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)

Chronic ammonia toxicity in experimental mice was induced by exposing them for 2 and 5 days to 5 % (v/v) ammonia solution. The enzymes concerned with glutamate metabolism (aspartate-, alanine- and tyrosine aminotransferases, glutamate dehydrogenase and glutamine synthetase) and (Na+ + K+)-ATPase were estimated in the three regions of brain (cerebellum, cerebral cortex and brain stem) and in liver. Glutamate, aspartate, alanine, glutamine and GABA, RNA and protein were also estimated in the three regions of brain and liver. A significant rise in the activity of (Na+ + K+)-ATPase in all the three regions of brain along with a fall in the activity of alanine aminotransferase was noticed. Changes in the activities of other enzymes were also observed. A significant increase in alanine and a decrease in glutamic acid was observed while no change was observed in the content of other amino acids belonging to the glutamate family. As a result of this, changes in the ratios of glutamate/glutamine and glutamate + aspartate/GABA was observed. The results indicated that the brain was in a state of more depression and less of excitation. Under these conditions the liver tissue was showing a profound rise in the activity of the enzymes of glutamate metabolism. The results are further discussed.
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PMID:Chronic metabolic effects of ammonia in mouse brain. 9 19

Intracoronary administration of contrast materials causes myocardial depression which is related to serveral physiochemical properties of the contrast solution. The role of variations in ambient calcium ions (Ca++) in mediating this effect was evaluated in 19 anesthetized dogs. Sodium meglumine diatrizoate caused decreases in left ventricular peak systolic pressure (LVPSP),-12.6 +/- 3.2%, and dp/dt at a left ventricular pressure (LVP) of 40 mm Hg, -14.3 +/- 4.1%. The total calcium (Cat) decreased from 10.2 +/- 0.2 to 6.5 +/- 0.2 mg%, while Ca++ decreased from 4.6 +/- 0.1 mg% to 2.3 +/- 0.7 mg%. In the presence of systemic hypocalcemia the myocardial depressant actions of this contrast materials were accentuated. Intracoronary administration of contrast material with added Ca++, calcium sodium meglumine metrizoate, caused no myocardial depression. Total calcium decreased only slightly (10.2 +/- 0.2 to 9.1 +/- 0.2 mg%), while Ca++ increased (4.8 +/- 0.1 to 5.1 +/- 0.2 mg%. During systemic hypocalcemia, the calcium metrizoate compound induced increases in LVPSP and dp/dt/LBP40. Thus, contrast materials caused myocardial depression which, at least in part, was related to reduction of ambient calcium through a dilutional and binding action. The addition of Ca++ to monomeric contrast materials reversed the myocardial depressant action and produced a transient rise in ambient Ca++.
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PMID:Alterations in calcium levels of coronary sinus blood during coronary arteriography in the dog. 9 41

Chair-restrained rhesus monkeys (Macaca mulatta) were inoculated subcutaneously with 10(2)--10(3) plaque-forming units of virulent Rickettsia rickettsii. The latent period for fever and rickettsemia was three to four days; death occurred six to eight days after infection. Total circulatory electrolyte levels and fluid volumes, including plasma, red blood cell, true circulatory blood, and extracellular fluid, increased. The expansion of the extracellular and plasma volumes resembled findings reported during severe Rocky Mountain spotted fever in humans, guinea pigs, and rabbits. Total water content of the liver also increased. Intracellular concentrations of K+, as well as total Na+ and K+, decreased in the diaphragm. Both the lung and medulla oblongata showed increased levels of intracellular Na+ and water with simultaneously decreased levels of extracellular Na+ and water. Such an intracellular overhydration of the medulla oblongata could contribute to death as a result of depression of the cardiovascular and respiratory centers. On the basis of the findings in monkeys, the intravenous infusion of fluids and electrolytes during clinical therapy of severe rickettsial infections should be considered extremely dangerous.
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PMID:Alterations of body fluid compartments and distribution of tissue water and electrolytes in rhesus monkeys with rocky mountain spotted fever. 9 95

The direct action of nitrate derivatives on myocardial contractility is not fully understood. The effects of Glyceryl Trinitrate (1 mM/L.) and Sodium Nitro prussiate (3 X 10(-5) M/L.) on papillary muscle were studied during 30 minutes hypoxia followed by 60 minutes reoxygenation: Both conditions were analysed every 5 minutes: 1. Contractility was assessed by maximal shortening velocity with no load (Vmax), maximal isometric force (PF), number of active cross-bridges and peak time (TPF), a characteristic of the period of activity. 2. Relaxation was assessed by the relaxation velocity (V relax) and the 1/2 relaxation time (THR). The two nitrate derivatives had the same effects: during anoxia, a notable reduction of the maximal force was observed; myocardial depression continued during the first 15 minutes of reoxygenation. After the 30th minute of investigation all parameters increased significantly (107-110 p. 100, p less than 0,01); TPF and THR returned to normal. A positive inotropic effect and improvement of the relaxation phase were observed at the end of reoxygenation. This effect is not attributed to improved segmental performance especially as it occurred at dosages close to those used in therapeutics.
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PMID:[Effect of nitrate derivatives on the contractility and relaxation of papillary muscle in hypoxia and reoxygenation]. 11 41

Plasma renin activity (PRA) in 40 diabetic patients and 42 healthy controls was investigated using the method of Pickens in modification of Serebrovskaja et al. (1967). PRA was slightly lower in the whole group of diabetes but the difference was not significant. The subgroup of 20 maturity-onset diabetics had significantly lower PRA in comparison with 22 controls of similar age, while PRA in juvenile diabetics did not differ significantly from matched controls. In patients without clinical signs and symptoms of microangiopathy PRA was as high as in the controls. In diabetics with microangiopathy PRA was significantly lower. PRA was also lower in patients with longer duration of the disease. The stimulation of juxtaglomerular apparatus with sodium free diet and diuretic drugs resulted in an increase of PRA both in controls and diabetics. This suggests a functional depression of PRA in diabetic patients. In diabetics with ketoacidosis PRA was higher than in control subjects and decreased after disappearance of ketoacidosis. A high level was recorded in a patient with hyperosmolar coma and a very low level in a patient with polyneuropathy and severe orthostatic hypotension. The possible mechanisms involved in the changes of PRA in diabetic patients are discussed.
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PMID:Plasma renin activity in diabetic patients. 11 36

Previous in vitro studies of the metabolism of the peripheral nerve have been based on incorporation of radioactive precursor into components isolated from whole nerve. In this study we have determined incorporation secifically into myelin components of peripheral nerve by isolating myelin after incubating whole nerves with lipid or protein precursors and by determining the specific activity of the components of that membrane. The effect of diabetes on such incorporation was also studied. In the rat, in vitro incorporation of DL-[1-14C]leucine into protein components of myelin was decreased by 30-88% in diabetic animals as compared to controls. The major polypeptide constituent of rat sciatic nerve myelin (mol st 28,000; 58.5% of total mass of proteins) was not labeled in either the diabetic or the control group. In diabetes incorporation rate into a polypeptide of mol wt 23,000, which constitutes 21% of total mass, was approximately one half that of controls. In polypeptides of mol wt 38,000-49,000, which are heavily labeled in normal animals, but constitute only about 5% of total mass of proteins, depression of incorporation was e-en more marked in the diabetics. While these marked differences in incorporation between diabetic and control animals were observed, the amount of protein and its distribution among the constituent polypeptides was the same in both groups. In young rats made diabetic with streptozotocin and young rabbits made diabetic with alloxan, there was a lower rate of incorporation of the lipid precursors, [1-14C]sodium acetate or [3H]water, into myelin components. In older animals of both species incorporation in the controls was considerably lower than in the yount animals, and the effect of diabetes was no longer apparent. In nondiabetic animals, the in vitro addition of insulin (10-7 M) stimulated incorporation of DL-[1-14C]leucine into myelin proteins 1.6-3.1 times that of controls. This stimulation by insulin in vitro was not seen in diabetic animals. In animals in which diabetes had spontaneously recovered, however, incorporation rate in the in vitro experiments approached that of controls and were significantly above that in animals whose diabetes persisted. Since myelin is the palsma membrane of the Schwann cell, these studies provide evidence that the Schwann cell is affected by insulin and that some aspects of the metabolism of myelin are altered in insulin-deficient states.
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PMID:Metabolism of peripheral nerve myelin in experimental diabetes. 12 35

The Km value for the dog heart (Na+-K+)-ATPase was 0.31 mM (MgATP), whereas the values for the concentrations of K+ and Na+ varied from 1.2 to 2.7 mM and 12 to 20 mM for half-maximal activation, respectively. The concentrations of ouabain and calcium for 50 percent inhibition of (Na+-K+)-ATPase activity varied from 2.4 to 3.2 muM and 0.5 to 1.2 mM, respectively, the inhibitory effects of these agents were pH dependent. This preparation bound about 50 nmoles of 1-anilino-8-napthaline sulfonate (ANS)/mg of protein and exhibited fluorescence attributable to the ANS-enzyme complex. Cations such as Na+,K+,Ca++, and Mg++ increased ANS-enzyme fluorescence intensity and the number of ANS binding sites but decreased the apparent ANS binding constant. The enzyme activity, ANS binding, and ANS-enzyme fluorescence were decreased by phospholipase A, phospholipase C, and trypsin treatments. Although ouabain inhibited enzyme activity and ANS-enzyme fluorescence markedly, it caused only a slight depression in ANS binding. These results extend support for the allosteric nature of the cardiac (Na+-K+)-ATPase and provide evidence for conformational changes during its activation by Na+ and K+.
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PMID:Characterization of partially purified heart sarcolemmal Na+-K+-stimulated ATPase. 13 Jun 58

We studied hearts from sham-operated and uninfected catheterized rabbits as well as from rabbits at early and late stages of cardiomyopathy and failure after 3 and 6 days of infection with Streptococcus viridans. No ultrastructural abnormalities or biochemical changes in membrane and myofibrillar activities were seen in 3-day uninfected hearts. In 6-day uninfected hearts there were decreased sarcolemmal M2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding and uptake, and myofibrillar Ca2+-stimulated ATPase as well as increased mitochondrial calcium uptake. Slight ultrastructural changes also were apparent in 6-day uninfected hearts. At both early and late stages of infective cardiomyopathy and failure there were varying degrees of depression in sarcolemmal Mg2+ ATPase, Na+-K+ ATPase, adenylate cyclase and calcium binding, microsomal calcium binding, calcium uptake and basal ATPase, and myofibrillar Ca2+-stimulated ATPase activities. However, sarcolemmal Ca2+ ATPase and myofibrillar Mg2+ ATPase activities were decreased only after 6 days of infection. Mitochondrial calcium binding and uptake were increased in early stages but decreased in late stages of disease. Furthermore in infected hearts there were defects in mitrochondrial respiration and phosphorylation. Generalized severe myocardial cell damage involving myofibrils, mitochondria, and the sarcotubular system was seen only in late stages of infection. The results demonstrate impairment of different membrane and contractile protein functions as well as ultrastructural abnormalities in bacterial cardiomyopathic hearts which were absent or of lesser magnitude in hearts with only hypertrophy. The findings reported here suggest to use that there is an association between heart failure and changes in function of cellular components during bacterial infective cardiomyopathy.
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PMID:Abnormalities in heart membranes and myofibrils during bacterial infective cardiomyopathy in the rabbit. 13 11

Using micropuncture techniques, the author studied the effect of vasopressin on renal function in young rats at three stages of development -- in the middle of the weaning period (22 days), after weaning was over (30 days) and at the beginning of the sexual maturation period (42 days). In the presence of a hypotonic load, a small dose of vasopressin (12 muU/100 g b.w., i.v.) was most effective in the youngest age group, where it reduced the urine flow by 82% both by increasing water reabsorption and by reducing the GFR. In this group, vasopressin lowered the TF/P Na+ ratio and raised the TF/P K+ ratio in the initial part of the distal tubules of the superficial nephrons, but raised water absorption only beyond the initial part of the distal tubules. Vasopressin reduced the urine flow by 72% in 30-day-old rats by raising water reabsorption beyond the initial part of the distal tubules. The only ion to be affected was K+, whose concentration rose in the final urine. In 42-day-old rats the effect of vasopressin was manifested in only mild depression of the GFR. In this age group, as distinct from younger animals, anaesthesia and surgery evidently led to endogenous vasopressin release, so that the small dose of exogenous vasopressin did not significantly influence the test parameters. This is also underlined by the significant difference between the control urine flow of the 42-day-old and the younger rats.
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PMID:The effect of vasopressin on renal function in young rats a clearance and micropuncture study. 13 28

The effects of iontophoretically applied Na+-, K+-dependent adenosinetriphosphatase (Na+,K+-ATPase) (EC 3.6.1.3) inhibitors (ouabain, digitoxin, digitoxigenin, strophanthin K, strophanthidin, thevetin A and B, ethacrynate, and harmaline) on the depression of rat cerebral cortical neurones by noradrenaline, 5-hydroxytryptamine, and histamine have been studied. The inhibitors antagonized depressions of spontaneously active neurones evoked by these amines, but not those evoked by gamma-aminobutyric acid, adenosine, adenosine 5'-monophosphate, or calcium. The antagonistic potencies of the various inhibitors appeared to be proportional to their known potencies as inhibitors of Na+, K+-ATPase. The data therefore support the hypothesis that amines depress central neurones by activating an electrogenic sodium pump.
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PMID:Antagonism of biogenic amine-induced depression of cerebral cortical neurones by Na+, K+-ATPase in inhibitors. 14 20


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