Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Graded doses of norepinephrine and methoxamine were given to rabbits over a standard 90-minute infusion period to assess their potential for inducing myocardial injury. Lesions of myofiber necrosis and leukocytic infiltration were graded semiquantitatively in animals killed 2 days later. A close correlation was found between the dose of norepinephrine and the histological score (r = 0.912, P less than 0.001). Mean arterial pressure rose from 100 mm Hg to a maximum of 129 mm Hg, and averaged 115 mm Hg during infusion of 2 micrograms/min per kg. However, heart rate fell from 287 beats/min to average 208 beats/min. The pressure-rate product, an index of metabolic demand, showed no significant change and did not differ from saline-infused controls. Beta-adrenergic blockade with practolol (4 mg/kg) or propranolol (1 mg/kg) failed to significantly reduce cardiac injury with norepinephrine. However, alpha-adrenoceptor blockade with phentolamine (10 mg), alone or in combination with either of the beta-antagonists, markedly reduced lesion formation as reflected by the histological score (P less than 0.02). Administration of the alpha-agonist methoxamine produced dose-related increases in the intensity of myocardial injury (r = 0.938, P less than 0.01), morphologically identical with those resulting from norepinephrine. Hemodynamic changes also were comparable. Phentolamine markedly reduced methoxamine injury. It may be concluded from these studies that norepinephrine cardiomyopathy results in large part from activation of the alpha-adrenergic system in the rabbit model. Ischemia or a supply-demand mismatch are unlikely mechanisms. We speculate that alterations in myofiber Ca++ translocation, uptake, and binding induced by alpha 1-receptor activation may contribute to membrane damage.
 ...
PMID:Contribution of alpha-adrenoceptor activation to the pathogenesis of norepinephrine cardiomyopathy. 613 55

The term "ischemic cardiomyopathy" was used initially to describe a clinical syndrome that was indistinguishable from primary congestive cardiomyopathy but due to severe, diffuse coronary artery disease. The term has been expanded to include the larger category of myocardial disease secondary to coronary artery disease. Using this expanded definition, we have discussed the varied clinical presentations of congestive ischemic cardiomyopathy and restrictive ischemic cardiomyopathy (stiff heart syndrome and right ventricular infarction), and how the effects of ischemia on left ventricular systolic and diastolic performance may cause these varied presentations. The prognosis of any ischemic cardiomyopathy is related primarily to the degree of ventricular dysfunction and the extent of coronary artery disease. Therapy is aimed at preventing or ameliorating myocardial ischemia and halting the progression of, or even reversing, the deterioration in myocardial function.
 ...
PMID:Ischemic cardiomyopathy. 614 79

This study presents experimental and clinical data in the use of I-123 labeled aromatic and aliphatic fatty acids. I-123 p-phenylpentadecanoic acid (p-IPPA) and I-123 heptadecanoic acid (HDA) were applied for myocardial scintigraphy. The feasibility of p-IPPA and HDA for myocardial scintigraphy was substantiated in animal experiments. Clinical studies were performed in patients with coronary artery disease (CAD) and cardiomyopathy (CMP). In CAD the results of fatty acid studies were compared with those of T1-201. Myocardial scintigraphy with p-IPPA and HDA was done with the patients supine and the collimator of the gamma camera in the LAO 45 grade position. Following intravenous administration of the labeled compounds data were continuously monitored. The regional distribution of the I-123 labeled fatty acids was assessed visually and supplemented with a semiquanitative analysis to estimate regional fatty acid uptake within the myocardium. The uptake was expressed as a ratio of background corrected regional myocardial activity to background activity (V. cava superior region). In initial studies data were accumulated for 40 minutes after intravenous HDA and for 50 minutes after intravenous p-IPPA, respectively. Data interpretation could be improved by an extended data acquisition (HDA: 70 minutes; p-IPPA: 90 minutes). In earlier experiments the decline in the myocardial count rate seemed to be monoexponential. However, in studies with prolonged data acquisition the myocardial time activity curve could be better described by two exponentials. Accordingly, the time activity curve was fitted with a biexponential function and the elimination half time of the initial and second component were determined. In addition, by extrapolation of the monoexponential slope of each component to zero, the size of each component was evaluated and the relative contribution of each phase on the myocardial elimination curve was expressed by a ratio of these extrapolated values. Our data provided evidence that I-123 labeled fatty acids can be used as metabolic tracers, as their kinetic behaviour was comparable to C-11 palmitate. Furthermore, in p-IPPA studies catabolites of its metabolic degradation were identified in plasma samples. Additionally it was shown in HDA studies that pharmacological interventions and acute ischemia were effective modulators of myocardial HDA utilization. In our patients we found a slower myocardial elimination half time for p-IPPA than for HDA; also the amount of p-IPPA utilized via the initial component was smaller than for HDA.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Myocardial scintigraphy with iodine 123-labeled fatty acids]. 622 70

Acute heart insufficiency was simulated in dogs, rabbits and rats with experimental myocardial infarction, hypothyrosis, thyrotoxicosis, autoimmune cardiomyopathy, myocardium hypertrophy by exerting additional mechanical load on the heart (graded aortic stricture, swimming, running in a tread-ban). Irrespective of the basic pathological process the development of acute heart insufficiency was associated with generalized damage of plasmalemma of the majority of functioning cardiomyocytes, registered with colloid lanthanum. Plasmalemma damage precedes intracellular ultrastructural alterations and is reversible. Sarcolemma damages in non-functioning cardiomyocytes revealed in the focus of severe ischemia in experimental myocardial infarction is on the contrary indicative of irreversible cellular changes. The distinctions demonstrate that mechanisms causing damages in sarcolemma membrane can be different in conditions of preserved coronary blood flow and in severe ischemia.
 ...
PMID:[Role of the sarcolemma in the morphogenesis of acute heart failure]. 623 4

Therapeutic modalities for ventricular tachycardia include antiarrhythmic drugs, direct current cardioversion, electrical pacing and surgical intervention. Lidocaine, procainamide and bretylium are all capable of controlling recurrent ventricular tachycardia; bretylium has the advantage of also being antifibrillatory and of raising the threshold for ventricular fibrillation. Lidocaine and bretylium are available only in i.v. form. Procainamide is available in i.v. as well as oral form. Other oral antiarrhythmic agents include quinidine, disopyramide, beta-blockers such as propranolol and verapamil. The latter may be useful in ventricular arrhythmias induced by ischemia; of these, only beta-blockers appear to significantly raise the threshold for ventricular fibrillation. Control of ventricular ectopy does not always preclude ventricular tachycardia and ventricular fibrillation. In treating ventricular tachycardia, bretylium tosylate is generally given 5 to 10 mg/kg i.v. over 10 to 20 minutes. Given too rapidly, it may cause nausea and vomiting. Orthostatic hypotension, a common side effect, generally abates with continued use and may be ameliorated with tricyclic antidepressants such as protriptyline. Significant supine hypotension may be encountered in patients with acute myocardial infarction and may be managed with pressor agents or fluids, or both. The antiarrhythmic efficacy of bretylium was analyzed in 40 patients. Five etiologic groups were defined by cardiac catheterization: 19 patients had atherosclerotic heart disease, 6 had primary myocardial disease, 4 had mitral valve prolapse, 4 had rheumatic heart disease and 7 had miscellaneous or no heart disease. All patients had recurrent ventricular tachycardia (VT); 23 had ventricular fibrillation (VF) as well. Other antiarrhythmic agents had failed in 38 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Therapy of ventricular tachycardia. 646 97

Male weanling rats were made copper deficient with a purified diet containing all known essential dietary nutrients except copper. Copper deficiency was verified by indirect (anemia, growth retardation, hypercholesterolemia, gross pathology, and abnormal electrocardiograms) and direct (tissue copper analysis) criteria. His bundle electrographic and electrocardiographic changes detected in the copper-deficient group consisted most notably of depressed His-Purkinje system conductivity and S-T segment depression. Phosphorus-31 nuclear magnetic resonance spectroscopic analysis of cardiac, renal, and hepatic tissue perchloric acid extracts revealed significant metabolic changes associated with the dietary copper deficiency, including a generalized marked decrease in ATP and phosphocreatine levels and a corresponding increase in inorganic orthophosphate and ADP levels in the various tissues. Tissue-specific changes consisting of elevated ribose 5-phosphate (heart), phosphocholine (heart), and inosine monophosphate (kidney) and decreased glycerol 3-phosphorylethanolamine (liver) and glycerol 3-phosphorylcholine (liver) levels were detected in copper-deficient rats. Microscopic examination of heart tissue from copper-deficient rats revealed extensive disruption of mitochondrial fine structure, including fragmentation of cristae and inner and outer mitochondrial membranes, which resulted in pronounced vacuolization throughout the tissue. Although the physiological and metabolic disturbances manifested in hearts from copper-deficient animals generally mimic myocardial responses to chronic ischemia, the observed changes are interpreted in a broader context to represent the appearance of a copper-dependent cardiomyopathy.
 ...
PMID:Physiological and metabolic characterization of a cardiomyopathy induced by chronic copper deficiency. 663 5

The purpose of this study was to determine whether an exercise-induced decrease in ejection fraction in patients with coronary artery disease and left ventricular dysfunction at rest represents ischemia or the nonspecific response of a compromised left ventricle to exercise stress. Accordingly, radionuclide ejection fraction responses of 246 patients with coronary artery disease and an ejection fraction at rest of less than 0.50 were compared with those of a "nonischemic" control group of 48 patients with idiopathic dilated cardiomyopathy and a similar degree of ventricular dysfunction. The significance of the ejection fraction response in the group with coronary artery disease was further examined by relating it to the angiographic extent of coronary artery disease, severity of angina, incidence of chest pain and electrocardiographic ST segment depression during exercise and long-term prognosis. The ejection fraction decreased by greater than or equal to 0.01 and greater than or equal to 0.05 during exercise in 48 and 28%, respectively, of the patients with coronary artery disease compared with only 8 and 2%, respectively, of the patients with cardiomyopathy. When exercise was limited by fatigue at a submaximal heart rate, the ejection fraction decreased in 25% of the patients with coronary artery disease but in none of the patients with cardiomyopathy. Patients with coronary artery disease whose ejection fraction decreased during exercise had a significantly higher incidence of three vessel disease, exercise-induced chest pain or ST depression and late mortality than did patients whose ejection fraction did not decrease. These relations were confirmed equally in subgroups of patients with moderate (ejection fraction 0.30 to 0.49) and severe (ejection fraction less than 0.30) left ventricular dysfunction. Thus, in patients with coronary artery disease and left ventricular dysfunction at rest, a decrease in ejection fraction during exercise is more likely to indicate ischemia than a nonspecific left ventricular response to exercise stress. In the individual patient, a decrease of 0.05 or greater, or a decrease during submaximal exercise, appears to be highly specific for ischemia. A decrease in ejection fraction identifies a subgroup of patients with a high prevalence of multivessel coronary artery disease and a high risk of death during long-term follow-up on medical therapy.
 ...
PMID:Mechanism and significance of a decrease in ejection fraction during exercise in patients with coronary artery disease and left ventricular dysfunction at rest. 669 May 59

Acute limb ischemia following aortic reconstruction is primarily related to intraoperative technical errors and is associated with significantly increased mortality. Elective aortic reconstruction was performed on 262 patients between 1975 and 1981. Surgical indications were aneurysm in 84 patients (32%), occlusive disease in 125 (48%), and both of these in 53 (20%). Acute limb ischemia developed postoperatively in 27 patients (10.3%); it was noted at the conclusion of the operation in five (19%) of them and within the first 48 hours in 22 (81%). The mortality was greater in the combined aneurysm and occlusive disease group than in the aneurysm-only and occlusive disease-only groups, primarily because of an increased incidence of myocardial disease in the combined group. Postoperative limb ischemia was mainly a result of technical error and resulted in increased mortality in all groups.
 ...
PMID:Acute limb ischemia following aortic reconstruction. A preventable cause of increased mortality. 670 5

Nineteen patients survived a cardiac arrest not associated with an acute myocardial infarction, and had a normal electrophysiologic study with no inducible ventricular tachycardia despite programmed stimulation with one to three extrastimuli at two or more ventricular sites. Among 14 patients who had obstructive coronary artery disease, cardiac arrest occurred during exertion or an episode of angina pectoris in 11; 24 hour ambulatory electrocardiographic recordings demonstrated infrequent or no premature ventricular complexes in 10 and an ischemic response occurred during stage I or II (Bruce protocol) in 6 of 9 patients who underwent exercise testing. Treatment of these patients consisted of myocardial revascularization (eight patients) or antianginal medications (six patients). Only three patients were also treated with an antiarrhythmic drug. Over a follow-up period of 26 +/- 15 months (mean +/- standard deviation), only one patient died suddenly. Two patients who had coronary artery spasm were treated with coronary vasodilator medications and had no recurrence of cardiac arrest over 7 and 36 months of follow-up, respectively. Three patients who had cardiomyopathy or no identifiable structural heart disease were treated with nadolol or amiodarone and had no recurrence of cardiac arrest over 3 to 27 months of follow-up. Among patients who survive a cardiac arrest and have a normal electrophysiologic study, those with obstructive coronary artery disease or coronary artery spasm generally have an excellent prognosis with treatment directed primarily at the underlying heart disease. The clinical features of these patients suggest that cardiac arrest was related to ischemia rather than a primary arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Clinical features and prognosis of patients with out of hospital cardiac arrest and a normal electrophysiologic study. 673 52

Application of vasodilators in evolving myocardial infarction has not yet received wide acceptance. Heretofore, clinical trials of a variety of vasodilator agents have been conducted without regard to the phase of the disease with its changing pathologic features and altering cardiac function. A classification of these phases based on the underlying myocardial disease--ischemia, necrosis, compensation, and healing--may allow a more rational interpretation of the available information. At present, vasodilators are not recommended during the ischemic phase, although some evidence suggests that preload modification by use of nitroglycerin may be beneficial in certain instances. Vasodilator drugs productive of arterial impedance reduction are probably of the greatest value late in the necrotic phase and in the compensation and healing phases. It is in these circumstances that heart failure becomes clinically manifest and maximal short-term efficacy of this intervention can be achieved. Impedance reduction, using agents such as sodium nitroprusside, will cause a prompt improvement manifested by a reduction in left ventricular filling pressure and in pulmonary congesting pressure and an increase in cardiac output. A significant improvement in short-term survival, at least, should be expected by judicious use of vasodilators.
 ...
PMID:Role of vasodilators in the changing phases of acute myocardial infarction. 680 48


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>