorrhage. Over two-thirds of the patients treated with intravenous cimetidine demonstrated a reduction in gastrointestinal symptom severity, and a statistically significant reduction in the mean severity rating for all patients was observed. Adverse reactions reported during cimetidine therapy were generally mild to moderate in severity and required discontinuance of therapy in only one patient. The most common complaint was headache. Intravenous cimetidine administered q8h offers a safe and cost-effective approach to H2-receptor blockade and reduction of gastric acid secretion in patients who are temporarily unable to take oral medication.
Ala Med 1990 Oct
PMID:Intensive care experience with intravenous cimetidine. 228 32

Intracoronary thrombi resulting in acute myocardial ischemia can often be lysed by thrombolytic agents. We examined the potential of a fibrin(ogen)-degradation product pentapeptide 6A (Ala-Arg-Pro-Ala-Lys), which increases coronary blood flow partly by stimulation of prostacyclin release, in reestablishing coronary blood flow in dogs with experimentally induced thrombus. An occlusive thrombus in the circumflex coronary artery was created by electrical stimulation of the endothelial surface. After the occlusive thrombus was stable without electrical current for at least 15 min, peptide 6A (5 mumol/min for 20 min intracoronary) or tissue-plasminogen activator (t-PA) [10 micrograms/kg/min for 20 min intravenously (i.v.)] was randomly administered. Peptide 6A administration reestablished coronary blood flow (peak 16 +/- 2 ml/min, mean +/- SE) in 6 of 12 animals with occlusive coronary thrombus. Mean time to blood flow reestablishment was 5.3 +/- 2.2 min, but the reflow was short lived (mean duration of reflow: 15.7 +/- 1.6 min). t-PA reestablished coronary blood flow (peak 19 +/- 3 ml/min) in 4 of 10 animals. The time of flow reestablishment was 12.0 +/- 3.9 min and the reflow persisted for 22.0 +/- 3.1 min. Peptide 6A administration was associated with an increase in coronary venous plasma 6-keto-PGF1 alpha, indicating stimulation of prostacyclin release. This study demonstrates the potential of peptide 6A in reestablishing coronary blood flow in a canine model of coronary thrombosis. This transient effect is associated with release of prostacyclin, which may be beneficial because of its vasodilator and platelet inhibitory effects.
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PMID:Effects of peptide 6A on coronary blood flow dynamics in canine coronary thrombosis. 248 73

Fractional myocardial extraction/release of glutamate, glutamine, alanine, ammonia, asparagine, glucose and lactate was studied in 12 subjects with normal coronary anatomy (controls) and 28 patients with coronary artery disease (CAD) during rest and atrial pacing. At rest patients with CAD showed an increased myocardial extraction of glutamate, glucose and lactate and an augmented glutamine and alanine release compared with controls. In all CAD patients myocardial ammonia and asparagine release was found at rest, while all controls showed myocardial extraction of these compounds. Myocardial glutamate extraction correlated positively with glucose and lactate extraction, glutamine and alanine release and inversely with ammonia release in CAD patients at rest. In patients with two- and three-vessel disease pacing-induced ischaemia resulted in a pronounced decrease in myocardial glutamate extraction and glutamine release, augmented myocardial production of ammonia and asparagine and a conversion of lactate extraction into lactate release. During pacing myocardial glutamate extraction was related to alanine and glutamine release and correlated inversely with ammonia and lactate release in these patients. The results indicate that glutamate extraction is closely connected with glucose and lactate extraction and ammonia binding via glutamine formation in the hearts of CAD patients and, thus, with the energy supply of ischaemic myocardium. An assessment of myocardial exchange of the nitrogenous compounds we have studied, complimentary to lactate, is a promising biochemical test for the identification of ischaemic heart disease in man.
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PMID:Features of myocardial metabolism of some amino acids and ammonia in patients with coronary artery disease. 270 69

The effect of intravenous glutamic acid infusion (3 mg/kg/min) was studied during myocardial ischemia and reperfusion in anesthetized dogs. Left ventricular ischemia was induced by underperfusion of the anterior descending and circumflex coronary arteries. Glutamic acid reduced the ischemic contractile depression 2 min after a 60%-reduction of the coronary blood flow. The left ventricular systolic pressure was decreased by 9% versus 22%, dP/dt by 16% versus 29%, left ventricular systolic pressure heart rate product by 16% versus 31%. Reperfusion with glutamic acid improved the recovery of cardiac performance without any increase in myocardial oxygen consumption. Glutamic acid infusion resulted in a 2-fold augmentation of glutamate uptake by the ischemic myocardium. It led to cessation of ammonia release by the heart due to activation of glutamine synthesis, enhancement of alanine formation coupled with pyruvate utilization and did not change lactate production. The mechanisms of the protective action of glutamic acid are discussed.
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PMID:[Correction of contractile function and metabolism in canine ischemic myocardium due to exogenous glutamic acid]. 286 92

The long-term effects of antianginal therapy on coronary blood flow and myocardial metabolism were studied in 35 patients with chronic stable angina. Arterial and coronary sinus blood samples and coronary blood flow measurements were obtained before and after 1 month of oral administration of propranolol or of the calcium antagonist nicardipine. When the data obtained at a fixed heart rate (10% to 15% above the pretreatment sinus rhythm) were compared, no significant differences were evidenced between the propranolol and the nicardipine groups. Coronary blood flow and myocardial oxygen uptake were unchanged with both drugs. Myocardial lactate uptake increased in 11 patients of the propranolol group (from -2 +/- 42 to 66 +/- 47 mumol/min, p less than .001) and in 11 patients of the nicardipine group (from 0 +/- 36 to 31 +/- 29 mumol/min, p less than .001). In these 22 patients, the increase in lactate uptake was accompanied by reductions in uptake of free fatty acids and by a decrease in the coronary sinus concentration of thromboxane B2 from 131 +/- 87 to 61 +/- 32 pg/ml (p less than .01), whereas the transcardiac release of prostacyclin increased. None of these changes in free fatty acids or in prostanoid handling were observed in the nine patients (five in the propranolol and four in the nicardipine group) in whom lactate uptake was not augmented. During pacing-induced tachycardia, the metabolic effects of the two drugs appeared different. Myocardial lactate uptake decreased more in the patients receiving propranolol than in those receiving nicardipine and the combined productions of alanine and glutamine rose by 3.2 +/- 5.8 mumol/min in the propranolol group while it decreased by 3.1 +/- 8.2 mumol/min in the nicardipine group (p less than .025 propranolol vs nicardipine). In conclusion, long-term antianginal therapy with propranolol or nicardipine improved several markers of myocardial ischemia in approximately two-thirds of the patients. Although the changes observed at low heart rates were similar with the two drugs, the data also suggest that better metabolic protection is provided by the calcium antagonist during pacing-induced tachycardia.
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PMID:Changes in myocardial metabolism during therapy in patients with chronic stable angina: a comparison of long-term dosing with propranolol and nicardipine. 369 57


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