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)

Cardiac depression in the isolated rat heart perfused with 4% ethanol was correlated with intracellular phosphate energetics and tissue water distributions. Energy metabolites were assessed using 31P magnetic resonance spectroscopy (MRS) and correlated to the mitochondrial redox state using epicardial surface fluorometry. Changes in myocardial water compartmentation were measured by using 1H NMR spectroscopy with an extracellular chemical-shift reagent (DyTTHA) and correlated to results of 2D echocardiography (2DE). During alcohol perfusion there was a significant decrease in developed pressure and in coronary flow. No change was seen in ATP, PCr, pHi, Pi, or NADH. After withdrawal of alcohol from the perfusate cardiac function reverted to control values without a depletion of energy levels. During alcohol perfusion 1H MRS showed a marked redistribution of water from the intra- to the extracellular space, corresponding to a 35% left ventricular wall thinning confirmed by 2DE. The results indicate that acute alcohol cardiac depression is related to a dehydration of myocardial cells, but is not associated with intracellular acidosis or energy depletion.
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PMID:31P and 1H magnetic resonance spectroscopy of acute alcohol cardiac depression in rats. 317 69

Persistent neutropenia (0-0.6 X 10(9) neutrophils/l) was documented during a 10-month period in a 4-year-old spayed female domestic shorthair cat that was presented for anorexia and depression. Salient abnormalities detected on physical examination were fever (40.3 degrees C), dehydration, and gingivitis. The cat was neutropenic (0.5 X 10(9) neutrophils/l) and enzyme-linked immunosorbent assay (ELISA) test for feline leukemia virus was negative. A bone marrow aspirate showed decreased numbers of mature granulocytic cells. In vitro bone marrow cultures for colony-forming units-granulocyte/macrophage (CFU-GM) were performed comparing bone marrow from the patient with that of a normal cat. The patient had fewer CFU-GM than the control. The number of CFU-GM increased when bone marrow mononuclear cells were cultured in the presence of 10(-5) and 10(-6) mol/l of hydrocortisone, but the cat did not respond to oral prednisolone therapy. The pathogenesis of the neutropenia in this cat remains obscure, but resembles the chronic idiopathic neutropenia syndrome of man.
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PMID:Chronic idiopathic neutropenia in a cat. 322 55

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.
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PMID:Hypernatremia in calves. 322 59

In a historical cohort study, acute renal failure developed in 16.5% of 157 patients with rhabdomyolysis over a two-year study period. Underlying clinical, laboratory, and causative factors associated with the development of acute renal failure were examined. Factors predictive of renal failure in this setting, determined by multiple logistic regression analysis, included the degree of serum creatine kinase, serum potassium, and serum phosphorus level elevation; the degree of depression of serum albumin level; and the presence of dehydration at presentation or sepsis as the underlying cause. The predictive model that was developed correctly classified 93% of subjects and was statistically validated.
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PMID:Factors predictive of acute renal failure in rhabdomyolysis. 338 1

Autonomic dysfunction was diagnosed in a 2.5-year-old spayed domestic shorthair cat. The cat had an 8-day history of progressive anorexia, signs of depression, constipation, weight loss, and intermittent regurgitation. Physical examination findings were signs of depression, dehydration, cachexia, bradycardia, bilateral nonresponsive mydriasis, prolapse of both nictitating membranes, dry oral and nasal mucous membranes, and urinary bladder atony. Thoracic radiography revealed megaesophagus. The cat lacked esophageal motility and had a decreased gastric emptying rate. Providing adequate fluid intake, electrolyte balance, and nutrition is a major problem in the management of dysautonomic cats. We were able to provide adequate nutritional support for this patient, using total parenteral feeding and, later, enteral nutrition using a nasogastric tube. Results of an ocular pharmacologic study indicated that the mydriasis and prolapse of the nictitating membrane were attributable to complete autonomic denervation of the eye. Using the method described, topical, autonomic-stimulating agents may assist the clinician in diagnosing dysautonomia in the feline. This report describes a syndrome that is well recognized in the United Kingdom and has the potential to develop in the United States.
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PMID:Dysautonomia in a cat. 339 54

The first cases of fulminant hepatic failure due to paracetamol poisoning were reported in 1966, and in the United Kingdom this condition is now responsible for more cases of acute hepatic failure than any other cause. Adults account for the majority of serious and fatal cases of paracetamol poisoning and it is extremely rare for young children to ingest sufficient paracetamol to cause more than minimal liver damage. A single measurement of the plasma paracetamol concentration is an accurate predictor of liver damage provided that it is taken not earlier than 4 hours after ingestion of the overdose. Peak disturbance of liver function occurs 2 to 4 days after the overdose, often accompanied by mild jaundice, after which recovery is usually rapid and complete. In a few patients, fulminant hepatic failure, manifested by increasing jaundice and encephalopathy, may develop by the third to fifth day. Acute renal failure may complicate paracetamol poisoning, often in the context of severe liver damage. Renal failure, which is often non-oliguric, typically becomes apparent 24 to 72 hours after overdosage. The treatment of paracetamol intoxication should include gastric lavage, which has been shown to be of value for up to 6 hours after ingestion of a paracetamol overdose. Further general treatment may include parenteral fluid replacement and a prophylactic infusion of dextrose (5-10%) in patients at risk of hepatic failure. Specific protective agents in those patients at risk of paracetamol-induced liver damage include N-acetylcysteine and methionine which are most effective if given within 8 to 10 hours of ingestion of the overdose. Hepatic and renal failure should be managed conventionally. In recent years in the United Kingdom there has been a gradual decline in the number of hospital admissions and the number of deaths from aspirin poisoning. Salicylates in overdose directly stimulate the respiratory centre and so cause a respiratory alkalosis. Metabolic acidosis occurs in severe poisoning because of impairment of the oxidative metabolism of energy substrates. At very high salicylate concentrations respiratory depression may occur, possibly associated with neuroglycopenia, adding respiratory acidosis to the worsening metabolic acidosis. In addition to a mixed acid-base disturbance, hypokalaemia and hypoglycaemia may be present. Nausea and vomiting increase the fluid deficit. If dehydration is sufficiently severe, decreasing cardiac output may hasten development of lactic acidosis and acute renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Non-narcotic analgesics. Problems of overdosage. 355 83

From the available experimental data a relatively clear picture can be established with regard to the physiological importance of some of the mechanisms involved in insect cold hardening. In freeze-avoiding insects, all potent ice-nucleating agents are removed or inactivated, leading to a depression of the supercooling points to about 20 degrees C. Accumulation of polyols causes a further depression with a magnitude of about twice the corresponding melting-point depression. Production of thermal hysteresis factors causes a stabilization of the supercooled state. In freeze-tolerant insects, potent ice-nucleating agents are produced in the extracellular body fluid, ensuring a protective extracellular freezing at a few degrees below zero. Accumulation of polyols causes a steep drop in the lethal temperature, due to a reduction of the amount of ice by a colligative mechanism. However, there is still much to be learned about the mechanisms by which ice-nucleating agents, polyols, and thermal hysteresis agents are acting. Furthermore, the regulatory mechanisms involved in the production and elimination of these components from the body fluid of the insects are not understood. Also, when it comes to the influence of environmental factors, like photoperiod and temperature, there is much to be learned. In addition to giving attention to these topics, future research should be focused on the possible role of other factors in cold hardening such as bound water, dehydration, low-molecular-weight solutes other than polyols, and the biochemical mechanisms forming the basis of the seasonal changes in the cold hardiness of insects.
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PMID:Physiology of cold tolerance in insects. 390 95

Fifty-four cases of death from hyperosmolar comas were examined pathoanatomically together with the postmortem biochemical analysis of the CSF and blood. Brain of animals with disturbances of the blood and CSF osmolarity was studied electron cytochemically and autoradiographically. It was discovered that the hyperosmolar comas are manifested by excosis and brain collapse. The brain is reduced in volume due to deep cell-extracell dehydration and alteration of the hematoencephalic barrier with the irreversible depression of the neuronal and glial metabolism. In 7 patients dying with the purulent-necrotic changes of vessels resulting from the hyperosmolar effect of verografin used for the carotid angiography, numerous perivascular hemorrhages developed in the brain. Dysequilibrium syndrome in hemodialysis is manifested by an acute brain swelling or by a formation at a later period of symmetrical ischemic-hemorrhagic necrosis in the thalamus and occipital lobes of the large hemispheres.
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PMID:[Pathologo-anatomical characteristics of hyperosmolar and other comatous conditions]. 392 35

The subacute toxic effects of cyclopiazonic acid (CPA; given orally) were characterized in the dog (CPA was purified from cultures of Aspergillus flavus). Four groups of dogs were given CPA in gelatin capsules for 90 days at the following dosage levels: 0.05, 0.25, 0.5, and 1.0 mg/kg of body weight; a 5th group was used as controls. All dogs administered the 0.5 and 1.0 mg of CPA/kg dosages and 1 dog given the 0.25 mg of CPA/kg dosage died or were humanely killed before the scheduled termination of the study. Clinical signs of intoxication appeared 2 to 44 days after dosing was started and consisted of anorexia and, in 1 to 2 days, vomiting, diarrhea, pyrexia, dehydration, weight loss, and CNS depression. Grossly, the entire alimentary tract had diffuse hyperemia with focal areas of hemorrhage and ulceration. Other lesions were renal infarcts, necrotizing epididymitis, and ulcerative dermatitis. Microscopic lesions included ulceration, necrosis, vasculitis, lymphoid necrosis, karyomegaly in several organs, and decreased mitotic activity in intestinal crypt epithelium. Ulcerative and necrotic lesions were usually associated with vascular lesions. Clinical pathologic changes were leukocytosis, neutrophilia, lymphopenia, monocytosis, and increased serum alkaline phosphatase activity.
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PMID:Cyclopiazonic acid mycotoxicosis in the dog. 392 55

One of the practical difficulties with the frequently proposed use of liposomes for delivery of water-soluble substances to cells in whole organisms is that liposomes are relatively unstable during storage. We have studied the ability of trehalose, a carbohydrate commonly found at high concentrations in organisms capable of surviving dehydration, to stabilize dry liposomes. With trehalose both inside and outside the bilayer, almost 100% of trapped solute was retained in rehydrated vesicles previously freeze-dried with 1.8 g trehalose/g dry phospholipid. Trehalose is very effective at inhibiting fusion between liposomes during drying, as assessed by freeze-fracture and resonance energy transfer between fluorescent probes incorporated into the bilayer. However, inhibition of fusion alone does not account for the preservation of the dry liposomes, since the concentration of trehalose required to prevent leakage is more than 10-fold that required to prevent fusion. We provide evidence that stabilization of the dry liposomes requires depression of transition temperature and consequent maintenance of the constituent lipids in the dry liposomes in a liquid crystalline phase.
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PMID:Preservation of freeze-dried liposomes by trehalose. 405 4


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