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

Cerebral blood flow (CBF) and central hemodynamics (CH) have been studied during anesthesia and after surgery in patients with tumours located in brain hemispheres. CBF and CH were determined by radiography. GOBA, diazepam and sodium thiopental were used for anesthesia. It has been shown that GOBA fails to normalize CBF both during and after surgery, diazepam normalizes blood flow in both brain hemispheres. Sodium thiopental leads to further CBF depression up to critical level in the affected hemisphere with parallel blood flow ingress in the intact brain hemisphere. It is concluded that the use of diazepam is advisable for anesthesia during surgery for tumours located in brain hemispheres.
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PMID:[Changes in the cerebral blood flow in neurosurgical patients during general anesthesia using antihypoxic agents]. 176 67

Dehydration, in childhood as in adulthood, may origin from an inadequate water ingestion or an excessive water elimination. Causes may be found in fever, vomiting, scalds, pulmonary hyperventilation, diabetes. Water loss during acute diarrhea in children can be even 6-7 times higher in comparison with an healthy child. Together with water, electrolytes are lost. We differentiate dehydration in isonatremic d. (70% of cases), hyponatremic d. (10%) and hypernatremic d. (20%) basing on Sodium loss. Important dehydration causes severe clinical symptoms as shock, renal and cardiocirculatory failure, convulsion, coma. Symptoms at the central nervous system level derivate both from hyperosmolarity in brain cells and from thrombosis or hemorrhages in subdural sites. Dehydration, following acute diarrhea, is slight when weight loss is lower than 5%. The child health conditions still remain good. Dehydration become moderate if weight loss reaches 5% and the child starts suffering. When the weight loss reaches 10%, dehydration is now severe and circulatory deficiency becomes evident. When it is higher than 10%, prognosis is very severe and shock and coma may be observed. In the present work, we illustrate the different ways of rehydration after acute diarrhea. Initially, oral rehydration must be established with one of the oral solutions, differing each other for amount of electrolytes and glucose. Recently, a new solution, "supersolution", has been presented differing from the other ones for electrolytes concentration and for the presence of rice starch instead of glucose. In most cases of diarrhea, oral rehydration appears adequate but sometimes an intravenous rehydration becomes necessary, e.g. in case of vomiting, CNS depression and in any case of severe gastroenteric symptomatology.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Dehydrated child]. 189 82

Sodium dimercaptopropanesulphonate (DMPS) and sodium dimercaptosuccinate (DMS) were discovered to be effective antidotes for acute poisoning of insecticides SCD [sodium ammonium dimethyl-2-(propane-1,3-dithiosulfate) monohydrate], nereistoxin (4-N,N-dimethylamino-1,2-dithiolane) and cartap (dihydronereistoxin dicarbamate). In mice, DMPS (250 mg/kg) or DMS (1000 mg/kg) ip 20 min before SCD increased LD50 of ig SCD from 97 to 374 or 251 mg/kg, respectively. The prophylactic effect of DMPS was better than that of DMS. Administration of DMPS prior to cartap increased LD50 of ig cartap from 130 to 375 mg/kg. The therapeutic effect of DMPS was also demonstrated in SCD-poisoned conscious rabbits. DMPS 62.5 mg/kg or DMS 500 mg/kg iv completely antagonized the neuromuscular blockade and respiratory depression caused by SCD, nereistoxin and cartap in anesthetized rabbits. The antagonism of SCD-induced neuromuscular blockade by cysteine (400 mg/kg, iv) was less effective and of shorter duration than that by DMPS and DMS. Dimercaprol 50 mg/kg im showed little effect on SCD-induced paralysis. The antagonistic actions of sulfhydryl compounds on neuromuscular blockade induced by these insecticides probably belong to chemical antagonism.
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PMID:[Antidotal effects of sulfhydryl compounds on acute poisonings by sodium ammonium dimethyl-2-(propane-1,3-dithiosulfate) monohydrate, nereistoxin and cartap]. 217 10

This study tested the hypothesis that membrane transport is the major biochemical system of the myocardium altered in furazolidone-induced cardiomyopathy (round heart disease), before the development of myocardial failure, and that metabolic enzymes and contractile proteins are less affected. Compared with controls, maximal percentage depression of activities of myocardium from furazolidone-treated birds were 40 for creatine kinase, 30 for glycolysis, 30 for glycogen, 20 for myofibrils, 20 for Krebs's cycle enzymes, 15 for fatty acid oxidation and 10 for total soluble protein. Sodium and potassium transport, antioxidant system activity, myosin, myosin isoenzyme patterns and amino acid aminotransferases were unaffected. In marked contrast, the calcium-transport ATPase activity of the sarcoplasmic reticulum had undergone a 60 per cent compensatory increase in activity. The pattern of biochemical changes observed is consistent with a role of ischaemia in the pathogenesis of round heart disease and indicates that calcium transport by the sarcoplasmic reticulum is the major biochemical system affected.
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PMID:Myocardial biochemical changes in furazolidone-induced cardiomyopathy of turkeys. 232 37

The effects of sodium selenite on the neuromuscular junction of the phrenic nerve-diaphragm of the mouse were studied. Nerve-evoked twitches of the diaphragm of the mouse, the frequency of miniature endplate potentials, the quantal content of endplate potentials and the compound action potentials of the axon were measured. Sodium selenite induced a slight increase of the amplitude of the twitch, followed by twitch depression. The amplitude of the twitch, increased by selenite, became more prominent after the suppression of the twitch induced by cadmium ions, d-tubocurarine or magnesium ions. It appeared that the increased amplitude of twitch was due to the facilitation of transmitter release, since selenite significantly increased the frequency of miniature endplate potentials, and the amplitude and quantal content of endplate potentials; the amplitude and half decay time of miniature endplate potentials were unaffected. Twitch depression induced by selenite was enhanced by ammonium ions, high potassium and low magnesium and attenuated by high calcium. During the period of gradual depression of the twitch, selenite decreased the amplitude of compound action potentials of the phrenic nerve axon and caused the disappearance of endplate potentials. Ammonium ions enhanced the blockade of axonal conduction induced by selenite. Moreover, the depolarizing agents, ammonium and high potassium also induced an initial increase of twitch amplitude followed by depression of the twitch. These findings indicate that selenite probably alters the release of the transmitter by depolarizing the nerve membrane. The effects of selenite were antagonized by glutathione and cyanide, suggesting that the binding of selenite to sulfhydryl groups of the membrane was essential for inducing its pharmacological actions.
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PMID:Effects of sodium selenite on neuromuscular junction of the mouse phrenic nerve-diaphragm preparation. 247 66

The effects of bupivacaine and lidocaine on cardiac conduction were compared in guinea pig ventricular muscle. Membrane potential was controlled using a single sucrose gap voltage clamp technique, and the maximum upstroke velocity of the action potential (Vmax) was used as an indicator of peak sodium current. Bupivacaine blocked cardiac sodium channels in a time- and voltage-dependent fashion. Although bupivacaine has a low affinity for rested and activated sodium channels, it avidly blocks inactivated channels (Kd = 9 X 10(-7) M). Bupivacaine-associated channels do not conduct and have their voltage dependence of inactivation shifted by about 33 mV to more negative potentials. At bupivacaine concentrations above 0.2 micrograms/ml, a substantial fraction of the channels become blocked during the cardiac action potential, while recovery from block during diastole proceeds relatively slowly with a time constant (tau) of 1,557 +/- 304 ms (n = 8). Thus, bupivacaine blocks sodium channels in a fast-in-slow-out fashion, and substantial block accumulates at 60-150 beats/min. In comparison, 5-10 micrograms/ml lidocaine also blocks a substantial fraction of channels during the action potential, but diastolic recovery from block is more rapid (tau = 153.8 +/- 51.2 ms, n = 4). Thus, lidocaine blocks channels in a fast-in-fast-out fashion. Consequently, even at toxic doses of lidocaine (i.e., 10 micrograms/ml), little accumulation of block occurs at normal heart rates. Sodium channel block by bupivacaine can be minimized by reducing heart rate, hyperpolarization, and shortening of action potential duration. However, alteration of these variables over clinically applicable ranges does not produce marked changes in bupivacaine effect. Our results provide a possible explanation for the clinical observation that when bupivacaine accidently gains access to the general circulation, cardiac conduction can be depressed seriously and such depression may be difficult to reverse.
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PMID:Mechanism for bupivacaine depression of cardiac conduction: fast block of sodium channels during the action potential with slow recovery from block during diastole. 258 Apr 63

The effects of ion substitution, inhibitors and variations in transmural p.d. on the movements of sodium and chloride across an in vitro preparation of rat gastric mucosa have been studied. The tissue maintained net steady-state transport of sodium in the mucosal-to-serosal direction in the absence of transmural gradients of electrochemical potential. Sodium transport was independent of the presence of chloride, and was abolished by 1 X 10(-5) M-amiloride. The inhibitor produced a decrease in short-circuit current equivalent to the depression of sodium transport, indicating that the sodium transport process was electrogenic. Variations in transmural p.d. showed that the sodium transport process included two components: one that varied with p.d. and one that was independent of it. These findings have been interpreted in terms of a system for sodium transport composed of three components: two rate-limiting entry mechanisms at the apical membrane, one of which can be represented as a conductive channel for sodium diffusion and the other as a neutral process possibly a sodium-hydrogen exchanger, and a voltage-independent pump at the basolateral membrane analogous to the constant-current pump models described in some other epithelia. The tissue maintained a net secretory movement of chloride in the short-circuited condition. The process responsible for net transport of chloride could be resolved into two components: one that was sodium dependent, electrogenic, and abolished by 8 X 10(-3) M-acetazolamide, and one that was independent of the presence of sodium, electrically silent and abolished by 5 X 10(-4) M-SITS (4-acetamido-4'-isothiocyano-2,2'-disulphonic acid stilbene). Both components of the chloride transport process varied with p.d. These findings were interpreted in terms of a system of three components: two entry mechanisms at the basolateral membrane including a coupled sodium-chloride influx process and a chloride-bicarbonate exchanger in parallel, and a rate-limiting conductive channel at the apical membrane. In addition, the studies on the effects of variations in transmural p.d. on chloride fluxes revealed a symmetrical voltage-independent component, dependent on the presence of chloride in the trans compartment, and it was suggested that this component may reflect the presence of a chloride-chloride exchange mechanism.
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PMID:Transport of sodium and chloride across rat gastric mucosa in vitro. 258 Sep 70

To shed light on the causes of Kaschin-Beck disease, which can be prevented by supplementation of the diet with sodium selenite, the interactions between inorganic selenium compounds (selenite and selenate) and humic/fulvic acid were investigated. Selenate was found to be slowly reduced to selenite by humic acid in acidic solution. Selenite was adsorbed on manganese dioxide and iron(III) oxide from solution to a much greater degree than on kaolin, humic acid, Yongshu soil, or silicon dioxide. Feeding mice a diet supplemented with sodium selenite increased the selenium concentration in the kidney, liver, spleen, lung, heart and blood. A diet containing sodium selenite and fulvic acid caused the selenium concentrations in the organs, with the exception of the spleen, to be lower than observed with the selenite-only diet. Selenium and fulvic acid increase the activity of glutathione peroxidase. Sodium selenite and fulvic acid injected in combination into the abdominal cavity of mice and rats were less toxic than either substance alone. Selenite and fulvic acid applied separately enhanced the luminosity of photobacterium phosphoreum T-3 at low concentrations but depressed the luminosity at higher concentrations. Selenite and fulvic acid in combination caused a larger enhancement and a smaller depression of the luminosity than observed with either substance alone. The hypothesis is formulated that Kaschin-Beck disease is caused by selenium levels insufficient to prevent the toxic effects of the organic compounds present in the drinking water of the regions in which the disease is endemic.
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PMID:The effects of humic acid on the chemical and biological properties of selenium in the environment. 295 9

One hundred and seventy-four patients who were receiving drug therapy for hypertension were asked to restrict their sodium intake for three months. At the end of that time their drug therapy was replaced with enalapril and the dose of the drug "titrated" to obtain a diastolic blood pressure of less than 90 mmHg. Sodium restriction caused a small fall in blood pressure and could be used as sole therapy in only 6% of patients. Enalapril therapy was instituted without problems and control of blood pressure below 90 mmHg was achieved in 62% of persons with monotherapy. The number of tablets of enalapril that were taken was reduced from 5.9 to 2.7; in most patients these were taken once a day. There were few side-effects and no depression of white cell count, no proteinuria and no deterioration of renal function. Seventy-six per cent of patients preferred the new regimen either because they felt better than with their previous therapy (52%) or because of the more simple regimen (24%). Enalapril was an effective, well tolerated antihypertensive agent and potentially has a major role to play in the management of patients with high blood pressure.
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PMID:Use of sodium restriction and enalapril in persons with moderate to severe hypertension. 303 55

Sodium was measured in beta-cell-rich pancreatic islets isolated from ob/ob-mice starved overnight. Exposure to glucose (5 or 20 mmol/l) resulted in about a 30% reduction of the sodium content whether or not the Na+/K+ pump was inhibited by removal of K+. The glucose effect was not potentiated after amiloride depression of Na+/H+ exchange, and it disappeared when combining removal of K+ with the addition of the hyperglycemic sulphonamide diazoxide (400 mumol/l). Tolbutamide (100 mumol/l) counteracted the reduction of sodium obtained with 5 mmol/l glucose both in the presence or absence of extracellular K+. It is concluded that closure of ATP-regulated K+ channels does not necessarily result in a lowering of the sodium content. The pancreatic beta-cells can be regarded as exceptional among the excitable cells in not responding to their natural physiological stimulus (glucose) with increase of sodium.
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PMID:Influence of glucose on the sodium content of beta-cell-rich pancreatic islets exposed to sulphonamides and amiloride. 306 44


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