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

Overdose cardiac effects of imipramine are due to fast Na channel blockade and are clinically reversed by administration of sodium lactate which induces alkalosis (about pH 7.50) and hypernatremia (about 8 mM). The mechanisms of this beneficial effect of Na lactate were explored in vitro on guinea-pig ventricular myocardium using the microelectrode technique. The time-course effects of the clinically relevant concentration of 10 microM imipramine on action potential characteristics were examined at pH 7.20 and pH 7.50. To test whether alkalinisation per se is important or whether an increase in Na concentration plays a major role in the reversal effect, preparations were exposed to increasing concentrations (1, 3, 10, 30, 100 mM) of either Na lactate, bicarbonate or chloride in the absence or in the presence of 10 microM imipramine at pH 7.50. The influence of elevating osmolality was evaluated with equivalent concentrations of sucrose. Imipramine alone significantly depressed Vmax and shortened action potential duration at all phases of repolarisation. All three high sodium solutions reversed imipramine effects. However the reversal effect was already obvious with 10 mM Na lactate and 10 mM NaHCO3 but not 10 mM NaCl. Osmolality did not reverse the imipramine-induced Vmax depression. The results suggest that at the clinically relevant 10 mM concentration, sodium lactate and bicarbonate may displace imipramine from its receptor site on the Na channel by causing alkalosis at the membrane level without profoundly affecting the driving force of the Na current, whereas at the upper concentrations, the increase in Na ion concentrations is predominantly involved in the reversal of imipramine effects.
 ...
PMID:Sodium lactate reversal of electrophysiological effects of imipramine in guinea-pig ventricular myocardium. 132 Oct 90

Blood volume and whole kidney and single nephron function were evaluated 2 and 10 days after nephrotoxic serum nephritis (NSN) induction in Wistar rats. Progressive proteinuria, hypervolemia and edema were observed in NSN rats. Sodium retention was associated with a progressive depression of single nephron glomerular filtration rate and elevated fractional tubular reabsorption rates. Since hypervolemia rather than hypovolemia was observed in this study, edema formation must have been a consequence of intrarenal rather than extrarenal phenomena.
 ...
PMID:Progressive hypervolemia despite hypoproteinemia and massive edema formation in rats with nephrotoxic serum nephritis. 169 61

The schema in Table 1 illustrates the inter-relationship between the major fluid and electrolyte disturbances with their primary site of involvement, that is, the CNS or peripheral nervous system (PNS), their primary effect (nervous system depression or irritability), and the major symptom complex associated with these sites and mechanisms (obtundation, seizures, muscle weakness, and tetany). As can be seen, a pattern emerges. Disorders of sodium and osmolality, whether hypernatremia (hyperNa), hyponatremia (hypoNa), hyperosmolality (hyperOsm), or hypo-osmolality (hypoOsm), all produce CNS depression with encephalopathy as the major clinical manifestation. Disorders of potassium, whether hyperkalemia (hyperK) or hypokalemia (hypoK), produce PNS depression with muscle weakness as the major clinical manifestation. On the other hand, disorders of magnesium and calcemia produce both CNS and PNS manifestations. Hypercalcemia (hyperCa) and hypermagnesemia (hyperMg) produce CNS and PNS depression with encephalopathy and muscle weakness, respectively, being the major clinical manifestations. Hypocalcemia (hypoCa) and hypomagnesemia (hypoMg) produce CNS and PNS irritability with seizures and tetany, respectively, being the major clinical manifestations.
 ...
PMID:Neurologic manifestations of fluid and electrolyte disturbances. 267 34

Hypernatremia (sodium chloride intoxication) is described in two calves due to presumed mixing errors of oral electrolyte solutions while undergoing therapy for neonatal diarrhea. The experimental induction of hypernatremia in two clinically normal calves is also reported. Physical findings in diarrheic calves included depression, weakness, dehydration, and diarrhea. Serum sodium concentrations were found to be 171.6 mEq/l and 208.0 mEq/l, respectively. Treatment with intravenous fluids was attempted in both cases, but one calf died after 6 hours and the other calf died after 2 days and exhibited periodic convulsions before death. Experimental induction with oral administration of 1 l of electrolyte concentrate, which contained approximately 2750 mEq sodium revealed that the normal calves would willingly consume the solution as mixed with milk and develop clinical signs of hypernatremia within 6 hours of administration. Serum sodium concentrations of 176.0 and 179.8 were found in the experimental calves and coincided with the onset of overt depression and weakness, at which time they were euthanatized. Cerebrospinal fluid electrolyte analysis paralleled the serum electrolyte alterations.
 ...
PMID:Hypernatremia in calves. 322 59

The causes, therapy for, and consequences of hypernatremia in elderly patients are not well understood. We found that in 15,187 consecutive hospital admissions, 162 (1.1%) patients who were at least 60 years of age had serum sodium levels that measured greater than 148 meq/L. Of that 162, 57% had become hypernatremic in the hospital; the remaining 43% were hypernatremic at hospitalization. The mean peak serum sodium level was 154 meq/L (range, 149 to 182), and mean water deficit, 9% of total body water (range, 6% to 30%). The most frequent primary causes were complications of surgery (21%), febrile illness (20%), infirmity (11%), and diabetes mellitus (11%), with more than 40 causal factors identified. Depression of sensorium correlated with severity of hypernatremia (p less than 0.001). The mortality rate (42%) was seven times that of age-matched hospitalized patients, but was not predicted by severity of hypernatremia. Mortality increased with increasing rates of fluid replacement (p less than 0.008). Hypernatremia in elderly patients is usually iatrogenic and often a marker for severe associated systemic illness.
 ...
PMID:Hypernatremia in elderly patients. A heterogeneous, morbid, and iatrogenic entity. 361 20

Ten clinically healthy cats were allotted into 2 groups. Group A was given the low (60 ml), and group B was given the high (120 ml) recommended dose of a commercial hypertonic sodium phosphate enema. Enema retention was enforced. All cats developed clinical and/or laboratory abnormalities, with group B cats being more severely affected. Clinical signs that occurred rapidly included depression, ataxia, vomition, bloody diarrhea, mucous membrane pallor, and stupor; tetany was not seen. One cat in group B died. Laboratory abnormalities included hypernatremia, hyperphosphatemia, hypocalcemia, hyperglycemia, calculated hyperosmolality, and metabolic acidosis with high anion gap probably due to hyperlacticacidemia. There were no significant gross or microscopic lesions associated with enema administration. Therefore, the use of hypertonic sodium phosphate enema at recommended doses is potentially dangerous to cats.
 ...
PMID:Clinical, biochemical, acid-base, and electrolyte abnormalities in cats after hypertonic sodium phosphate enema administration. 401 52

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.
 ...
PMID:Practical toxicologic diagnosis. 649 3

The sodium and water intakes of a group of infants treated for diarrhea and dehydration in 1972-73, when hypernatremia was common, and a group of infants treated for diarrhea and dehydration in 1978-79, when hypernatremia was rare, were compared. Infants from both study periods whose intake was poor and who received feedings containing sodium in concentrations greater than 17 mEq/liter were more likely to develop elevated serum sodium concentrations. In a group of infants recovering from diarrhea, the effect upon the serum concentration of sodium of varying water and sodium intake was studied. Those treated with small amounts of a solution containing 30 mEq sodium per liter regularly demonstrated an elevation of serum sodium, whereas those treated with large amounts of the same solution regularly demonstrated a depression. It is concluded that infants with diarrhea should receive feedings containing sodium in concentrations less than 17 mEq/liter unless a high fluid intake can be assured.
 ...
PMID:Sodium and water content of feedings for use in infants with diarrhea. 719 44

Although valproic acid has gradually gained its popularity in the treatment of various seizure disorders, overdose of valproate is not common. An 18-y-old man with a history of epilepsy controlled by sodium valproate and clonazepam attempted suicide with an ingestion of 45 g sodium valproate. He presented to our service with drowsiness and irritability. Extremely high serum ammonia (623 ug/dL) and elevated serum valproate concentration (575 ug/mL) were found on admission. Several metabolic abnormalities, including hypernatremia, hypocalcemia and metabolic acidosis, as well as, increased serum transaminase levels were also recorded. With supportive measures, he became clear 24 h later and was discharged 6 d after ingestion. Serial follow-up of his serum valproate and ammonia levels disclosed a close relationship between these 2 measurables. After acute overdose of valproic acid, patients usually present with mild and generally reversible depression of the central nervous system. However, impairment of liver function, hyperammonemia, fluid-electrolyte disturbances, coma, seizures, hypotension and even death may occur following valproate overdose. Symptomatic and supportive measures are the mainstay in the treatment of valproic acid overdose. With prompt diagnosis and early institution of treatment, a complete recovery should be anticipated.
 ...
PMID:A case of severe hyperammonemia and unconsciousness following sodium valproate intoxication. 983 Jun 96

Sodium retention is a frequent effect of cancer in humans and animals, but the mechanism involved is not yet understood. In the Walker-256 tumor, sodium retention has been considered to be a late effect, secondary to retention in the tumor mass, and/or to adrenal hypertrophy. Normally, (in rats receiving single tumor implants), the development of different tumor systemic effects (TSE) such as anorexia, sodium and fluid retention, anemia and immune depression in rats is synchronous within each individual but random among individuals of a given group in which they appear 6-47 days, or more, after inoculation. In present study, multifocal simultaneous inoculations of tumor cells resulted in a rapid and synchronous initiation of TSE (in 3-4 days) in all rats when no local effects of metastases could mask the results. Sodium retention is a special tumor effect on Na+ balance and a very sensitive indicator of TSE initiation. The results from multifocally inoculated rats were averaged in each (sub-clinical (SubC), moderate (mCP) and grave (gCP)) clinical phase and compared to food-restricted (FR) rats. There was a significant, early decrease in urinary Na+ excretion during mCP when compared to SubC and FR. The renal sites involved were studied in awake, unrestrained animals by measuring of sodium, creatinine and lithium clearances. There was an initial increase in the absolute proximal (mCP: 21.4 +/- 1.7 vs FR: 16.0 +/- 1.1 mmol/min/100 g b.w., p < 0.05) and post-proximal (mCP: 11.1 +/- 0.4 vs FR: 6.6 +/- 0.4 mmol/min/100 g b.w., p < 0.001) Na+ reabsorption, which were partially compensated for by a rise in glomerular filtration rate (mCP: 213 +/- 11.4 vs FR: 162 +/- 10.2 microL/min/100 g b.w., p < 0.01) and by a fall in fractional proximal Na+ reabsorption (mCP: 62.8 +/- 2.2% vs FR: 70.1 +/- 1.7%, p < 0.05), despite significant Na+ and fluid retention. The terminal phase of illness (gCP) culminated with a marked decrease in creatinine clearance, suggesting a significant fall in renal function. The multifocal model proved useful for studying the initial TSE, since the sites of action would, in principle, be easy to identify. These observations may be of physiological interest since TSE may result from the abnormal production of physiological modulators.
 ...
PMID:Re-assessment of the renal hydrosaline dysfunction in rats bearing the Walker-256 tumor. 1110 65


1 2 Next >>