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At least 19 recordsLinked to original sources
PubMed1977

Pathology of acute ischemic myocardium. Special references to (I) evaluation of morphological methods for detection of early myocardial infarcts, and (II) lipid metabolism in infarcted myocardium.

Morphological changes of early myocardial infarction within 24 hours after the onset of the acute attack were described together with a review of the literatures. For the practical purpose in detecting very early infarcts, enzymatic histochemistry is the most reliable method. Other methods previously reported such as wavy pattern of the muscle fibers and fuchsinophilia are still controvertial. Lipid metabolism in the infarcted myocardium of dogs was studied both morphologically and biochemically. Up to 3 hours, after the coronary ligation, the tissue lipids accumulated in the necrotic areas with a rise of triglyceride, but later than 6 hours the lipids decreased and were lost from the necrotic tissue, while the surrounding living cells were accumulated with neutral lipids. Serum free fatty acids were elevated in the coronary sinus blood in 6 hours after the ligation. Linolic acids were contained in high proportion in both coronary venous blood after 6 hours, and normal myocardial phospholipid. These results may lead to another possible factor in addition to catecholamine activity to elevate serum FFA in acute myocardial infarction that fatty acids may be released partly from tissue phospholipid and once ever accumulated triglyceride.

Aged↗
PubMed1975

[Steinert's syndrome and the myocardium. Total gene expression by the myocardium].

As revealed by a very thorough cardiological study of Steinert's disease in 13 cases, it would appear that the incidence of cardiac involvement observed in this disease is not merely frequent; it is, in fact, usual, systematic, and forms an integral part of the pathological picture in the same way as peripheral muscular dystrophy. One is aware of the diagnostic interest of this fact in the juvenile or abortive forms of the disease. The cardiac involvement is an indication of the complete expression of the gene towards striated muscle tissue, whether skeletal or myocardial. Finally, it opens new perspectives on the prophylactic attitude to be adopted for such patients; regular and systematic cardiological checks, moderation in the prescription of digitalis and anti-arythmia drugs, implantation of a cardiac pacemaker before an auriculo-ventricular syncopal block occurs.

Adolescent↗
PubMed1976

Observations on the ultrastructure of developing myocardium of rat embryos.

Timed pregnancies were obtained in Sprague-Dawley rats and early ultrastructural differentiation of myocardium of embryos of 10, 11, 12, 13, and 14 days were investigated and compared with that of newborn. Ten-day myocardium is characterized by loosely packed cells; the cytoplasm is typified by a dearth of organelles. Both thick (myosin) and thin (actin) filaments become identifiable for the first time in the 10-day myocardium where the heart is pulsating but circulation is not established. These filaments are not visible in the embryos of 9-day-old myocardium. The formation of these filaments is observed to continue throughout the period covered in this investigation. Concomitant with the appearance of the myofilaments is the synthesis of Z band material. By the eleventh day of gestation and during the subsequent days there is a rapid proliferation and differentiation of most of the organelles. The myofilaments become organized into fully formed striated fibrils. Intercalated discs appear as small wavy lines on the eleventh day and become plicated in later stages and serve as cell boundaries and points of attachment for myofilaments and fibrils. There is a perceptible change in the number and morphology of mitochondria from the tenth to eleventh day and later stages of development when the heart becomes functional. Similarly, there is a rapid proliferation and differentiation of granular endoplasmic reticulum and Golgi bodies. Large quantities of free ribosomes are dispersed in the cytoplasm of 10-day myocardium; however, in later stages there is a progressive reduction in the distribution of these particles. An intimate association of ribosomes and polysomes with the developing myofibrils is discernible. The T-system and sarcoplasmic reticulum begin to appear in 11-day myocardium. The embryonic myocardium displays intense mitotic activity throughout its development and a unique feature of embryonic myocardial cells is the simultaneous occurrence of myofilament synthesis and mitotic activity within the same cells.

Animals↗
PubMed1978

[Blood supply of the compact and spongy myocardium of fish, amphibia and reptiles].

Coronal arteries were injected with lead carbonate suspension and with Indian ink and cleared preparations 150--300 mkm thick were made in 195 hearts of fish, amphibians and reptiles and studied roentgenographically. It was stated that in Chondrichthyes (shark, skate) and in Chondrostei (beluga, stellate sturgeon, sturgeon), as well as in alligator both compact and spongy myocardium of the cardiac ventricle possess blood vessels. In teleostei, amphibians and reptiles (except alligator) spongy myocardium is avascular and receives its nutrition from the ventricle. In view of the data on the presence of blood vessels in the spongy myocardium in some vertebrates, it is impossible to accept the theory suggested by Grant and Regnier according to which vessels in the heart walls appear only in connection with compactization of the myocardium. Vascularization of the spongy myocardium is closely connected with oxygen saturation of the blood flowing through the heart. When this saturation is not satisfactory, the spongy myocardium has blood vessels. In alligator, vascularization of the spongy myocardium is connected with the fact that the heart has four chambers and there are arterial and venous blood streams.

Alligators and Crocodiles↗
PubMed1976

Electron microscopical and enzyme histochemical changes in the rat myocardium during prolonged autolysis.

The effect on rat myocardium of autolysis at 19 degrees C, for up to 20 days, was studied by electron microscopy and enzyme histochemistry. The enzymes studied included monoamine oxidase (MAO), sytochrome oxidase (CytO), non-specific esterase ((Ns.E.), phosphorylase (P-ase), succinate dehydrogenase (SDH) and various NAD- and NADP-linked dehydrogenases. The myocardium lost its histochemical P-ase activity within a few hours of autolysis, whereas the activity of all other enzymes remained quite normal for at least about 4 days, except that of MAO and SDH, which were normal for about 8 and 12 days, respectively. The myocardial cells lost activity of various enzymes in a patchy manner during prolonged autolysis and practically all histochemical enzyme activity disappeared within 20 days. The early period of autolysis was accompanied by rapid ultrastructural changes of myocardial cells. During prolonged autolysis the gross architecture of the myocardium was lost gradually by the 12th to 20th days. Mitochondria were the organelles most resistant to the effects of autolysis, and numerous mitochondria with morphologically solid inner and outer membranes were seen among the totally disintegrated myocardium 20 days after death. The loss of P-ase activity coincided with the loss of glycogen. The loss of MAO, SDH and CytO activities was not closely related to the morphological preservation of mitochondria, but, in accordance with other enzymes, was more closely related to the disintegration of the over-all myocardial structure. The present results showed that the architecture of the myocardium, and especially that of the mitochondria, was surprisingly resistant to the effects of autolysis at room temperature. Also several enzymes of the myocardium other than those examined so far maintained quite stable histochemically demonstrable activity during prolonged autolysis. These observations give support to the possibility of making the diagnosis of myocardial infarction at postmortem more accurate than with the present morphological and histochemical routine methods.

Alcohol Oxidoreductases↗
PubMed1976

[Maximum velocity of load-free shortening Vmax, myocardial capacity and "contractility indices" in the hypertrophic myocardium].

Based upon literature and our own experimentation on Goldblatt rats, the significance of a decrease of the maximal shortening velocity of the myocardium at zero load (Vmax) in the hypertrophied, chronically pressure-loaded heart is discussed. In the hypertrophied myocardium with varying concentrations of the contractile structures, the developed tension under isometric conditions (sigma) and the maximum rate of tension development (d sigma/dtmax) can indicate significant deviations from the values of controls of the same age, without, however, making it possible to draw from these changes absolute conclusions about the elementary contractile process. With the enhanced concentration of contractile proteins, the mentioned isometric values, as well as the maximum instantaneous power (cross-sectionally related) of the myocardium can be increased during a stage of hypertrophy in which Vmax is already reduced. The decrease of Vmax shows a rough correlation with the reduction of the specific ATPase activity of actomyosin and is already observed at moderate degrees of hypertrophy (30 to 50%). The time course of the change of both parameters in experimental hypertrophy suggests a causal relation between the changes of those two parameters and the failure of the myocardium in later stages of a chronic overload. Under the condition of reliable estimation, Vmax allows for, also with changed actomyosin concentration, an assessment of the elementary contractile process. On the other hand, Vmax does not present a sufficient measure for the cross-sectionally related power capacity of the hypertrophied myocardium. The possible dissociation between the unloaded shortening velocity and the cross-sectionally related power capacity could, in certain cases, explain an unsatisfactory correlation between Vmax and the clinical state of the heart. The so-called empirical indices of contractility, which are not always clearly related to basic physiological characteristics of the myocardium, should be interpreted with particular reserve in relation to the hypertrophied cardiac muscle.

Actomyosin↗
PubMed1976

Regional contractility. Selective depression of ischemic myocardium by verapamil.

The effects of verapamil (0.02-0.2 mg/kg) on contractility in normal and partially ischemic myocardium were compared with the changes following propranolol (0.01-1.0 mg/kg). Regional contractile function was studied in open-chest dogs with ultrasonic crystals and ischemia was controlled by graded occlusion of a carotid-to-coronary artery shunt. Reduction in shunt perfusion pressure (40-55 mm Hg) resulted in hypokinesia. Verapamil depressed contractility in ischemic myocardium in 5/5 dogs, but did not alter the maximum velocity of shortening (max V) or end-diastolic segment length in normal myocardium. Propranolol in doses sufficient to depress ischemic myocardium also depressed contractile function in normal myocardium. In two dogs without coronary occlusion, verapamil (up to 1.0 mg/kg) increased end-diastolic segment length but did not reduce max V. We conclude that verapamil selectively depresses ischemic myocardium, a finding that may have clinical implication since ischemic injury can be decreased by reducing contractility (and thereby MVO2).

Animals↗
PubMed1977

Studies on digitalis. X. Digitoxin metabolites in human myocardium and relationship between myocardial and serum concentrations of digitoxin in patients on maintenance treatment.

The levels of digitoxin and cardioactive metabolites were measured in 42 atrial biopsies with a 86Rb method modified for analysis of myocardial samples. The mean value was 91.0 ng/gm wet weight (SD 54.4). Myocardial and serum concentrations were compared in 23 patients; there was no significant correlation. The ratio of total drug concentration in myocardium and serum ranged from 1 to 38 with a mean value of 5.4. Calculated from the free drug concentrations, the mean myocardial serum ratio was 200, which reflects the high affinity of digitoxin and cardioactive metabolites to the myocardium. The metabolic pattern of cardioactive and inactive metabolites (conjugates with glucuronic and sulfuric acid) was studied in autopsy samples from left ventricular myocardium from 7 patients. Significant differences between the myocardial and serum patterns of cardioactive and inactive metabolites were demonstrated. The myocardium contained less unchanged digitoxin (25.7%) and more hydrolyzed (55.4%) and conjugated (54.1%) metabolites than serum (57.6%, 31.0%, and 33.1%, respectively). Hydroxylated metabolites in myocardium (15.8%) were not significantly changed compared to serum (10.0%).

Adult↗
PubMed1979

Resistance of contracting myocardium to swelling with hypoxia and glycolytic blockade.

The interrelationship of myocardial metabolism, performance and tissue hydration was examined in isolated contracting rat, guinea pig and dog myocardium. Myocardial metabolism was altered by blocking aerobic, and both aerobic and anaerobic metabolism. Myocardial water content and distribution were measured in rat myocardium using 3H-inulin and 51Cr-EDTA as extracellular markers. Myocardial hydration was also evaluated by light and electron microscopy. The relative susceptibility of non-contracting slices of rat and guinea pig myocardium and kidney to swelling secondary to these interventions was also explored. Hypoxia resulted in a partially reversible reduction in mechanical function; hypoxia plus glycolytic blockade led to irreversible severe contracture and total loss of tension development. Neither hypoxia nor hypoxia plus glycolytic blockade resulted in increased total tissue or extracellular water in previously contracting preparations or in non-contracting slices of myocardium. On the other hand, there were significant increases in cellular water in similarly treated kidney slices after each intervention. Thus, despite severe, irreversible derangements of mechanical function, myocardium did not swell under conditions which produced swelling in renal cortex.

Animals↗
PubMed1978

Long-term preservation of ischemic myocardium in the dog by hyaluronidase.

The administration of hyaluronidase is a promising intervention to protect the ischemic myocardium in man, but evidence of the extent to which it may reduce the ultimate size of an infarct is not well-defined. Hence, open chest, anesthetized dogs were randomized into 10 control dogs which received saline and eight treated dogs which received three doses of hyaluronidase (500 NF units/kg I.V.) at 15 minutes, 2 hours and 24 hours after occlusion of the left anterior descending coronary artery (CAO). Regional myocardial blood flow (RMBF) assessed by the microsphere technique was measured 12 minutes after CAO. The chest was then closed and the dogs were allowed to recover. Twenty-one days after CAO, the hearts were excised, divided into 1 cm thick slices and incubated in triphenyl tetrazolium chloride. Infarct size was then determined by planimetry. The left ventricular myocardium was divided into multiple samples for RMBF analysis. In control dogs 23.2 +/- 2% of the left ventricle was infarcted, compared to only 9 +/- 2.8% (P less than 0.001) in hyaluronidase-treated dogs. RMBF in noninfarcted myocardium directly adjacent to the infarct was similar to that in the normal zone remote from the infarct in the control dogs; however, in the hyaluronidase-treated dogs, blood flow in the myocardium adjacent to the infarct was significantly reduced to 68% of normal (P less than 0.01) in the outer myocardial wall and to 86% of normal (P less than 0.02) in the inner myocardial wall, which indicates that this tissue, at least in some part, was in jeopardy, but was salvaged by hyaluronidase. Epicardial electrocardiographic data showed that three weeks after CAO, Q waves were less frequent and smaller in hyaluronidase compared to untreated dogs. Preservation of the frequency and magnitude of R waves was greater in the hyaluronidase-treated group at three weeks. We conclude that hyaluronidase resulted in long-term preservation of the ischemic myocardium.

Animals↗
PubMedDate not supplied

[Protein fractions and their enzymatic activity in the rat myocardium after a flight on the Cosmos-690 biosatellite].

Gamma-irradiation of rats in the ground-based experiment decreased the activity of aspartate aminotransferase of sarcoplasmatic proteins of the myocardium and increased the activity of adenosine triphosphate of myosin of the myocardium 1 and 26 days post-test. Gamma-irradiation of flight rats also reduced the activity of aspartate aminotransferase of sarcoplasmatic proteins of the myocardium; however, the activity of ATPase of myosin of the myocardium was lowered both 1 and 26 days postflight. It is suggested that irradiation-induced inhibition of synthetic processes delayed the synthesis of myosin with a normal activity and diminished the protein content in the T fraction of myocardium on the 1st postflight day.

Animals↗
PubMedDate not supplied

[Shifts in the electrolyte and energy metabolism of rat myocardium in experimental hypercorticism].

Experiments were conducted on 612 albino male rats; a complex study was made in the myocardium of K+, Na+, Ca2+, Mg2+, Cl-, water, creatinphosphate, inorganic phosphorus, adenylic system components. A study was made of the effect of exogenous hypercorticism created by the administration of prednisolone, hydrocortisone and DOCA on the cardiac metabolism. Potassium-sodium tissue homeostasis in the myocardium proved to be stable under these conditions. Glucocorticoid hypercorticism was characterized by a reduction of creatinphosphate and by the accumulation of inorganic phosphate. DOCA administration failed to be significantly reflected on the balance of the phosphate macroerg balance. Glucocorticosteroids caused an increase in the Mg2+ and a reduction of the Cl- level, whereas DOCA brings about an increase of Ca2+ and Cl- in the myocardium. Dosaged sharp physical load is accompanied by the K+ cumulation in the myocardium. In the case of 2-hour swimming this is combined with a "stable" condition of the energy processes. When swimming is continued up to 5 hours there occurs a distinct disturbance of the balance of disintegration and resynthesis of the phosphate macroergs in the cardiac muscle. Administration of the corticosteroids under study against this background produced no significant influence on the character of the shifts in the electrolyte-energy metabolism, and failed to prevent the normal course of the restorative processes in the myocardium at the immediate period after the exercises.

Adenine Nucleotides↗
PubMedDate not supplied

Noncompetitive catecholamine-antagonism of acetylcholine in the sympathectomized mammalian ventricular myocardium.

The effect of the vagus transmitter on the ventricular myocardium varies qualitatively as well as quantitatively in different warm-blood species. In the ventricular myocardium of birds (duck, hen), a part of the acetylcholine sensitivity remains even after catecholamine depletion. In contrast, the inhibitory effects of acetylcholine on the ventricular myocardium of mammals (rat, guinea pig, cat, dog, man) depend on the activity of the sympathicus. In the chemically sympathectomized (6-OH-DA) cat ventricular myocardium, a cholinergic innervation is, histochemically, clearly demonstrable. Correspondingly significant effects of endogenous (i.e. releasable by field stimulation) and exogenous acetylcholine can be seen if the contraction force is enhanced by exogenous catecholamines. This preparation is, therefore, a good model for the demonstration of a catecholamine antagonism of acetylcholine. Using this model, on the basis of dose-response relationships, it is possible to demonstrate that a noncompetitive catecholamine-antagonism of acetylcholine indeed exists in the mammalian ventricular myocardium independent of a cholinergically mediated reduction in the norepinephrine release.

Acetylcholine↗
PubMed1978

Effects of graded coronary constriction on regional oxygen and carbon dioxide tensions in outer and inner layers of the canine myocardium.

This study was undertaken to investigate the effects of graded coronary constriction on regional gas tensions of the myocardium. In 12 open chest dogs, tissue carbon dioxide (PtCO2) and oxygen (PtO2) tensions were measured simultaneously in outer and inner layers of the myocardium using a mass spectrometer. In normal condition, higher PtO2 and lower PtCO2 were observed in outer layer than in inner layer. With application of coronary constriction, increase in PtCO2 and decrease in PtO2 were observed in both layers of the myocardium, but the response to the ischemic stimuli by applying coronary constriction in inner layer was different from that in outer layer. Severe coronary constriction, more than 90% in its diameter, was necessary to produce significant changes in both gas tensions in both layers of the myocardium. Decrease in PtO2 was found in the condition of less severe coronary constriction and to be greater in inner layer than in outer layer of the myocardium. In terms of the changes in PtCO2, inner layer was also more susceptible to the ischemic stimuli than outer layer. The greater and earlier elevation of PtCO2 in inner layer than in outer layer is regarded as one of the possible mechanisms of the reduction of myocardial contraction in the early stage of myocardial ischemia.

Animals↗
PubMed1978

Technetium-labeled heparin: preliminary report of a new radiopharmaceutical with potential for imaging damaged coronary arteries and myocardium.

Heparin has been labeled with [99mTc] pertechnetate and its ability to image damaged coronary vessels and myocardium during and following myocardial ischemia has been studied in experimental animals. The data obtained indicate that Tc-99m heparin localizes in damaged myocardium and coronary vessels in canine models of temporary myocardial ischemia and reperfusion and in damaged myocardium during fixed coronary occlusion. Scintigraphic detection of damaged myocardium was possible in both models, but the highest levels of Tc-99m heparin in damaged myocardial tissue were found in those dogs with temporary coronary occlusion and reflow. The data suggest that Tc-99m heparin may be of value as a positive imaging agent when coronary arteries or myocardium are injured and either reperfusion is allowed and/or significant blood flow persists in the damaged area.

Animals↗
PubMed1977

Transaxial tomographic imaging of canine myocardium with 11C-palmitic acid.

Radiopharmaceuticals incorporated directly into the metabolic pathways in myocardium provide a useful means for evaluating such processes. Palmitic acid, a major physiologic substrate of myocardium, has a well-understood role in myocardial metabolism. Accordingly, 11C-palmitic acid was the substrate chosen for use in conjunction with positron emission transaxial tomography to obtain images of canine myocardium. This procedure provides high-contrast images of tranverse sections of the myocardium, with good target-to-nontarget ratios (in the image), over a period of 5 to 85 minutes. Clearance half-times for blood and myocardial tissue were found to be 4.8 and 330 min, respectively. In normal myocardium, images obtained with 11C-palmitic acid were those obtained with 13NH3 and 11CO-hemoglobin. In vivo images of hearts with myocardial infarcts showed a clear delineration of infarcts and normal tissue.

Ammonia↗