Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin accelerates the entry of glucose and amino acids into muscle cells by acting upon the 'carrier-facilitated' transport mechanism. For glucose this process is passive and leads to equilibration of intracellular and extracellular concentrations. In heart muscle, glucose transport is a rate-limiting step for glucose uptake. During hypoxia and ischemia the heart turns to anaerobic glycolysis for energy production and therefore, maximal glucose transport becomes important. Insulin is necessary to insure proper protein synthesis, probably at the level of membrane-bound polyribosomes. However, during myocardial hypoxia, insulin alone cannot restore the associated depression in protein synthesis. Although insulin hyperpolarizes the cell, a change in the ratio of intracellular to extracellular activities of potassium is not its primary mode of action. An insulin-induced configurational change in the plasma membrane could simultaneously account for the effects of insulin on sodium and potassium permeability and the action on facilitated transport. Intracellular levels of cyclic adenylate may be reduced by insulin in adipose tissue because of inhibition of adenyl cyclase or stimulation of phosphodiesterase. However, at this time there is little evidence that insulin alters cyclic AMP levels in the heart. Insulin secretion is depressed in patients with heart disease in proportion to the reduction of cardiac index sustained. Since the ischemic heart is dependent upon glucose as the major fuel, insulin lack may deprive the heart of adequate substrate.
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PMID:Insulin: fundamental mechanism of action and the heart. 18 67

Although the time course of changes in myocardial function during ischemia has been demonstrated for the papillary muscle, this time course in the intact heart is less well understood. Accordingly, in 24 isolated, isovolumic, perfused dog hearts, coronary perfusion pressure (PP) was lowered to various fixed levels. Left ventricular developed pressure (LVP) rapidly fell and reached 63 +/- 3% of control at 1 minute of ischemia 50 +/- 5% at 6 minutes; this was due primarily to an abbreviation of time to peak tension (TPP). dP/dt was 70 +/- 3% of control at 1 minute and 56 +/- 5% at 6 minutes. The rate of relaxation as reflected by negative dP/dt declined as well to 49 +/- 4% of control at 1 minute of ischemia and to 41 +/- 4% control at 6 minutes. These changes were directly correlated with the decrease in PP. When PP was restored to normal, an overshoot of LVP and dP/dt was noted, peaking at 1 minute, returning to control by 5 minutes, and then gradually declining to 90 +/- 2% of control following 25 minutes of recovery. Depression of the rate of relaxation was reduced, but persisted throughout recovery. Diminution of force development early in ishcemia is due primarily to decreased duration of contraction accompanied by a decrease in relaxation rate. Later, the rate of force development also falls, but some preservation of force development may result from the return toward normal of the duration of contraction.
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PMID:Experimental myocardial ischemia: dynamic alterations in ventricular contractility and relaxation with dissociation of speed and force in the isovolumic dog heart. 18 14

A new approach to study the effect of ischemia on the brain of the awake gerbil is described. The measurement of NADH fluorescence from the surface of the cortex is done by a time-sharing fluorometer/reflectometer connected to the brain via a flexible light guide and an implanted cannula. The response of the gerbil brain to anoxia and spreading depression is described. By unilateral occlusion of the carotid artery an increase in NADH was measured in the ipsilateral hemisphere.
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PMID:Pyridine nucleotide oxidation-reduction state of the cerebral cortex in the awake gerbil. 21 12

A brief review is given of recent results which indicate that several stressful situations are accompanied by an increase in cerebral metabolic rate, mediated by extrinsic or intrinsic catecholamines. These situations include withdrawal of nitrous oxide supply in paralyzed animals ("immobilization stress"), amphetamine intoxication, hypoxia, and hypercapnia. Studies of hypercapnia (and hypoxia) suggest that activity in cerebral noradrenergic systems is enhanced by cellular acidosis. Data obtained during recirculation, following severe, transient ischemia, indicate that in spite of a general depression of cerebral metabolism (and neuronal function) some neuronal systems, notably the noradrenergic ones, show evidence of increased activity.
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PMID:Brain energy metabolism and catecholaminergic activity in hypoxia, hypercapnia and ischemia. 29 Jul 38

Cerebral ischemia was induced in normothermic, artificially ventilated rats, anesthetized with 70% N2O or 150 mg/kg of phenobarbitone, by bilateral occlusion of the common carotid arteries and by simultaneous depression of the mean arterial blood pressure to 50 mm Hg. The levels of tyrosine, dopamine (DA), noradrenaline (NA), tryptophan, 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were measured after 15 min of ischemia as well as after 30 min of recirculation. In separate experiments (70% N2O) the rate of accumulation of DOPA and 5-hydroxytryptophan (5-HTP) was determined in three different brain regions (striatum, limbic forebrain and hemispheres) during recirculation. During ischemia, the monoamine pattern was unaffected. Following recirculation, increases in DA, 5-HIAA, tyrosine and tryptophan were found irrespective of the type of anesthesia used. Pronounced postischemic decreases in NA and 5-HT were observed in animals anesthetized with nitrous oxide but not in those given phenobarbitone. During recirculation the rate of tyrosine hydroxylation increased in all three brain regions while tryptophan hydroxylation was reduced. It is tentatively concluded that following transient, global cerebral ischemia, neuronal activity is low or eliminated in dopaminergic and serotoninergic neurons and high in noradrenergic neurons.
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PMID:Influence of transient ischemia on monoamine metabolism in the rat brain during nitrous oxide and phenobarbitone anaesthesia. 30 81

The effect of coronary arterial bypass surgery on exercise-induced ventricular arrhythmias and their relation to sudden death was examined in 102 patients with stable angina pectoris randomly assigned to medical and surgical therapy (54 and 48 patients, respectively). Symptom-limited treadmill tests were performed at entry and at 1 and 5 years. The surgical group demonstrated significant improvement in exercise performance at 1 year compared with the medical group, and at 5 years exercise-induced ischemia as evidenced by S-T depression and exertional angina remained substantially decreased in the surgical group with little change in the medical group. However, the frequency and severity of exercise-induced ventricular arrhythmias in each group remained unchanged at 1 and 5 years from those at entry. Similar results were obtained from an evaluation of ventricular arrhythmias in the electrocardiogram at rest. With the exception of exercise-induced ventricular tachycardia and fibrillation, no relation was found between ventricular arrhythmias and sudden death. Coronary bypass grafting does not decrease the frequency or severity of exercise-induced or resting ventricular arrhythmias. In patients with stable angina pectoris, with the exception of ventricular tachycardia and fibrillation, exercise-induced ventricular arrhythmias are poor predictors of sudden death. The data suggest that exercise-induced ventricular arrhythmias may not be related to ischemia but to other effects of exercise such as cardiac stimulation by catecholamines or other factors.
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PMID:Effect of coronary arterial bypass surgery on exercise-induced ventricular arrhythmias. Long-term follow-up of a prospective randomized study. 31 62

The significance of asymptomatic episodes of ischemic type S-T segment depression was studied in 20 patients with coronary heart disease. Continuous 10 hour electrocardiographic recordings accompanied by detailed daily diaries of activity and symptoms were obtained periodically during a mean time of 16 months. All patients had ischemic type S-T depression associated with angina pectoris during treadmill exercise. Measurements of heart rate, S-T depression and exercise level at the onset of angina obtained during repeated controlled exercise tests at the start of each study period were compared with the measurements recorded during daily activity. After 2,826 hours of recording, 411 transient epidsodes of ischemic type S-T depression were noted during usual daily activity. Only 101 (25 percent) of these episodes were associated with angina. The remaining episodes were unrelated to other symptoms or to posture. All occurred at heart rates significantly lower than those observed at the onset of angina during exercise testing. Of these episodes of asymptomatic S-T depression, 72 percent occurred only at rest or during very light activity such as slow walking or sitting. Nitroglycerin administered hourly significantly reduced the frequency of these episodes, thus supporting the concept that they represent painless ischemia. Because the episodes of asymptomatic ischemic type S-T depression occurred more frequently than angina during usual daily activity and were evident at heart rates and activity levels well below those expected to evoke ischemia, they may be caused by factors other than those that cause angina.
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PMID:Transient asymptomatic S-T segment depression during daily activity. 40 3

An experimental study was performed in rhesus monkeys (M. mulatta) to examine the contribution of Bunnell tendon suture to the production of postoperative tendon adhesions. It was found that Bunnell suture used with atraumatic technique caused a significant depression of in vitro tendon surface plasminogen activator activity, allowing the in vivo persistence and fibrous organization of fibrinous postoperative adhesions to sutured areas. Bunnell suture also produced coagulation necrosis of the sutured area of tendon. Collagen, which replaced the destroyed areas, was oriented randomly and frequently was continuous with surface tendon adhesions to surrounding connective tissues. Bunnell suture appears to be a cause of tendon adhesions in subhuman primates. The importance of fibrin and depressed local fibrinolysis in the relationship of tendon ischemia and adhesion formation is discussed.
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PMID:Some effects of Bunnell suture on otherwise uninjured tendons in subhuman primates. 41 Nov 89

We have recently detected accumulation of lysophosphoglycerides, catabolites of phospholipids, in ischemic myocardium early after coronary occlusion. In the present study we delineated effects of selected concentrations of albumin-bound lysophosphatidyl choline (LPC) comparable to those accompanying ischemia in vivo on action potentials of isolated canine Purkinje fibers. Lysophosphoglycerides induced concentration-dependent (0.75-3.0 mM) decreases in resting membrane potential, overshoot of phase 0, maximal velocity of upstroke (Vmax) of phase 0, and action potential duration. The highest concentrations (2.0-3.0 mM) induced fractionation of the action potential into several components, unresponsiveness to external stimulation, and enhanced automaticity at normal and reduced membrane potentials. LPC induced a rightward shift in the membrane response curve, a 40-fold prolongation of conduction time, and an increase in the ratio of effective refractory period to action potential duration such that the effective refractory period persisted beyond action potential duration, resulting in postrepolarization refractoriness. These electrophysiological alterations were entirely reversible after 70 minutes of perfusion without LPC, with the exception of a persistent depression in the Vmax of phase 0. Lysophosphatidyl ethanolamine (LPE) elicited alterations in action potentials indentical to those elicited by LPC. Furthermore, LPC (3.0 mM) induced comparable alterations in action potentials recorded from isolated rabbit papillary muscles. Since lysophospholipids accumulate early after myocardial ischemia, and since concentrations equivalent to those occurring in vivo induce electrophysiological alterations resembling those seen in ischemic myocardium in vivo, lysophosphoglycerides may be of major importance as biochemical mediators of malignant dysrhythmia induced by ischemia.
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PMID:Potential arrhythmogenic electrophysiological derangements in canine Purkinje fibers induced by lysophosphoglycerides. 42 75

We used intracellular microelectrodes to study the electrophysiological effects of combinations of components of ischemia and their relation to the occurrence of ventricular arrhythmias in the specialized conducting system of isolated canine right ventricles. The middle area of the free wall was exposed to various test solutions in the center compartment of a three-chambered bath; the base and apex of the preparation were superfused with normal Tyrode's solution in the outer control compartments. Hypoxia (Po2 40 mm Hg), lactic acidosis (pH 6.5), and orciprenaline (10(-6) M), either alone or combined, failed to affect the action potential amplitude or the conduction velocity of the subendocardial fibers, and no arrhythmias occurred. The action potential duration and the effective refractory period were markedly prolonged by lactic acidosis. Exposure of the test regions to 15 mM K+ plus orciprenaline resulted in marked decreases in action potential amplitude and conduction velocity. Abnormalities of impulse transmission through the depressed area included high degrees of rate-dependent block, one-way block, warming-up phenomenon, and the Wenckebach phenomenon. Such conditions regularly provoked the appearance of single, sustained, or concealed reentrant depolarizations. The combined effects of hypoxia, 15 mM K+, and orciprenaline resulted in further depression of the already depressed action potential in the depolarized fibers. Our results indicate that regional increases of extracellular K+ may be the predominant factor of the components of ischemia we studied which facilitates the initiation of reentrant arrhythmias.
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PMID:Effects of some components of ischemia on electrical activity and reentry in the canine ventricular conducting system. 42 79


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