Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because the Na+ pump is considered to modulate the contractile force development by the cardiac muscle and depressed cardiac pump function is the hallmark of congestive heart failure, we characterized the sarcolemmal Na(+)-K(+)-ATPase activity in failing rat hearts after myocardial infarction. For this purpose, the left ventricular coronary artery was ligated, and hearts were examined 4, 8, and 16 wk later; sham-operated animals served as controls. Hemodynamic assessment revealed the presence of abnormal cardiac function at 4, 8, and 16 wk. Although accumulation of ascites in the abdominal cavity was present in experimental animals at 4 wk, other clinical signs of congestive heart failure in experimental rats including lung congestion and cardiac dilatation were evident 8 and 16 wk after induction of myocardial infarction. The depression in Na(+)-K(+)-ATPase activity in purified sarcolemmal membrane from the uninfarcted experimental left ventricle at 8 wk was associated with depressed Vmax without any changes in the affinities for Mg-ATP, Na+, and K+ or the pH optimum for the enzyme. The Kd values of both the high- and low-affinity binding sites for [3H]ouabain, which is believed to interact with Na(+)-K(+)-ATPase, were increased; however, no change in the density of either class of ouabain binding site was evident. The depression of Na(+)-K(+)-ATPase activity in failing hearts at 16 wk of myocardial infarction was not different from that observed at 8 wk but the enzyme activity was not altered at 4 wk of coronary occlusion. These data support the view that depression of Na(+)-K(+)-ATPase activity may serve as an adaptive mechanism during the development of congestive heart failure.
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PMID:Sarcolemmal Na(+)-K(+)-ATPase activity in congestive heart failure due to myocardial infarction. 131 80

To examine the status of sarcoplasmic reticulum (SR) with respect to Ca2+ transport in congestive heart failure due to myocardial infarction, the left coronary artery in rats was ligated for 4, 8, and 16 wk. The left heart function was assessed with an intraventricular pressure transducer, and SR membrane fractions from the right ventricle and the viable left ventricle were isolated for measuring the ATP-dependent Ca2+ uptake activities. In comparison to sham-operated controls, SR Ca2+ uptake activity was decreased in viable left ventricle of the experimental animals at 4, 8, and 16 wk. On the other hand, SR Ca2+ uptake activity in the right ventricle was increased at 4 and 8 wk, but no change was apparent at 16 wk of coronary occlusion. The decrease in SR Ca2+ uptake in left ventricle and increase in right ventricle were associated with corresponding changes in maximal velocity values without any alterations in the affinity for Ca2+. These opposite changes in the right and left ventricles were dependent on the scar size as well as time after inducing the myocardial infarction. The SR Ca(2+)-stimulated adenosinetriphosphatase activity was decreased in left ventricle and increased in the right ventricle from 4 wk experimental animals. The results suggest differential remodeling of the SR membranes with respect to Ca(2+)-pump mechanisms in left and right ventricles during the development of congestive heart failure.
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PMID:Differential changes in left and right ventricular SR calcium transport in congestive heart failure. 131 49

Moderate and severe stages of congestive heart failure due to the loss of myocardium upon coronary occlusion in rats was associated with an increase in alpha-adrenergic receptors and a decrease in beta-adrenergic receptors in the viable left ventricle. However, at early stages of heart failure the number of beta-adrenergic receptors was decreased without any changes in the number of alpha-adrenergic receptors. The affinities of these receptors to alpha receptor antagonist (3H-prazosin) and beta receptor antagonist (3H-dihydroalprenolol) were not altered in the failing hearts. On the other hand, the pattern of changes in both alpha- and beta-adrenergic receptors in heart membranes treated with oxygen free radical generating system was different from that seen in the failing hearts. In particular, the affinities for these receptors were decreased whereas the number of beta-receptors was increased and the number of alpha-receptors was decreased or unchanged. These results indicate that alterations in the adrenergic receptors in heart failure are not due to the formation of oxygen free radicals.
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PMID:Changes in adrenergic receptors during the development of heart failure. 146 Dec 61

It is well known that changes in serum potassium cause ventricular arrhythmias as a result of clearly documented changes in the electrophysiological characteristics of single fibers. Hypopotassemia induced by thiazide and loop diuretics may contribute to the incidence of sudden cardiac death in patients with hypertension and those with congestive heart failure. In addition, hypopotassemia appears to be an independent risk factor for lethal ventricular arrhythmias occurring in the setting of acute myocardial infarction and contributes significantly to arrhythmias associated with starvation and alcoholism. The increase in myocardial extracellular potassium that occurs in the ischemic zone after coronary occlusion is clearly a major factor in the genesis of lethal ventricular arrhythmias that occur in this setting. A decrease in serum magnesium is also believed to be arrhythmogenic, and magnesium depletion is thought to play a role in many of the arrhythmias associated with hypopotassemia. Moreover, the administration of magnesium salts may be effective in the management of life-threatening ventricular arrhythmias. However, definite evidence establishing a causal relation between ventricular arrhythmias and hypomagnesemia or intracellular magnesium depletion is lacking. Changes in intracellular calcium contribute to the arrhythmias associated with acute ischemia and with reperfusion and may be important in the genesis of ventricular tachycardia induced by exercise and by digitalis. Thus, electrolyte and metabolic abnormalities clearly underlie lethal ventricular arrhythmias in a wide variety of clinical situations and should be routinely considered as potential etiologic factors in patients with life-threatening ventricular arrhythmias, particularly those with hypertension and congestive heart failure who are receiving thiazide and loop diuretics.
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PMID:Electrolyte abnormalities underlying lethal and ventricular arrhythmias. 172 8

In a group comprising a total of 217 patients with a recent myocardial infarction, who were treated with streptokinase the authors provided evidence that early recanalization of the coronary occlusion occurred after superselective intracoronary administration in 81 and 83% of the patients. After intravenous streptokinase administration they recorded early recanalization in 62%. They found a significant diminution of the infarction focus and improved left ventricular function, as compared with patients treated in the "classical" way by antiarrhythmic drugs, beta-blockers and vasodilatating drugs. The follow up of some other indicators is also in favour of significant improvement after thrombolytic treatment--thrombi in the left ventricle, cardiac decompensation, development of an aneurysm, myocardial rupture. Conversely an argument against thrombolytic treatment are more frequent haemorrhagic complications--16%. However, in these complications no deaths were recorded nor the need of an operation or discontinuation of maintenance anticoagulant treatment. In reperfused patients no hospitalization mortality was recorded. Reocclusions occurred most frequently during the first four weeks after treatment and only after intracoronary administration--10%. According to the authors this is due to residual stenoses more serious ones, 75% of the lumen--the higher incidence of reocclusions in significant stenoses is statistically evident. The only prevention of reocclusions is immediate follow up of PTCA after intracoronary thrombolysis. The intravenous administration of streptokinase in myocardial infarctions is according to the authors a safe method and they recommend its use in all coronary units in the CSSR.
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PMID:[Myocardial infarct. Results and tactics in reperfusion therapy]. 262 Mar 38

The cardiovascular effects of 1,2-dihydro-6-methyl-2-oxo-5-(imidazo[1,2-a]pyridin-6-yl)-3-pyridine carbonitrile hydrochloride monohydrate (E-1020), a new nonglycoside, noncatechol cardiotonic agent, were investigated in dogs. In anesthetized dogs, E-1020 (10-100 micrograms/kg i.v.) dose-relatedly increased cardiac contractility (LV dP/dtmax), enhanced cardiac index and decreased systemic vascular resistance accompanying relatively small reduction in mean aortic pressure and a mild increase in heart rate. Coronary and femoral arterial blood flow were increased by either systemic intravenous or topical administration of E-1020. The degree of increase in myocardial oxygen consumption was only slight (10% at 30 micrograms/kg i.v.). The inotropic effect of E-1020 was not markedly affected by pretreatment with beta-adrenoceptor blockade, reserpine or other cardiotonic agents such as dobutamine or ouabain. In two experimental heart failure models induced by an excessive dose of propranolol or by coronary occlusion following volume-loading, E-1020 (30 micrograms/kg i.v.) rapidly reversed the cardiac depression. In chronically instrumented conscious dogs, E-1020 (30-100 micrograms/kg i.v. or 0.3-10 mg/kg p.o.) produced dose-dependent increases in LV dP/dtmax with minor increases in heart rate. E-1020 did not exacerbate arrhythmias of several experimental models in anesthetized dogs even at high dose of 100 micrograms/kg i.v. These results indicate that E-1020 is an intravenously and orally effective cardiotonic agent with vasodilating property, and that it may be beneficial in the treatment of acute and chronic congestive heart failure.
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PMID:Cardiovascular effects of the new cardiotonic agent 1,2-dihydro-6-methyl-2-oxo-5-(imidazo[1,2-a]pyridin-6-yl)-3-pyridine carbonitrile hydrochloride monohydrate. 2nd communication: studies in dogs. 271 42

Beta blockers reduce myocardial oxygen demand and are therefore useful in ischemic states. They reduce angina pectoris and reduce the risk of death when administered long-term after acute myocardial infarction. Some studies suggest that when administered early after coronary occlusion they can reduce myocardial infarct size. Relative contraindications to beta blockers, such as a history of congestive heart failure, chronic obstructive lung disease, atrioventricular conduction defects and low blood pressure, limit their use. Conventional beta blockers have a relatively long duration of action and are either contraindicated or must be used with particular caution in patients with these contraindications. Esmolol is an ultrashort-acting beta blocker with a biologic half-life of 9 minutes. Therefore, such an agent may be useful in patients with ischemic heart disease in whom reducing heart rate would be beneficial but in whom there is concern that beta blockers might not be tolerated. Esmolol reduced myocardial infarct size in 2 experimental studies of coronary occlusion followed by reperfusion, and improved the recovery of the stunned myocardium when administered during experimental myocardial ischemia. Esmolol's brief duration of action may make it safer than conventional beta blockers for the management of patients with unstable angina or myocardial infarction.
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PMID:Experimental and clinical observations on the efficacy of esmolol in myocardial ischemia. 286 48

The reported study determined whether timolol would afford a protective effect by preventing the coronary occlusion-induced arrhythmias associated with the increase in plasma norepinephrine (NE) and epinephrine (E). Ten anesthetized cats received saline or timolol (5 mg/kg, IV) five minutes after coronary occlusion of the left anterior descending coronary artery 10 to 14 mm below its origin. Coronary occlusion produced arrhythmia in three of the cats that received saline and in four of the cats that received timolol. Three of the saline-treated cats died in cardiogenic shock; two were sacrificed six hours postocclusion. Four of the timolol-treated cats died in congestive heart failure postcoronary occlusion. There was a gradual increase in NE (P greater than .05) and E (P less than .05) in both groups after coronary occlusion. Death produced a significant increase in NE and E levels. Timolol did not modify the occurrence of arrhythmias and the associated increase in plasma NE and E that developed after coronary occlusion and at death.
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PMID:The effect of timolol given five minutes after coronary occlusion on plasma catecholamines. 339 27

Two patients are described, each with a large left ventricular aneurysm and severe coronary artery disease, and each with an ejection fraction lower than 30% and in congestive heart failure. In both, the left latissimus dorsi (LD) muscle was used in the repair of the ventricular aneurysm because preoperative studies demonstrated that there was concomitant coronary artery disease, and there was a strong suggestion that resection of the entire aneurysm would seriously compromise the residual ventricular capacity. One patient had an 18-year history of coronary occlusion with two infarctions. A large, calcified ventricular aneurysm developed, and despite vigorous medical treatment, intractable congestive heart failure and angina persisted. The diffuse coronary artery disease made this patient a poor candidate for bypass grafting. The other patient sustained an acute myocardial infarction 5 months prior to operation. The left anterior descending coronary artery was totally occluded, and a large apical aneurysm developed along with an akinetic anterior wall and septum. After his heart attack, the patient had progressive dyspnea on exertion. Following operation in both patients, the transpositioned LD, then a component in the repair of the left ventricular wall, was electrically trained to synchronously contract with each systole, driven by a standard dual-chamber cardiac pacemaker. Steady improvement and a return to normal activities were observed in both patients. There was an indication of improved ejection fraction with synchronous contraction of the skeletal muscle.
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PMID:Paced latissimus dorsi used for dynamic cardiomyoplasty of left ventricular aneurysms. 366 86

Experiments were undertaken to examine whether and how intravenous infusion of ISDN ameliorated hemodynamics of anesthetized dogs with congestive heart failure. A model of acute congestive heart failure with markedly high left ventricular end-diastolic pressure (LVEDP) and low cardiac index (CI) was induced by occlusion of the left anterior descending coronary artery (LAD) following 30-min infusion of dextran solution containing propranolol in halothane anesthetized open-chest dogs. Five minutes after occlusion of LAD, intravenous infusion of ISDN (100 and 500 micrograms/kg/min for 5 min) decreased the elevated LVEDP, aortic pressure and systemic vascular resistance, and enhanced the reduced CI. These changes produced by ISDN were significant (P less than 0.05 or P less than 0.01) as compared with values just before infusion of ISDN. ISDN at the same doses slightly reduced LVEDP, but did not increase CI in normal dogs which were not subjected to the coronary occlusion and dextran infusion. These results indicate that intravenous infusion of ISDN reduces both pre- and after-load and increases CI in dogs with heart failure, demonstrating that ISDN is useful for the vasodilator therapy of heart failure.
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PMID:[Effects of intravenous infusion of isosorbide dinitrate (ISDN) on acute experimental congestive heart failure]. 667 26


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