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

Coronary collateral development in response to chronic myocardial ischemia is modulated by the integrated release of a variety of growth factors. Protamine, a specific inhibitor of angiogenesis in vitro and in vivo, may attenuate coronary collateral development. The purpose of this investigation was to characterize a model of canine coronary collateral development and to ascertain the effects of protamine on collateral perfusion in response to chronic myocardial ischemia. Ischemia-induced coronary collateral enhancement in response to daily, repetitive, 2-minute left anterior descending (LAD) coronary artery occlusions over 22 consecutive days was demonstrated in control (saline treated) dogs by time dependent, significant (p < 0.05) increases in collateral blood flow to ischemic myocardium. Concomitant with increases in collateral perfusion, myocardial contractile function during LAD occlusion was progressively normalized, and percent coronary flow repayment was reduced successively. These indicators of collateral development were attenuated significantly by administration of subcutaneous protamine. The present findings demonstrate that a model of brief, repetitive, coronary artery occlusion in chronically instrumented dogs sensitively elicits extensive enhancement of the coronary collateral circulation in response to chronic myocardial ischemia. In contrast, protamine attenuates coronary collateral development through its actions as an inhibitor of angiogenesis.
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PMID:Modulation of coronary collateral angiogenesis: a canine model of neovascularization induced by chronic ischemia. 754 94

Aortic cross-clamping with inadequate myocardial preservation has been shown to cause postoperative decreases in myocardial performance following coronary artery bypass graft surgery. We have demonstrated a mild decrement in myocardial beta-receptor function associated with cold cardioplegia in a normal animal model; in normal human hearts, however, response to beta-adrenergic inotropic stimulation was diminished significantly. Beta-receptor dysfunction also is associated with chronic myocardial ischemia that is associated with severe ischemic heart disease. Although the change in beta-receptor function with acute regional myocardial ischemia associated with severe ischemic heart disease is not understood fully, we found that the intensity of regional ischemia significantly affects functional recovery after cardiopulmonary bypass (CPB). Myocardial stunning does not appear to be significant in this dysfunction; however, alterations in beta-receptor density and function may play a critical role in post-CPB ventricular function.
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PMID:Acute regional myocardial ischemia and recovery after cardiopulmonary bypass: effects of intensity of antecedent ischemia. 757 33

Direct evidence from pathologic-anatomical studies in victims of sudden cardiac death has been given for acute ischemia (caused by either an acute thrombus, plaque fissuring or an organizing thrombus) to play a major role in the genesis of sudden cardiac death. Furthermore, indirect data on the effects of drugs in the setting of acute myocardial infarction have demonstrated that treating patients with beta-blocking agents is more beneficial than treating them with a pure anti-arrhythmic drug such as lidocaine. Whereas lidocaine, which also reduces the incidence of ventricular fibrillation in the setting of acute myocardial infarction, may produce an excess of mortality, beta-blockers reduce ventricular fibrillation and are associated with a prolonged survival. Further, indirect evidence on the role of ischemia in ventricular arrhythmias is given in patients with chronic ischemic heart disease by several studies on coronary revascularization and by studies on antiarrhythmic drugs versus beta-blockers in the same situation. In conclusion, there is clear evidence from studies of coronary revascularization and from studies on drug intervention in different patient populations with ischemic heart disease at risk for ventricular arrhythmias and/or for sudden cardiac death that ischemia plays an important role in the genesis of these arrhythmias.
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PMID:Therapeutic consequences of newer studies addressing the problem of myocardial ischemia and ventricular arrhythmias. 763 2

In this work, an x-irradiation/high fat/high cholesterol diet-induced atherogenic model was invoked to examine the effects of severe diffuse atherosclerosis on myocardial metabolism in the in vivo porcine heart. This model was studied using spatially localized 31P-nuclear magnetic resonance (NMR) to monitor pH and the levels of inorganic phosphate, phosphomonoesters, creatine phosphate, and adenosine triphosphate as a function of workload transmurally in control swine and in animals suffering from chronic ischemic heart disease. These preliminary studies revealed that the development of severe atherosclerosis and the accompanying chronically diseased state produce changes in high energy phosphates and that increases in rate pressure products result in demonstrable signs of ischemia in the myocardium which span the entire left ventricular wall. Ischemic changes include a global increase in inorganic phosphate and corresponding decreases in creatine phosphate, ATP, and pH. Importantly, changes in intracellular pH are noted with even the slightest increase in workload suggesting that these diseased hearts display elevated glycolytic activity. By challenging these animals with increased cardiac workload, we directly visualize how the chronically compromised heart responds to severe oxygen challenges in a clinically relevant model of this situation.
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PMID:31P-nuclear magnetic resonance studies of chronic myocardial ischemia in the Yucatan micropig. 781 9

Acute or chronic myocardial ischemia may develop in patients with pulmonary atresia with intact ventricular septum and right ventricular-dependent coronary circulation. In such cases an aorta to right ventricle shunt may be used to reverse this ischemia. This report summarizes our experience with the placement of an aortic to right ventricular shunt in 5 patients. The shunts were made of Gore-Tex and ranged from 4 mm to 8 mm. Associated procedures were bidirectional Glenn (n = 2) and Fontan (n = 2). All 5 patients survived the procedure with documented early graft patency and no evidence of ischemia.
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PMID:Aortic to right ventricular shunt for pulmonary atresia and intact ventricular septum. 878 54

It is known that angiotensin converting enzyme (ACE) inhibitors not only prevent the formation of angiotensin II, but also potentiate the activity of bradykinin. We investigated the effects of the ACE-inhibitor ramipril in two models of cardiac ischemia. In anesthetized dogs with a coronary occlusion of 6-h duration, both ramiprilat and bradykinin significantly reduced infarct-size. This effect was prevented by the co-administration of the bradykinin antagonist HOE 140. In rats with a coronary occlusion of 6-weeks duration, ramipril administration significantly reduced infarct-size and prevented the development of left ventricular hypertrophy. Thus, ramipril showed a cardioprotective activity in models of acute as well as of chronic myocardial ischemia. These effects are probably mediated by the potentiation of bradykinin.
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PMID:[Reduction of infarct size and remodeling after ramipril]. 785 82

For many years ischemic heart disease involving the right ventricle had received little attention. During the last 15 years, the initial works of Cohn, Isner, and others spawned a number of clinical and experimental studies that extended the understanding of the pathophysiology of ischemia in the right ventricle. Most of the work has been done in the setting of acute myocardial infarction, and information is still lacking in other conditions, such as chronic ischemic heart disease and perioperative right ventricular dysfunction. Acute right ventricular infarction rarely occurs in the absence of left ventricular necrosis and in most cases is the extension of an inferior left ventricular infarct. The majority of patients with right ventricular infarction only exhibit subtle signs of ischemic dysfunction. Elevated right atrial pressure is found only in the typical syndrome of elevated venous pressure; low output syndrome can be found only in 20% of the cases, and cardiogenic shock secondary to right ventricular necrosis is found only in 10%. It is also important to note that there is not a clear correlation between the severity of ischemic right ventricular dysfunction and the necrotic area. The discrepancy may be due to ischemia without necrosis of the right ventricular wall (stunned myocardium), but the intact pericardium and the necrosis of the interventricular septum may also play an important role. In the most severe form of ischemic right ventricular dysfunction, the entire right ventricular wall is akinetic. Right atrial, right ventricular, and pulmonary artery pressures become similar in magnitude and shape, and the pulmonary valve is opened during diastole, demonstrating a passive blood flow from the right atrium to the left ventricle through the low resistance pulmonary capillary bed. Volume loading, administration of dopamine or dobutamine, and careful use of vasodilators under hemodynamic monitoring are the therapeutic measures to control the severe forms of acute ischemic right ventricular dysfunction. The use of thrombolytic agents has decreased the incidence of right ventricular dysfunction after acute myocardial infarction. Mortality is high in the severe forms of acute ischemic right ventricular dysfunction, but after discharge from hospital the prognosis is good and right heart failure is unusual, even in those patients with shock during the first days of evolution of the infarct.
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PMID:Ischemia right ventricular dysfunction. 794 82

Recent studies suggest that granulocytes (PMNs) play a role in the pathogenesis of acute and chronic myocardial ischemia and extension of myocardial injury. Granulocytes can release a variety of mediators tissue injury and synergize with these different mediators, cytokines and other cells resulting in amplification of neutrophil stimulation and rising to additional products with enhanced endothelial injury. Free radicals released by PMNs during ischemia or reperfusion produce deleterious effects on cell membranes, endothelial cells and myocardium. Experience in humans shows the modification of PMNs function in angina and during myocardial ischemia: upon reperfusion PMNs accumulate and produce an inflammatory response leading to endothelial injury. Rabbit derived antiserum dependent-reduction of circulating PMNs in the dog or using monoclonal antibody anti-CD11b/CD18 of PMNs resulted in smaller myocardial infarction. Another aspect of PMNs function is related to leukotriene C4 release; the vasoconstrictor effect of this leukotriene on coronary arteries is synergistic with that induced by platelet-released thromboxane A2, and the decrease in coronary flow produced by the combination of both substances is greater than the sum of changes caused by the two eicosanoids separately administered. The potential role of leukocytes, oxygen radicals, leukotrienes and granulocyte enzymes in the pathophysiology of myocardial injury due to regional ischemia and reperfusion is an area of intense investigation. This overview will not attempt to be exhaustive. Experimental and clinical studies to elucidate these events should not only provide insight into acute and chronic pathologic tissue damage, but may also lead to the identification of important new targets of pharmacologic intervention.
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PMID:[The role of the granulocytes in ischemic cardiopathy]. 807 42

Identification of viable myocardium in patients with impaired left ventricular function, who are possible candidates for revascularization, represents an important clinical question. Modern methods of revascularization provide a therapeutic alternative to conventional pharmacological therapy even in patients with advanced ischemic heart disease. Modern diagnostic techniques make it possible to assess not only the extent of ischemia under exercise conditions, but also the presence of viable tissue in patients with severe coronary artery disease and impaired ventricular function. Currently, the most accurate methods for scintigraphic quantification of viable myocardial tissue are metabolic investigations with positron emission tomography (PET). Because of the limited availability of PET other methods like thallium-201-scintigraphy play an important clinical role. Modifications of thallium-201-scintigraphy, for example the introduction of reinjection protocols have improved the recognition of viable tissue and decreased the diagnostic difference to PET. We recommend as standard diagnostic procedure for assessment of tissue viability thallium-201-scintigraphy with reinjection. In patients with severely depressed left ventricular function and equivocal thallium-201-scintigraphy findings, PET should be considered as further diagnostic test. Low dose dobutamine-echocardiography is emerging as alternative test for evaluation of contractile reserve in dysfunctioning left ventricular segments. Its clinical role, however, remains to be determined. Besides the clinical application of these methods, newly developed radiotracers, together with PET, may provide insights into the mechanism of metabolic adaptations in patients with repeated episodes of ischemia. Furthermore, correlation of clinical data with in vitro histological and biological tissue analysis in the same patients may provide a better understanding of metabolic alterations observed in chronic ischemic heart disease.
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PMID:[Scintigraphic evaluation of the ischemically damaged myocardium in patients with reduced left ventricular function. From clinical aspects to the cell]. 858 63

Guanine nucleotide-binding regulatory proteins (G proteins) play a major role in the regulation of a number of physiological processes, such as stimulation or Inhibition of adenylate cyclase activity or gaiting of ionic channels. Myocardial ischemia could induce the changes in receptor-G protein signal transduction system in the heart. Therefore, this article will focus on the role and alterations of G proteins (especially, Gs and Gi) in myocardial ischemia. The Gi protein rapidly loses functional activity during very early myocardial ischemia. In contrast to Gi protein, the function of Gs protein during this phase has not been evaluated. Moreover, the changes in Gs protein after 30 min of ischemia are contradictory. However, the sensitization of the adenylate cyclase activity in the very early phase of acute ischemia is gradually replaced by a decrease in adenylate cyclase activity with prolonged ischemia. The decrease in the function and amount of Gs protein may be one of the factors that induce these changes. The function of Gs protein was also decreased in the canine hearts with ischemia and reperfusion. In contrast to ischemia and reperfusion, there are no significant alterations in G proteins and modulation of adenylate cyclase in the stunned myocardium. It has become increasingly evident that Gi protein may play an important role in the cardioprotective effects of preconditioning. When beta-adrenoreceptor densities are reduced in chronic myocardial ischemia, decreased in the amount and function of Gi protein and increased amount of Gs protein may play the role in preservation of the adenylate cyclase activity. These alterations in G proteins may play the important role in the myocardial function during myocardial ischemia.
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PMID:The guanine nucleotide-binding regulatory proteins (G proteins) in myocardium with ischemia. 890 69


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