Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of calcium current agonist BAY K 8644 on transmembrane potential of guinea pig papillary muscle (PM) and sheep Purkinje fibers (PF) were studied. The action potentials (AP) and contractions (C) were recorded. C both of PM and PF increased (two-four times) in response to BAY K 8644 (0.5-5 microM) addition. The AP duration of PM increased slightly (20%) while PF AP duration increased progressively with the time even at low BAY K 8644 dose (0.5 microM). At 5th min, early afterdepolarizations (EAD) occurred. After 10 min drug application PF became inexcitable at high plateau level. TTX and ethmozin (1 microM) restored AP. Thus, changes in ionic currents balance in PF towards the increase in inward calcium current by BAY K 8644 resulted in additional steady state potential at plateau level. The latter might induce EAD and re-entry around functionally inexcitable PF. The similarity of mechanisms of arrhythmias induced by ischemia with the presented model is discussed.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1989
PMID:[Asymmetrical changes in electrical activity of Purkinje fibers and muscle cells after administration of BAY K 8644. A new model of cardiac arrhythmia]. 247 20

Seventeen patients were studied: 10 with stable angina and coronary atherosclerosis, and 7 with "intact" coronary arteries (a control group). All patients underwent coronarography and catheterization of the coronary sinus. Blood samples were obtained from the left ventricle and coronary sinus in 3 points: at rest, peak pacing, 10 min after pacing. All patients with stable angina had positive atrial pacing test (pain and/or ECG deviations and lactate production), in control group similar changes were not observed. However, no statistically significant difference was found in platelet factor (IV) 4 levels between the groups and following pacing; the level of platelet factor IV was near 90 ng/ml. It is concluded that patients with stable angina during pacing-induced ischemia had no significant platelet activation, which may provoke thrombotic events.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1989
PMID:[The platelet factor 4 content of the blood in induced myocardial ischemia in patients with stable stenocardia]. 260 90

The article deals with the effect of permanent, temporal and total myocardial ischemia on the oxidation of acetate, hexanoate, palmitoylcarnitine and palmitoyl-CoA in isolated rabbit heart mitochondria. All the three models of ischemia in different experimental situations demonstrated a similar degree of fatty acid oxidation suppression independent of the length of acyl residue, the suppression being the greatest during the first hours and in total ischemia. Both in the control and in ischemia, respiratory activity was at its highest level with acetate, decreasing in the order above. Thus, the rate of Krebs' cycle reactions and of respiratory chain does not limit medium- and long-chain fatty acid oxidation. It is nevertheless established that suppression of their oxidation in ischemia is completely determined by the decrease of cytochrome S and of endogenous substrate intermediates of Krebs' cycle in the mitochondria; decreased adenine nucleotide and carnitine-palmitoyl-transferase transport (other authors' data) is not critical, at least in early ischemia (0.5 h). Ischemic mitochondria are characterized by incomplete palmitoylcarnitine oxidation.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1985
PMID:[Mechanism of ischemic disorders of fatty acid oxidation in heart mitochondria]. 298 85

To study the character of the mechanism of protective action of phosphocreatine on ischemic myocardium the effects of phosphocreatine (PCr) and phosphoarginine (PArg) were compared. PCr and PArg were shown to expose identical Ca2+-chelating properties and were used as their Na-salts. Only PCr protected the cardia function during ischemia and simultaneously inhibited the accumulation of lysophosphoglycerides, products of phospholipid degradation. PArg failed to exert both of these effects. By an EPR probe method PCr was shown to increase the order of structural organization of phospholipids in the cardiac sarcolemmal vesicles. The results show that the effect of PCr on ischemic myocardium is not due to nonspecific changes in the ion composition of a solution, but most probably due to highly specific effect of phosphocreatine on the phospholipid membrane of the cardiac cells sarcolemma.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1988
PMID:[High specificity in the molecular mechanism of the protective action of phosphocreatine on the myocardium in ischemia]. 323 54

Systemic haemodynamic and myocardial blood flow effects of ryodipine and nifedipine have been studied during acute transitory coronary occlusion in the open-chest anesthetized dogs. Acute ischemia has been done by occlusion of left anterior descending coronary artery for 5 min. Cardiac output and blood flows in the ischemic, lateral border and intact areas of the myocardium were defined with 15 mcm plastic radiolabelled microspheres. Drugs were administered intravenously in equihypotensive doses. Both drugs prevented fall of cardiac index during occlusion, decreased arterial pressure and total peripheral resistance but heart rate remained unchanged. Ryodipine as well as nifedipine considerably increased blood flow (42 +/- 15% and 85 +/- 23%, respectively, P less than 0.05) in the intact zones of the left ventricle, but they did not affect the blood flow in the ischemic zone.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1988
PMID:[Effect of the calcium antagonists foridon and nifedipine on systemic hemodynamics and myocardial blood flow in dogs with acute myocardial ischemia]. 340 43

The state of myofibril creatinkinase and contractile properties of chemically skinned myocardial fibers of rat after 70-90 min ischemia and 15-30 min reperfusion was studied. In spite of sharp fall in the total creatinkinase activity in the tissue, the enzyme activity in myofibrils does not change greatly. Ischemia does not change the functional abilities of myofibril creatinkinase as well as characteristics of Ca-activated contraction of skinned fibers. The results show that irreversible loss of myocardial contractile activity after prolonged ischemia and reperfusion is not connected with violation of myofilament characteristics or deterioration of functional association between myofibril creatinkinase and ATPase.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1987
PMID:[Contractile properties and creatine kinase activity of myofilaments after ischemia and reperfusion of the rat heart]. 342 20

The effect of K+ (13.5 and 26 mmol). Cs+ (10 mmol), verapamil (500 nmol) and desipramine (100 nmol) added to the perfusate before the induction of 25-min total ischemia on the release of noradrenaline (NA) and adenine nucleotide degradation products (ANDP) and on myocardial contractility recovery has been studied on the isolated guinea-pig heart. It has been shown that desipramine-induced inhibition of catecholamine transport through axoplasmic membrane was accompanied by a considerable decrease in NA and ANDP release from ischemic myocardium. The experiments on KCl, CsCl and verapamil have demonstrated that the degree of preischemic contractility reduction determines ANDP myocardial loss and contractility recovery in reperfusion. Linear correlation observed in all the experimental series between the degree of endogenous NA release and overall ANDP release suggests that the magnitude of NA release in ischemia is determined by the energetic myocardial status. NA loss approaches zero if adenine nucleotide pool is not reduced to minimal critical values.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1987
PMID:[Relationship between adenine nucleotide breakdown and catecholamine losses in myocardial ischemia and the recovery of contractile function during reperfusion]. 360 37

Using 31P-NMR technique it was shown that exogenous phosphocreatine (10 mM) added in the cardioplegic solution provided higher levels of recovery of intracellular ATP (approx. 60% vs. 26% in the control) and phosphocreatine (90% vs. 43%) in perfused rat hearts after 35 min of total ischemia. Simultaneously significantly higher levels of contractile recovery (90% vs. 35%) and a three-fold decrease in creatine kinase release into the perfusate were observed. These effects of exogenous phosphocreatine can be related to either intracellular action of this compound or its interaction with cellular membrane.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1985
PMID:[Study of the protective effect of phosphocreatine on the ischemic myocardium during cardioplegia using the P-31 NMR method]. 400 52

Acute heart insufficiency was simulated in dogs, rabbits and rats with experimental myocardial infarction, hypothyrosis, thyrotoxicosis, autoimmune cardiomyopathy, myocardium hypertrophy by exerting additional mechanical load on the heart (graded aortic stricture, swimming, running in a tread-ban). Irrespective of the basic pathological process the development of acute heart insufficiency was associated with generalized damage of plasmalemma of the majority of functioning cardiomyocytes, registered with colloid lanthanum. Plasmalemma damage precedes intracellular ultrastructural alterations and is reversible. Sarcolemma damages in non-functioning cardiomyocytes revealed in the focus of severe ischemia in experimental myocardial infarction is on the contrary indicative of irreversible cellular changes. The distinctions demonstrate that mechanisms causing damages in sarcolemma membrane can be different in conditions of preserved coronary blood flow and in severe ischemia.
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR 1984
PMID:[Role of the sarcolemma in the morphogenesis of acute heart failure]. 623 4