ABSTRACT
Low-molecular weight peptides prepared according to an original procedure from a cattle heart possess a protecting effect on the myocardium during ischemia. Peptides in doses of 10(-7) g/ml and less improve the indexes of contractility function of the isolated heart after total ischemia and correct respiration warranting cardiomyocytes survival during hypoxia. However, in different models high doses of heart peptides (5 x 10(-6) g/ml and more) are shown to inhibit contractility, to stop respiration, the action of the peptides increasing with myocardial ischemia degree.
Subject(s)
Heart/drug effects , Peptides/pharmacology , Animals , Cattle , Dose-Response Relationship, Drug , Drug Evaluation, Preclinical , Guinea Pigs , In Vitro Techniques , Molecular Weight , Myocardial Contraction/drug effects , Myocardial Infarction/drug therapy , Myocardial Infarction/physiopathology , Myocardial Ischemia/drug therapy , Myocardial Ischemia/physiopathology , Peptides/isolation & purification , Peptides/therapeutic use , RatsABSTRACT
It has been established that cordialin inhibits selectively succinic acid oxidation and intensifies the exudation of a NADH2 substrate which is energetically more advantageous, and in this way has a favorable effect on energy metabolism, evidence of which is increase of the ATP content in the myocardium. Cordialin correction of the biologic energy of cardiomyocytes in hypoxia and ischemia prevents the accumulation of lipid drops in the cells of the peri-infarction zone, which reflects the high intensity of the processes of fatty acids beta-oxidation. As a result of this glycolysis activation is unnecessary (which is confirmed by high glycogen content, both of a qualitative and quantitative character, in the myocardium and low concentrations of glucose and lactate in the blood) and, consequently, the sequelae of acidosis are prevented.
Subject(s)
Cardiovascular Agents/pharmacology , Energy Metabolism/drug effects , Heart/drug effects , Hypoxia/drug therapy , Myocardial Ischemia/drug therapy , Peptides/pharmacology , Animals , Cardiovascular Agents/isolation & purification , Female , Guinea Pigs , Intercellular Signaling Peptides and Proteins , Male , Myocardium/cytology , Peptides/isolation & purification , RatsABSTRACT
Based on experimental studies the possibility of cordialin use in acute ischemia is being substantiated. On the first day of the animals' mortality and increased life duration of cells in ischemia zone, delaying the injury region expansion. But later in rats, that were given cordialin, slowing down of injury zone recovery and scar tissue formation was demonstrated. Cordialin use in early stages of myocardial infarction is suggested. In experiments on isolated heart cordialin is reported to decrease the intensity of processes of lipids' peroxide oxidation in intact and ischemic myocardium. But in reperfusion cordialin activates LPO, that is associated with heart contracting activity inhibition. The results of the study may serve as an experimental basis for cordialin use on the first day of MI development. Its further use needs the correction of its ability to slow down the processes of necrotic tissue recovery.
Subject(s)
Cardiovascular Agents/therapeutic use , Heart/drug effects , Myocardial Infarction/drug therapy , Peptides/therapeutic use , Animals , Biopsy , Cardiovascular Agents/pharmacology , Guinea Pigs , In Vitro Techniques , Intercellular Signaling Peptides and Proteins , Malondialdehyde/analysis , Myocardial Contraction , Myocardial Infarction/pathology , Myocardial Infarction/physiopathology , Myocardial Reperfusion , Myocardium/pathology , Peptides/pharmacology , Rats , Time FactorsABSTRACT
An increased density of blood revealed in myocardial infarction patients served the basis for a simple and highly informative method developed by the authors to early diagnose myocardial infarction when other methods are not sensitive. The high density of blood is registered upon placing a drop of blood into flakes with sodium chloride solution of different concentration.
Subject(s)
Blood Chemical Analysis , Myocardial Infarction/diagnosis , HumansABSTRACT
Cardiolin therapy influence on the periinfarction zone cardiomyocyte ultrastructure, sarcolemma permeability for colloidal lantan, myocardium energy level were studied in 25 white noninbred rats with experimental myocardial infarction. 6 hours after coronary occlusion ultrastructural damage in treated rats was less pronounced and mitochondria energy efficiency ratio was higher than those in the control group. 24 hours after the occlusion the tendency to normalization of the cardiomyocyte damage in treated rat myocardium was demonstrated, while in non-treated animals ischemic damage becomes irreversible, this being confirmed by the test with colloidal lantan. Cardiolin therapy prevents the infarction zone expansion by decreasing ischemic damage of periinfarction cardiomyocytes and by stimulating regeneration processes in these cells.
Subject(s)
Myocardial Infarction/drug therapy , Peptides/therapeutic use , Animals , Coronary Vessels/ultrastructure , Microscopy, Electron , Myocardial Infarction/pathology , RatsABSTRACT
The experiments on white rats with induced myocardial infarction have studied the influence of dalargin on the infarction size and peri-infarction zone ultrastructure. 24 hours later the decrease in the infarction zone size was detected in rats who had received dalargin in a dose of 50 and 100 micrograms/kg. In the peri-infarction zone the increase in glycogen quantity, the lower degree of lipid infiltration, the increase in mitochondrial number and mitochondrial energy effectiveness coefficient were noted, as compared to control animals. Sarcolemma of cardiomyocytes from the peri-infarction zone in rats on dalargin was impermeable for colloidal lanthanum. The decrease in the infarction size under the effect of dalargin is explained by its influence on the survival of cardiomyocytes in the peri-infarction zone.
Subject(s)
Enkephalin, Leucine-2-Alanine/analogs & derivatives , Enkephalin, Leucine/analogs & derivatives , Heart/drug effects , Myocardial Infarction/drug therapy , Myocardium/ultrastructure , Animals , Dose-Response Relationship, Drug , Drug Evaluation, Preclinical , Enkephalin, Leucine/therapeutic use , Microscopy, Electron , Mitochondria, Heart/drug effects , Mitochondria, Heart/ultrastructure , Myocardial Infarction/pathology , RatsABSTRACT
The effect of opiate peptides (leu-enkephalin, met-enkephalin and beta-endorphin) as well as of enkephalin synthetic analogs (two tetrapeptides and dalargin hexapeptide) on the activity of blood enzymes CPK and LDG1, the scope of myocardial infarction and ultrastructure of periinfarction cardiomyocytes has been studied on 200 white outbred rats with simulated myocardial infarction. The endogenous opiate peptides and dalargin hexapeptide were found to significantly decrease CPK and LDG1 activity and to diminish the size of the infarction. The effect is related to the drugs influence on the survival of periinfarction cardiomyocytes that can be proved electron-microscopically and using colloid lanthanum test.
Subject(s)
Endorphins/therapeutic use , Heart/drug effects , Myocardial Infarction/drug therapy , Myocardium/enzymology , Animals , Creatine Kinase/blood , Drug Evaluation, Preclinical , L-Lactate Dehydrogenase/metabolism , Myocardial Infarction/enzymology , Myocardial Infarction/pathology , Myocardium/ultrastructure , RatsABSTRACT
Finding opiate receptors in the heart, definition of their role in contractility and blood flow regulation (2) as well as our previous data on the decrease of Leu-enkephalins contents in the blood of patients with myocardial infarction (5) are the theoretical prerequisites for the elucidation of the role of Leu-enkephalins in the pathogenesis of acute myocardial infarction.
Subject(s)
Enkephalins/physiology , Myocardial Infarction/etiology , Animals , Blood Circulation/drug effects , Enkephalins/blood , Female , Male , Myocardial Contraction/drug effects , Myocardium/ultrastructure , Rats , Receptors, Opioid/physiology , Receptors, Opioid/ultrastructureABSTRACT
The ultrastructure of sinus and atrioventricular nodes was studied in white rats with experimental myocardial infarction. 24 hours after the induction of the disease mitochondrial enlargement characterized by the increase in their area, decrease in the number of cristae and the decline in the rate of mitochondrial energy effectiveness was detected. Different degrees of nuclear chromatin aggregation and membrane permeability for colloidal lanthanum were observed. Characteristic types of conduction cellular lesions were revealed in experimental myocardial infarction.