Myocardial Stunning
Mostrando 1-12 de 19 artigos, teses e dissertações.
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1. Anesthesia Management for a Patient Undergoing Pulmonary Endarterctomy without Cardiopulmonary Bypass
Abstract Pulmonary endarterectomy is a curative procedure for chronic thromboembolic Pulmonary Hypertension. As usual, cardiopulmonary bypass circuit is required. However, there are several complications attributed to extracorporeal circulation. Hemodilution, systemic inflammatory response syndrome and leukocyte sequestration are circulation related complica
Braz. J. Cardiovasc. Surg.. Publicado em: 02/12/2019
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2. New method in myocardial viability detection with 18F-fluoro-desoxi-glucose using a low-carbohydrate diet: a comparative study with euglycemic hyperinsulinemic clamp / Nova técnica para pesquisa de viabilidade miocárdica com 18F-fluoro-desoxi-glicose utilizando dieta restrita em carboidratos: estudo comparativo com o clamp hiperinsulínico euglicêmico
INTRODUÇÃO: Em pacientes com infarto do miocárdio (IM) e disfunção cardíaca, a evidência de viabilidade miocárdica é primordial, e o exame tomográfico por emissão de pósitrons com 18F-fluoro-desoxi-glicose (18FDG-PET) é o padrão-ouro para essa identificação. Existe preferência, na literatura, pela realização do clamp hiperínsulínico eugl
Publicado em: 2008
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3. Evidence for an essential role of reactive oxygen species in the genesis of late preconditioning against myocardial stunning in conscious pigs.
Conscious pigs underwent a sequence of 10 2-min coronary occlusions, each separated by 2 min of reperfusion, for three consecutive days (days 1, 2, and 3). On day 1, pigs received an i.v. infusion of a combination of antioxidants (superoxide dismutase, catalase, and N-2 mercaptopropionyl glycine; group II, n = 9), nisoldipine (group III, n = 6), or vehicle (
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4. Direct evidence that protein kinase C plays an essential role in the development of late preconditioning against myocardial stunning in conscious rabbits and that epsilon is the isoform involved.
Brief ischemic episodes confer marked protection against myocardial stunning 1-3 d later (late preconditioning [PC] against stunning). The mechanism of this powerful protective effect is poorly understood. Although protein kinase C (PKC) has been implicated in PC against infarction, it is unknown whether it triggers late PC against stunning. In addition, the
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5. Haemodynamic and energetic properties of stunned myocardium in rabbit hearts.
OBJECTIVE--To amplify the description of myocardial stunning. DESIGN--Control versus 30 min after a 20 min no flow ischaemia. EXPERIMENTAL ANIMALS--15 isolated rabbit hearts perfused with erythrocyte suspension. MAIN OUTCOME MEASURES--Left ventricular systolic function in terms of aortic flow, peak systolic pressure (LVPmax), dP/dtmax, and the end systolic p
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6. Gene program for cardiac cell survival induced by transient ischemia in conscious pigs
Therapy for ischemic heart disease has been directed traditionally at limiting cell necrosis. We determined by genome profiling whether ischemic myocardium can trigger a genetic program promoting cardiac cell survival, which would be a novel and potentially equally important mechanism of salvage. Although cardiac genomics is usually performed in rodents, we
The National Academy of Sciences.
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7. Late preconditioning against myocardial stunning. An endogenous protective mechanism that confers resistance to postischemic dysfunction 24 h after brief ischemia in conscious pigs.
Conscious pigs underwent a sequence of 10 2-min coronary occlusions, each separated by 2 min of reperfusion, for three consecutive days (days 1, 2, and 3 of stage I). The recovery of systolic wall thickening (WTh) after the 10th reperfusion was markedly improved on days 2 and 3 compared with day 1, indicating that the myocardium had become preconditioned aga
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8. Hemodialysis-Induced Cardiac Injury: Determinants and Associated Outcomes
Background and objectives: Hemodialysis (HD)-induced myocardial stunning driven by ischemia is a recognized complication of HD, which can be ameliorated by HD techniques that improve hemodynamics. In nondialysis patients, repeated ischemia leads to chronic reduction in left ventricular (LV) function. HD may initiate and drive the same process. In this study,
American Society of Nephrology.
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9. Pathophysiology and pathogenesis of stunned myocardium. Depressed Ca2+ activation of contraction as a consequence of reperfusion-induced cellular calcium overload in ferret hearts.
Contractile dysfunction in stunned myocardium could result from a decrease in the intracellular free [Ca2+] transient during each beat, a decrease in maximal Ca2+-activated force, or a shift in myofilament Ca2+ sensitivity. We measured developed pressure (DP) at several [Ca]0 (0.5-7.5 mM) in isovolumic Langendorff-perfused ferret hearts at 37 degrees C after
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10. Dobutamine echocardiography and myocardial contrast echocardiography. Two new techniques for the assessment of myocardial viability.
As investigators have discovered that cardiac regions displaying resting wall motion abnormalities are not the necessary equivalent of myocardial scar (and therefore of irreversible injury) but are potentially viable regions rendered dysfunctional by stunning or hibernation, a new field of medicine has developed to identify viable myocardium that can improve
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11. Recurrent ischemia in the canine heart causes recurrent bursts of free radical production that have a cumulative effect on contractile function. A pathophysiological basis for chronic myocardial "stunning".
Open-chest dogs (total number used, 117) underwent 10 5-min coronary occlusions (O) interspersed with 10 min of reperfusion (R). When systolic thickening fraction was measured 9 min after each R, the first O-R cycle was found to cause the largest decrement, with only a slight additional loss during the next four cycles and no further loss during the last fiv
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12. Acidosis during early reperfusion prevents myocardial stunning in perfused ferret hearts.
Cellular calcium overload figures prominently in the pathogenesis of the contractile dysfunction observed after brief periods of ischemia (myocardial stunning). Because acidosis is known to antagonize Ca influx and the intracellular binding of Ca, we reasoned that acidosis during reperfusion might prevent Ca overload and ameliorate functional recovery. We me