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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Silent myocardial ischemia seems a relatively frequent manifestation of coronary insufficiency. The practice of more and more sophisticated tests to detect myocardial ischemia shows that it is a relatively frequent pathological occurrence. It occurs in patients with an abnormality or a transient or constant failure of the alarm system, represented by pain during the ischemia. It is an heterogenous picture which may take the appearance of a completely silent ischemia (the metabolic, hemodynamic and electrical consequences of ischemia being the only symptoms of coronary insufficiency, demonstrated by the presence of severe, angiographic or anatomical, stenoses); of a silent transient ischemia (with alternance of symptomatic and silent episodes or with silent episodes after myocardial infarction); of myocardial necroses without pain or ischemic myocardiopathies. It is the consequences of either an ischemia which is too moderate to reach the pain threshold, or a severe ischemia in patients presenting alterations of the transmission system and of the perception of pain. It has metabolic, hemodynamic and anatomical consequences which may lead to necrosis or degeneration and fibrosis of the myocardium. The prognosis of a painless disease is difficult to make but it does not seem to be as poor as the one of the usual forms of ischemic cardiopathies. Medical treatment is mandatory, and surveillance of its efficacy must be systematic using the techniques of detection of the ischemia.
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PMID:[Silent myocardial ischemia]. 382 50

Experiments were made on 56 white noninbred male rats with transitory coronary insufficiency (duration of myocardial ischemia 10, 40 and 120 min, the length of subsequent reperfusion 10 and 40 min). It was discovered that there were changes in the ultrastructure of cardiocytes and vessels of the microcirculatory bed both in the area of ischemia and reperfusion and in the distant heart regions, an increase in myocardial cell and microvessel lesions during postischemic reperfusion not only in the area of ischemia but also in distant zones. In addition, a reduction was noted in the degree of ischemic and reperfusion myocardial injury during the prophylactic use of myophedrine. The mechanisms of the protective action of myophedrine in acute transitory coronary insufficiency are discussed.
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PMID:[Reperfusion damages to the heart in acute transitory coronary failure and their prevention with myophedrin]. 401 48

To evaluate changes in magnesium levels with treadmill exercise-induced coronary insufficiency, 59 consecutive patients were studied. In addition to electrocardiographic monitoring, hematocrit, total protein, whole blood, serum and red blood cell magnesium determinations were made before and after exercise testing. Fifteen patients had positive exercise test, 18 did not complete, and 26 had negative exercise test. There was no significant difference in the serum and red blood cell magnesium on the basis of stress test results for ischemia. Although whole blood magnesium, hematocrit, and total proteins increased (P less than .05) in both groups, we did not find a significant change in magnesium homeostasis.
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PMID:Observations on serum and red blood cell magnesium changes in treadmill exercise-induced cardiac ischemia. 401 38

Experiments on dogs with acute coronary insufficiency were made to show that nonachlazine in doses of 3 and 5 mg/kg considerably reduces or even prevents the rise of S-T segment on the epicardial electrogram depending on the intensity of ischemia. Hydroxyfedrine in doses of 0.1 and 0.3 mg/kg deteriorates the electrogram. Nonachlazine prevents an increase in the content of lactate and in the lactate/pyruvate ratio in the blood outflowing from the focus of ischemia. On the contrary, hydroxyfedrine raises the characteristics in question. Nonachlazine improves blood supply of the ischemized myocardium, increases the retrograde coronary blood flow and redistributes blood in favour of the affected myocardial area. Hydroxyfedrine lowers the retrograde blood supply of the area of ischemia and redistributes blood in favour of the unaffected areas of the heart.
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PMID:[Effect of antianginal agents with a beta-adrenostimulating component of their action on the ischemic myocardium]. 612 32

Disturbances in properties of the sarcoplasmic reticulum (SR) Ca-pump are found under conditions of experimental coronary insufficiency and confirmed by a decrease in the Ca2+-ATPase activity and in ability to the 45Ca uptake by SR membranes. Simultaneously the Ca2+ uptake by mitochondria increases. It is established that a rise in the total Ca content in the myocardium tissue is accompanied by its redistribution between the subcellular membrane structures and its accumulation in mitochondria. The found shifts may underlie disturbances in energy supply and a decrease in the contractile myocardium function with ischemia.
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PMID:[Calcium accumulating ability of various membrane structures of the myocardium in experimental coronary insufficiency]. 623 53

Experiments on 77 white random-bred male rats weighing 200 +/- 10 g have shown that combinations of high unsaturated fatty acids (HUFA) containing the precursors of prostaglandin synthesis, arachidonic and linoleic acids, produce a powerful antiarrhythmic action during transitory coronary insufficiency. The effect was seen not only during ischemia but also during subsequent myocardial reperfusion. The combination of HUFA containing arachidonic and linoleic acids as precursors of prostaglandin synthesis exerted a more demonstrable antiarrhythmic action than that without arachidonic acid. The degree of the ischemia-induced depression of contractile process was less versus control, provided HUFA combinations contained arachidonic acid.
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PMID:[Effect of different combinations of exogenous higher fatty acids on cardiac function during coronary ischemia and reperfusion]. 642 42

Ischemic cardiopathy in its various clinical manifestations, whether acute (angina pectoris or myocardial infarction) or chronic (chronic coronary insufficiency), has shown in recent years particular hemorheological characteristics of its own. The observation of patients with such diseases has allowed us to record the existence of modifications in the parameters indicative of rheological damage. Numerous studies have been made, many of which are still in progress, with the aim of clarifying the relationships between these data and the disease. In our experience an increase in blood and plasma viscosity and a decrease in red cell deformability are often present in a manner which is statistically significant, if these patients are compared with normal subjects. Hemorheological change is more evident in the acute forms of myocardial ischemia. In fact, in angina pectoris the occurrence of pain is always accompanied by an increase in blood viscosity and by a worsening of red cell deformability both during spontaneous crises and during provocative tests. The hemorheological damage tends to diminish fairly rapidly when the crisis is over, even if the level of stabilization proves to be still higher than normal. In myocardial infarction higher levels of viscosity appear for a brief period after the onset with a slight tendency to diminish up until the 30th day. With the aim of ascertaining whether the alteration is more evident precisely at the point where the ischemia occurs, we chose a necessarily limited number of subjects, undergoing coronarography and atrial pacing for diagnostic purposes, and decided to control the hemorheological data not only in the systemic venous blood but also in the blood taken from the coronary sinus. Our data has shown that the level of viscosity and of red cell filtrability, in the blood taken from the coronary sinus, is worse than those of the systemic venous blood and that, after atrial pacing, in negative pacing subjects the variations are of slight significance whilst in positive pacing subjects we observe a rapid increase in viscosity and a decrease in red cell filtrability. This seems to confirm what we have already observed in the limbs affected by peripheral ischemia, and to demonstrate the existence of a local hyperviscosity syndrome which, even in the myocardium, appears to be dependent on the tissue ischemia.
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PMID:[Hemorrheological changes in ischemic heart disease]. 667 96

Red blood cell filterability, platelet aggregation and blood fibrinogen levels were evaluated in 46 vasculopathic patients with a history of peripheral insufficiency (15 subjects), cerebral insufficiency (16 subjects) and coronary insufficiency (15 subjects). In comparison with a control group of 24 normal subjects, filterability was depressed, platelet aggregation was enhanced and there was a higher plasma concentration of fibrinogen even one month after the last clinical episode of acute ischemia.
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PMID:[Preliminary study on erythrocyte filterability and other hemorrheological parameters in arteriosclerotic vascular disease]. 667 24

Experiments conducted on 240 albino non-inbred male rats, using models of transitory coronary insufficiency of various duration (the period of myocardial ischemia lasted 10, 40 and 120 min), showed impaired energy supply to the heart in both periods of its ischemia and reperfusion in relation to three principal stages; first the synthesis of ATP, then the transportation and utilization of its energy. The period of ischemia was associated with disorders of predominantly the ATP synthesis and to a lesser degree of the transport and utilization of its energy. In the period of the post-infarction resumption of the coronary blood flow mostly affected were the mechanisms of the transportation and absorption of ATP energy by the effector apparatus of cardiomyocytes. At the early stage of myocardial reperfusion after a prolonged (40 and 120 min) local ischemia, the heart was damaged to a greater degree than in continuing ischemia of the same duration. The development of transitory coronary insufficiency following the preliminary administration of the antihypoxant gutimin is characterized by less marked disorders in the process of cardiac energy supply both in the period of myocardial ischemia and at the early stage of the reperfusion.
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PMID:[Mechanisms of disordered cardiac energy supply in transient coronary insufficiency]. 674 83

Experiments on 93 white random-bred male rats weighing 200 +/- 10 g have shown that during myocardial ischemia under transitory coronary insufficiency, there is an increase in platelet adhesive capacity, acceleration of fibrinogenesis, staged time course of formation of the fibrin-platelet structure of the blood clot, depression of its velocity and lysis degree, as well as of fibrin polymerization. Postischemic reperfusion of the coronary blood flow is not followed by normalization of all the hemostatic indicators under study even after a short-term (10 min) myocardial ischemia. Reperfusion after a long-term (40 min) ischemia gives rise to depression of coagulation and fibrinolytic activity, while that after a still longer ischemia (120 min) is characterized by discordant changes in the parameters of the systems indicated. It is assumed that similar shifts in hemostasis can be observed in patients with different patterns of coronary insufficiency.
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PMID:[Changes in various hemostasis indices during transient coronary insufficiency with different durations of myocardial ischemia]. 683 Sep 52


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