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

In the experimental animal, acute ischemia by interruption of coronary blood supply is accompanied by a steepening of the slope of the left ventricular pressure-volume and pressure-segment length relations. This increase in chamber stiffness is associated with an increase in myocardial stiffness assessed from the slope of the diastolic stress-strain relation. Supply-type ischemia in humans brought about by balloon inflation during coronary angioplasty leads to an upward shift of the pressure-length relation of the ischemic and the adjacent segment combined with a steepening of the slope. In demand ischemia produced by rapid pacing in patients with coronary artery disease, an increased radial stiffness modulus at any level of radial stress was present when compared with that during the resting state. These alterations of the stress-strain relation suggest that the physical properties of the myocardium change during both supply and demand ischemia. The increased diastolic myocardial stiffness appears to result, at least in part, from increased residual interaction between actin and myosin filaments.
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PMID:On whether there is a true increase in myocardial stiffness during myocardial ischemia. 264 91

To detect myocardial cell damage, serum samples of 42 consecutive patients with angina at rest were screened for cardiac myosin light chains, which were detected in 22 patients (52%). In 17 of these patients there was a persistent release of myosin light chains lasting until the 4th hospital day, whereas in 7 patients myosin light chains were only detectable during the initial 24 h after admission. The presence of myosin light chains correlated with signs of ischemia in the electrocardiogram (ECG) (p less than 0.05) and with the extent of coronary artery narrowing (p less than 0.05). Cardiac myosin light chains were elevated in serum only if there was a greater than or equal to 75% diameter narrowing in at least one major vessel. In all five patients who developed transmural myocardial infarction during the course of their hospital stay, myosin light chains were detectable greater than or equal to 28 h before the diagnosis of myocardial infarction could be established by ECG criteria and conventional serum enzymes. Thus the detection of circulating cardiac myosin light chains enables one to identify a subgroup of patients with angina at rest having more severe coronary artery disease with a worse outcome.
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PMID:Circulating cardiac myosin light chains in patients with angina at rest: identification of a high risk subgroup. 334 52

The muscle proteins of rabbits with the compartment syndrome caused by tourniquet were studied by SDS-polyacrylamide gel electrophoresis and the compartment pressure post-ischemia was measured. The post-ischemic pressure in the anterior compartment increased more than that in the deep-posterior compartment. The phoretic patterns of structural and soluble proteins changed after ischemia, and their degeneration appeared to depend on the degree of pressure increase. In ischemic contracture, the patterns of myosin light chains of type 1 fibers changed to those of type 2 fibers. This indicated the possibility of fiber type transformation from type 1 to type 2 in ischemic contracture.
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PMID:[Experimental studies on a compartment syndrome caused by a tourniquet]. 339 50

The purpose of this study was to make clear the changes of structural proteins in the ischemic contracture muscle. Ischemia experiments were conducted on the forelimb of canines. Contracture proteins (myosin, actin, alpha-actinin) were isolated and analysed by using SDS-polyacrylamide gel electrophoresis. In the muscle group after 7-hour-ischemia, the muscle structural proteins were changed remarkably, along the time course after the release of tourniquet. After 7 days, myosin heavy chain decreased to 1/2 to 1/3 the original value. It was especially myosin heavy chain that changed remarkably among muscle structural proteins. Actin showed changes after 10-hour-ischemia.
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PMID:[The study of structural proteins in the ischemic contracture muscle]. 343 76

Acute exposure of the heart to ethanol does not appear to alter the rate of young guinea pig cardiac protein synthesis when assayed in vitro. In contrast, the primary metabolite of ethanol, acetaldehyde, markedly diminishes synthesis despite its chronotropic and inotropic effects. On the other hand, after 11-13 weeks of ethanol-drinking during growth and maturation, the synthetic capacity of the working right ventricle was decreased when measured in vitro with normal perfusate. Assay of synthesis of the contractile proteins myosin heavy and light chains, actin and tropomyosin suggests a change in synthesis or pool size of actin reflected in an alteration of relative synthesis of this protein compared to that of heavy chains. The relative synthesis of the other proteins remained at control levels. When hearts from ethanol-drinking and matched control animals were perfused under conditions of severe ischemia, there was a profound fall in protein synthesis in all hearts, and ethanol did not enhance the inhibition of synthesis. However, the hearts from ethanol-drinking animals showed a more marked and significant impairment of maintaining ejection pressure with a marked increase in coronary resistance as the perfusion progressed. It is postulated that some impairment of protein metabolism may occur during prolonged ethanol exposure, which may influence the cardiac response of another induced stress, e.g., ischemia.
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PMID:Ethanol and cardiac protein synthesis. 391 35

An ATPase activity of myosin was decreased in the ischemic zone of myocardium within 24 hrs after experimental infarction in dogs. The intensity of Ca2+-dependent phosphorylation of the myosin preparation was also decreased and the rate of phosphorylation in the light chain (with molecular mass 18,000) was increased. These alterations found in the ATPase properties and phosphorylation of myosin are important for studies of pathogenetic alterations in myofibril contractile function in acute ischemia of myocardium.
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PMID:[Ca2+-dependent phosphorylation and ATPase activity of cardiac muscle myosin in experimental myocardial infarction]. 624 76

The diastolic portion of the cardiac cycle can be divided into sequential phases: isovolumic ventricular relaxation; rapid ventricular filling; slow, or passive, ventricular filling; and atrial contraction. Contraction and relaxation are to some extent interrelated; however, relaxation is not simply a passive reversal of events during systole. Rather, relaxation is an energy-consuming process which involves dissociation of calcium from the actin-myosin-complex and reuptake of calcium by the sarcoplasmic reticulum. Left ventricular diastolic function is determined by the interrelationship of several/factors, including some intrinsic to the left ventricular chamber (completeness of left ventricular relaxation, time course of left ventricular contraction, and elastic and viscous properties of the myocardium) and others extrinsic to the left ventricle (pericardial and pleural pressure, right ventricular contraction, and coronary perfusion pressure). Acute ischemia alters diastolic left ventricular function by: slowing isovolumic relaxation, delaying left ventricular filling and altering passive elastic properties of the myocardium. Slowing of isovolumic relaxation is measured as a fall in the maximal rate of left ventricular pressure decline (peak negative dP/dt) and as an increase in the time constant (T) of left ventricular pressure fall. Delayed left ventricular filling is manifested regionally as a reduced rate of septal and posterior wall thinning (by echocardiography) and globally as a reduced rate of chamber filling (by gated radionuclide angiography).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemodynamics in ischemia: diastolic phase]. 652 97

Isovolumic relaxation abnormalities have been noted in the ischemic left ventricle, but altered end-diastolic distensibility, as well as the role of right ventricular distention, is debated. Accordingly, left ventricular end-diastolic pressure and myocardial segment length were studied in the open-chest dogs with critical (90% diameter reduction) stenoses on both left anterior descending and circumflex coronary arteries. Regional segment length was measured with ultrasonic crystals placed subendocardially, and ischemia was induced by pacing tachycardia for 3 minutes. Transient vena caval occlusion was done to unload the right ventricle and to produce a series of left ventricular end-diastolic pressure and left ventricular end-diastolic segment length points before and after pacing tachycardia. After pacing tachycardia, left ventricular end-diastolic pressure (9.3 +/- 0.9 to 16.9 +/- 1.5 mm Hg, P less than 0.001) and time constant T of left ventricular isovolumic pressure decline (46 +/- 3 to 60 +/- 5 msec, P less than 0.01) increased, with an increase in left ventricular end-systolic segment length (9.8 +/- 0.3 to 10.5 +/- 0.3 mm, P less than 0.001), and a decrease in fractional shortening (17.6 +/- 1.7 to 14.5 +/- 1.3%, P less than 0.01) in the ischemic region, although right ventricular end-diastolic pressure was unchanged. With vena caval occlusion, right ventricular diastolic pressure fell promptly to near zero, followed by decrease in left ventricular pressure and segment length. In each dog, the left ventricular end-diastolic pressure-end-diastolic segment length relation shifted upward after pacing tachycardia. Pacing tachycardia was performed again in six dogs without stenoses. In this group, fractional shortening was preserved after pacing tachycardia (15.7 +/- 2.3 to 15.3 +/- 2.3%, NS), and left ventricular end-diastolic pressure (9.4 +/- 1.8 to 9.8 +/- 1.8 mm Hg, NS) was unchanged. The left ventricular end-diastolic pressure-segment length relation did not shift upward after pacing tachycardia. These data indicate that extrinsic compression of left ventricle by right ventricle is unlikely to be responsible for the upward shift in this model, and the upward shift in end-diastolic left ventricular pressure-segment length relations, as well as dynamic left ventricular diastolic pressure-segment length, supports the concept that persistent myosin-actin interaction throughout diastole plays an important role in the diastolic abnormalities in this angina physiology model.
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PMID:Left ventricular diastolic pressure-segment length relations and end-diastolic distensibility in dogs with coronary stenoses. An angina physiology model. 674 30

We examined myosin of fast and slow skeletal rat muscles regenerating after ischemia and bupivacaine injection in denervated limbs. Four days after injury two-dimensional gel electrophoresis revealed the presence of the embryonic light chain in the myosin isolated from the portion of muscle showing a homogeneous population of new small fibers by histological examination. Two weeks after injury this subunit was absent, whereas the two light chains, LC1F and LC2F, became prominent. One month after injury the still denervated soleus muscle maintained this light chain pattern. Gel electrophoresis in native condition of the myosin and peptide mapping of electrophoretically purified heavy chains confirmed that the muscle regenerating in absence of the nerve accumulated a myosin that had the general features of a fast, not slow, myosin but contained definite differences from the former.
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PMID:Myosin light and heavy chains in muscle regenerating in absence of the nerve: transient appearance of the embryonic light chain. 682 48

Ischemia is known to produce damage to subcellular organelles, such as nuclei and mitochondria, in myocardial tissue. We tested the hypothesis that during myocardial ischemia various cytoskeletal and contractile proteins also undergo changes. We induced total global ischemia by incubation in buffer of tissue samples from six human left ventricles that were obtained from heart transplant recipients. Samples were removed from the incubation medium at different time intervals and investigated by immunohistochemistry using monoclonal antibodies against myosin, actin, tropomyosin, troponin T, myomesin, desmin, tubulin, and vinculin. The degree of ischemic injury was determined by electron microscopy. Ischemic cardiomyopathic human tissue showed disturbances of the localization pattern of myosin, actin, tropomyosin, and troponin T as early as 10 minutes after the onset of ischemia; this disruption was complete at 20 minutes. Tubulin also started changing at 10 minutes, but complete disruption was only evident after 120 minutes. Desmin and myomesin showed an intermediate response; changes began at 30 to 40 minutes, and disruption was complete at 90 to 120 minutes. Vinculin was most resistant to ischemia. Ultrastructurally, the tissue showed moderate reversible ischemic injury during the entire period of 180 minutes. Measuring the exposure time in seconds allowed quantitation of the intensity of the fluorescence. We reached the following conclusions: (1) Ischemia causes damage to the contractile proteins sooner than to the cytoskeleton and subcellular organelles. (2) Diseased human hearts are extremely susceptible to the effects of ischemia. These findings are important for the situation of induced cardiac arrest in heart operations and for preservation of donor hearts for transplantation.
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PMID:Ischemia induces early changes to cytoskeletal and contractile proteins in diseased human myocardium. 760 73


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