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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical signs and lesions of Nubian goats and Desert sheep orally dosed with fresh and dry leaves and stems of Ipomoea carnea at 2.5, 5 and 10 g/kg/day were studied. The signs of Ipomoea poisoning were inappetence, depression, weakness of the hind limbs, dyspnea, staggering, and pallor of the visible mucous membranes. The main lesions were focal necrosis and fatty vacuolation of centrilobular hepatocytes, accumulation of fibroblasts in hepatic portal tracts, degeneration or necrosis of the cells of the renal proximal convoluted tubules, hemorrhage in renal cortices, in renal medullas and in cardiac muscle fibers, focal pulmonary edema, and emphysema and straw-colored fluid in serous cavities. Increased serum aspartate amino transferase and ammonia concentrations, and decreased concentrations of total protein, calcium and magnesium in the serum of Ipomoea-poisoned animals were detected. Hematological changes indicated the development of normocytic normochromic anaemia.
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PMID:The effects of Ipomoea carnea on goats and sheep. 362 12

Sodium selenite was fed in the diet in concentrations of 3, 1 and 0.50 ppm to hybro-type chicks for 4 weeks from the age of 7 d. The chemical's effects on growth and tissues were investigated. One and 3 ppm dietary levels of selenium caused depression of growth, fatty change, focal necrosis, congestion of the sinusoids and slight fibroplasia in the liver, congestion and degeneration and/or necrosis of the cells of the proximal renal tubules and of the cardiac muscle fibers and hemorrhage in the thigh and breast. These changes were accompanied by an increase in the activity of sorbitol and glutamic dehydrogenases (SDH and GDH) and in the concentration of potassium, and a decrease in the levels of total protein, calcium and zinc in the serum. Susceptibility to hemorrhage and damage to kidneys and liver persisted for 3 weeks after the test diet was withdrawn. One-half of 1 ppm-selenite meal produced no adverse effects on the chicks.
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PMID:Effects of various levels of dietary selenium on hybro-type chicks. 370 35

Ryanodine and caffeine have the ability to diminish sarcoplasmic reticulum (SR) calcium release in cardiac muscle cells. To determine whether these agents also share a common mechanism of action, we compared their effects on rat papillary muscles using two different experimental approaches. First, using the protocol of Jundt et al. (19), in which quiescent rat papillary muscles were exposed to sodium-free solutions, we found that 1 microM ryanodine decreased resting force, phosphorylase alpha activity, and the scattered light intensity fluctuations (SLIF) due to calcium-dependent myofilament interactions. In contrast, 10-20 mM caffeine increased both resting force and phosphorylase alpha levels and initially increased then decreased SLIF to below detectable levels. In a second series of experiments, contractures were elicited by exposing rat papillary muscles to 125 mM KCl. Pretreatment with ryanodine (1 microM) or caffeine (10 mM) abolished the initial phasic component of this response, while increasing the subsequent tonic component. These effects were different from those of isoproterenol, which decreased tonic contracture force. The depression of twitch force produced by ryanodine developed more rapidly in the presence of 125 mM KCl than in normal buffer, suggesting that the negative inotropic effects of this agent may, in part, depend on membrane depolarization. The results of these experiments suggest that ryanodine and caffeine affect SR calcium release through different mechanisms of action. Ryanodine appears to decrease, while caffeine initially increases, cytoplasmic calcium. Once these effects have occurred, the alterations of SR function produced by both agents can similarly alter other inotropic responses.
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PMID:Comparison of effects of ryanodine and caffeine on rat ventricular myocardium. 370 54

Previous work has demonstrated that myocardial ischemia results in a breakdown of the excitation-contraction coupling system of cardiac muscle associated with lysosomal activation. It has been hypothesized that lysosomal activation during the course of myocardial ischemia is mediated by the production of oxygen free radicals. We have tested the hypothesis that myocardial ischemia results in the activation of lysosomal phospholipase C and disruption of calcium transport in sarcoplasmic reticulum (SR) mediated by oxygen free radicals. Three groups of dogs were studied: sham-operated controls (n = 6); normothermic global ischemia of 30-min duration (n = 6); and 30 min of normothermic global ischemia pretreated with intracoronary superoxide dismutase (SOD, 10 micrograms/ml) plus catalase (25 micrograms/ml). In vitro, isolated SR demonstrated a significant depression of calcium uptake rates and Ca2+-stimulated, Mg2+-dependent ATPase activity at both pH 7.0 and 6.4 with the depression at pH 6.4 greater than 7.0. This depression of SR function was significantly inhibited in hearts pretreated with SOD plus catalase. In sham-operated controls, acid-induced dysfunction was associated with substantial loss of phospholipid phosphorus and major changes in phospholipid composition. SR contained an extremely active, ion-independent sphingomyelinase-phospholipase C (SM-PLC) that had maximal activity at pH 4.5-5.0. This SM-PLC was activated when control SR was incubated at acid pH and the specific activity of SM-PLC was decreased 50% in SR isolated from normothermic global ischemia. Activity remained at control levels in hearts pretreated with SOD plus catalase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sarcoplasmic reticulum dysfunction: phospholipid alterations induced by lysosomal phospholipase C. 377 91

Myoglobin, an intracellular iron containing protein that binds oxygen reversibly, has been shown in model systems to facilitate the diffusion of oxygen and thereby maintain the mechanical function of exercising canine skeletal muscle and of hypoxic benthic fish hearts. Since no such role has yet been established for mammalian cardiac muscle small diameter (less than or equal to 0.70 mm) isolated kitten papillary muscles were stimulated at 24 X min-1 under isometric conditions in a physiological bath maintained at 30 degrees C with an oxygen tension of approximately equal to 450 mm Hg (59.8 kPa) to obtain a level of oxygenation just adequate to meet the metabolic needs of the muscles, as confirmed experimentally. Myoglobin was inactivated by adding 2 X 10(-3) mol X litre-1 sodium nitrite to the bath to abolish the facilitated diffusion of oxygen in the presence or absence of glycolytic blockade by 10(-4) mol X litre-1 sodium iodoacetate. This resulted in a 22(8)% (with blockade) or 10(3)% (without blockade) decrease (p less than 0.05) in the maximal rate of relaxation (-dT/dtmax) of the papillary muscles. Since the depression in mechanical function was reversible by increasing the bath oxygen tension to approximately equal to 600 mm Hg (79.8 kPa) it is concluded that the myoglobin facilitated diffusion of oxygen plays a role in maintaining the mechanical function of mammalian cardiac muscle under normal conditions. Furthermore, the maximal rate of relaxation of cardiac muscle is a sensitive indicator of the presence of hypoxia.
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PMID:Myoglobin facilitated oxygen diffusion maintains mechanical function of mammalian cardiac muscle. 379 52

Reports of electrocardiographic abnormalities in association with myoglobinuria have been sparse and have included conduction disturbances, ST segment shifts, and T-wave changes. In many instances, these changes were noted in patients with underlying heart disease. We report a case of a 34-year-old woman with ST segment depression and T-wave inversion in the inferolateral leads during the acute episode of myoglobinuria. There was no demonstrable underlying heart disease, and there was parallel resolution of these ECG changes with myoglobinuria. We conclude that these ECG changes were produced by cardiac muscle involvement in a manner similar to that observed in skeletal muscle in myoglobinuria.
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PMID:ECG abnormalities in myoglobinuria: review of the literature. 381 48

The electrophysiologic properties of flecainide, a new potent antiarrhythmic drug, are poorly defined. In this study, they were investigated by standard microelectrode technique in isolated cardiac muscle from rabbit and dog hearts. The concentrations of flecainide used were between 0.1 and 10.0 micrograms/ml. Flecainide produced a concentration-dependent decrease in maximal rate of rise of phase 0 of the action potential (Vmax), action potential amplitude and overshoot potential with an increase in the effective refractory period in ventricular muscle. Vmax was reduced by 52.5% after 1 microgram/ml of flecainide (p less than 0.001) and by 79.8% after 10.0 micrograms/ml (p less than 0.001). The corresponding values for Purkinje fibers were 18.6% (p less than 0.01) and 70.8% (p less than 0.001), respectively, but in these fibers the effective refractory period was shortened at the lower concentration and restored to control value at the higher concentration. The depression of Vmax by flecainide was frequency-dependent. The action potential duration was lengthened by flecainide in ventricular muscle and shortened in Purkinje fibers. At high concentrations (10 micrograms/ml), flecainide depressed slow channel-dependent fibers. Purkinje fiber automaticity induced by isoproterenol was slowed by flecainide. The data indicate that the overall electrophysiologic effects of flecainide in isolated cardiac muscle are complex with a major depressant action on Vmax that may account for its dominant antiarrhythmic effects. It is also possible that the differential effects of the compound on the action potential duration and refractoriness in ventricular muscle and Purkinje fibers contribute to the known arrhythmogenic potential of the drug.
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PMID:Effects of flecainide on the electrophysiologic properties of isolated canine and rabbit myocardial fibers. 396 15

During intensive growth of animals, the main parameters of myocardial contractility were reduced. Poststressor depression of the contraction of isolated papillary muscles was more marked in adult than in young animals. Thus, aging of animals was accompanied by reduced cardiac muscle contraction. It is inferred that strong stress influence might result in a deep depression of the cardiac function in question, threatening the physiological possibilities of adaptation.
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PMID:[Effect of the age of animals on disorders of the contractile function of the heart muscle under stress]. 403 63

1 The actions of 4-(2-hydroxy-3-isopropylaminopropoxy) phenyl acetamide (ICI 66082), a new beta-adrenoceptor blocking drug, on the twitch response of the isolated papillary muscle of the rabbit and on dP/dt max and free heart rate of a denervated dog heart preparation, are described.2 ICI 66082 (up to 1 mg/ml) did not produce any depression of the twitch response of the rabbit papillary muscle. ICI 66082 antagonized the action of isoprenaline on this preparation at a concentration of 0.01 mug/ml.3 ICI 66082 (0.5-1.0 mg/kg intravenously) reduced the control value of dP/dt max in four dog preparations by a mean value of 529 mmHg/s (s.e. mean +/- 139 mm Hg/s), with no significant change in free heart rate. Antagonism of the effect of isoprenaline on dP/dt max and on free heart rate was demonstrated with ICI 66082 (0.1 mg/kg).4 ICI 66082 (1.0-1.5 mg/kg) produced no significant changes in dP/dt max or in free heart rate in four dogs pretreated with reserpine. A significant reduction (16% of the control value) in dP/dt max was observed with ICI 66082 at a high dose of 40-50 mg/kg.5 It is concluded that ICI 66082 is a competitive antagonist against the actions of isoprenaline on cardiac muscle, has no negative inotropic action (unless the dose exceeds 40 mg/kg) and lacks intrinsic sympathomimetic activity.
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PMID:The actions of a new beta-adrenoceptor blocking drug, ICI 66082, on the rabbit papillary muscle and on the dog heart. 415 70

1 The effects of propranolol, oxprenolol and practolol on the isometric twitch responses to electrical stimulation of isolated diaphragm muscles from the rat and of isolated papillary muscles from the rabbit are described.2 Depression of the twitch responses of the diaphragm muscle was produced by propranolol (20 mug/ml), by oxprenolol (100 mug/ml) and by practolol (500 mug/ml).3 Depression of the twitch responses of the papillary muscles was produced by propranolol (20 mug/ml) by oxprenolol (100 mug/ml) and by practolol (200 mug/ml).4 No increase of twitch tension was produced by oxprenolol or practolol on either tissue.5 It is concluded that propranolol, oxprenolol and practolol produce negative inotropic actions on isolated cardiac muscle by a mechanism unrelated to blockade of beta-adrenoceptors and which occurs at doses which are well in excess of those doses required to produce beta-blockade.
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PMID:The effects of three beta-adrenoceptor blocking drugs on isolated preparations of skeletal and cardiac muscle. 415 91


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