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

Left ventricular performance was evaluated in seven canine right heart bypass preparations during and after the intraauricular administration of sodium bicarbonate (100 ml, 1100 Osm, 60 mEq). Under conditions of constant cardiac input and left ventricular volume, sodium bicarbonate produced mild and brief left ventricular depression, as manifested by a decline of left ventricular dp/dt with simultaneous rise of left ventricular end-diastrolic and left atrial pressures. These findings occurred as aortic impedance fell. Identical results accrued in paced and unpaced preparations. The data lends credence to the proposition that a sudden rise in blood pCO2 produces increased transport of CO2 across the cardiac membranes with intracellular acidosis. However, the data is also compatible with hyperosmolality induced contractile depression. Possible clinical implications are discussed.
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PMID:Effect of sodium bicarbonate on canine left ventricular function. 1 35

A 1-month-old Jersey calf died of oxalate nephropathy. The calf had access to antifreeze (ethylene glycol) 3 days prior to death. Since ethylene glycol toxicosis had not been reported in cattle, the effects or oral administration of ethylene glycol were studied in 7 calves and 3 cows. The toxic dose ranged from 2 to 10 ml of ethylene glycol per kg of body weight. Clinical signs were increased respiration, staggering gait, paraparesis, depression and later, recumbency and death. Hemoglobinuria and epistaxis were seen at doses of 10mg/kg of body weight. Azotemia, hypocalcemia and neutrophilia were constant findings whereas acidosis, plasma hyperosmolality and hemolytic anemia were seen in the animals receiving the higher doses. A diagnosis of ethylene glycol toxicosis must be based upon a history of ingestion and the presence of calcium oxalate crystals in body tissues (especially the kidney and brain).
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PMID:Ethylene glycol toxicosis in cattle. 47 24

In cardiac muscle, moderate degrees of hyperosmolality of the type encountered physiologically or clinically (i.e., less than 200 mosM above control) characteristically exert a positive inotropic effect, which presumably is mediated by increased Ca2+ availability for binding to troponin. In contrast, skeletal muscle displays significant contractile depression on exposure to hyperosmotic solutions, even at mild degrees of hypertonicity. To determine whether a similar potential for hyperosmolarity-induced depression also exists in cardiac muscle, right ventricular papillary muscles from cats were exposed to hypertonic solutions of mannitol or sucrose under circumstances in which positive inotropic effects were precluded by prior exposure to a bathing solution of 4.0 mM Ca2+ and paired electrical stimulation to maximize intracellular Ca2+ before addition of the hyperosmotic substances. In contrast to their usual positive inotropic effects, hypertonic solutions under these conditions caused cardiac depression at all osmolarities tested. Developed tension and its maximal rate of development (dT/dt) decreased by 18% at 50 mosM above control, by 30% at 100 mosM, by 36% at 150 mosM, and by 42% at 200 mosM (P less than 0.01 for all). Time to peak tension and resting tension were not changed significantly. When the muscles were returned to control solutions, tension development also returned toward normal. The data are compatible with the hypothesis that, within the range tested, all degrees of hyperosmolarity exert a significant negative inotropic influence on cardiac muscle, as is true in skeletal muscle; manifestation of this effect of increased tonicity normally would be obscured at low degrees of hyperosmolality, however, by an overriding positive influence that is absent in skeletal muscle.
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PMID:Negative inotropic influence of hyperosmotic solutions on cardiac muscle. 121 82

Using a freezing point depression method osmolality in the intestinal tissue of four mammals (gerbils, guinea-pigs, rabbits and rats) was estimated in vivo, during fluid transport from an isotonic electrolyte-glucose solution. Net fluid transport was also measured. In gerbils, guinea-pigs and rabbits tissue osmolality was also estimated during in vitro conditions. A marked hyperosmolality was observed in vivo in the upper parts of the villi of all four mammals studied. The tissue osmolality was significantly higher than that seen in the same species during in vitro conditions. A villus hyperosmolality was observed also in species which exhibited a net fluid secretion (guinea-pig, rabbit ileum), indicating that the fluid secretion emanated from the intestinal crypts. Based on the results of the present experiments and on observations made in earlier experiments performed on the cat, it is proposed that the villus hyperosmolality is created by a countercurrent multiplier present in the intestinal villus. The hyperosmolar compartment in the villus tissue creates the force that drives fluid from lumen to tissue.
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PMID:Tissue osmolality in intestinal villi of four mammals in vivo and in vitro. 177 35

The effect of contrast media on the left ventricular function of the heart was assessed by left coronary administration of contrast media using canine models. Following insertion of the catheter into the left coronary artery, 0.5 ml/kg of a test solution was injected at a rate of 1 ml/s. The test solutions included isotonic saline, meglumine/sodium diatrizoate, iopamidol and ioxaglate. The mean systemic pressure, left ventricular end-systolic and end-diastolic pressures and the first derivative of left ventricular pressure were continuously measured until five min post-injection. Left ventricular function decreased immediately by 15 s post-injection and recovered quickly by one min. The inhibition of myocardial contractility was observed with diatrizoate and ioxaglate to the same degree. These changes were statistically more pronounced than those with iopamidol, which showed changes similar to those with saline in all parameters except for the positive inotropic effects. These observations suggest that not only hyperosmolality but also ionic composition and chemotoxicity are the factors responsible for the myocardial depression and that no single factor dominates in their effects.
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PMID:Effect of contrast media on left ventricular function during left coronary arteriography in dogs. 263 51

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.
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PMID:Neurologic manifestations of fluid and electrolyte disturbances. 267 34

1. Focal electrographic seizures arose in the CA1 region of rat hippocampal slices bathed in elevated (8.5 mM) external potassium [( K+]o). High [K+]o also induced spontaneous interictal bursts that originated in area CA3 and propagated to CA1. To examine the contribution to electrographic seizure initiation of excitatory mechanisms that are influenced by extracellular volume, we studied the effect of hyperosmotic expansion of interstitial volume on seizure occurrence, interictal bursts, and excitatory synaptic transmission. The tissue electrical resistance was also measured leading up to and during seizures. 2. Media made 5-30 mosmol/kg hyperosmotic by addition of agents restricted to the extracellular space (mannitol, sucrose, raffinose, L-glucose, dextran) rapidly and reversibly abolished [K+]o-induced spontaneous CA1 seizures in 86% of slices tested. However, similar increases in osmolality effected by agents that access the intracellular compartment (D-glucose, glycerol) did not influence electrographic seizure occurrence. Hyperosmotic changes with plasma membrane impermeable compounds, but not permeable compounds, produced significant concentration-dependent decreases (1-10%) in the electrical resistance of CA1 stratum pyramidale. Because tissue resistance is proportional to extracellular volume, these results suggest that hyperosmotic suppression of electrographic seizures is associated with expansion of the extracellular space in hippocampal slices. 3. Measurement of electrical resistance of the CA1 stratum pyramidale during spreading depression and electrographic seizure revealed an increase in tissue resistance to 122% and 108% of control, respectively. Furthermore, a slight (approximately 2%) but significant increase in electrical resistance gradually occurred over the 20 s immediately preceding seizure generation. The observed increase in tissue resistance suggests extracellular space is decreased during these events. 4. Hyperosmolality did not alter CA3 interictal burst frequency. However, burst intensity, estimated from the total length of the burst waveform, was significantly reduced in both the CA3 (83% control) and CA1 region (67% control) when osmotic changes were imposed by plasma membrane impermeant compounds. Additionally, media made hypoosmotic by removal of 7.5 mM NaCl reversibly increased burst intensity. 5. High [K+]o potentiated excitatory synaptic transmission and excitatory postsynaptic potential (EPSP) spike coupling.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of extracellular space in hyperosmotic suppression of potassium-induced electrographic seizures. 272 35

Eight dogs with ethylene glycol intoxication were treated with 4-methylpyrazole, an alcohol dehydrogenase inhibitor. Dogs had clinical signs referable to ethylene glycol ingestion including ataxia, depression, vomiting, polyuria, and dehydration. Metabolic abnormalities included high anion gap metabolic acidosis, serum hyperosmolality, isosthenuria, and monohydrate and dihydrate calcium oxalate crystalluria. Serum and urine ethylene glycol concentrations were determined to confirm ingestion of ethylene glycol. A 50-mg/ml solution of 4-methylpyrazole in propylene glycol was administered iv as follows: initial treatment, 20 mg/kg of body weight; at 17 hours after admission, 15 mg/kg; at 25 hours after admission, 5 mg/kg. By 24 hours after admission, all dogs had clinical and metabolic improvement. Of the 8 dogs, 7 were released within 3 days of admission. Four of the 8 dogs returned for follow-up evaluation, at which time biochemical or hematologic abnormalities were not observed.
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PMID:4-Methylpyrazole as treatment for naturally acquired ethylene glycol intoxication in dogs. 258 8

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.
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PMID:Clinical, biochemical, acid-base, and electrolyte abnormalities in cats after hypertonic sodium phosphate enema administration. 401 52

Electrical activity in cells directly exposed to water-soluble radiographic contrast agents was investigated by intracellular and extracellular recordings from neurons in in vitro rat hippocampus slices. Measurements included extracellular field potentials, intracellular resting membrane potential and membrane conductance, postsynaptic events, action potential configurations and spontaneous electrical activity. The neurons were exposed to test solutions of an ionic contrast agent, sodium diatrizoate, and a nonionic contrast agent, metrizamide, as well as control solutions. The ionic contrast agent produces bursts of action potentials having epileptogenic characteristics which is temporally followed by a depression of all electrical activity. The nonionic contrast agent produces minimal convulsive-like electrical bursts, but does produce a consistent depression of transmembrane electrical potentials, though in a lesser degree than the ionic contrast agents. The excitatory electrical events appear to be related to large depolarizing post-synaptic events while the later electrical depression is at least partially due to hyperpolarization. The depressing effects may be related to the hyperosmolality of the test solutions; however, no excitatory changes are related to hyperosmolality. These results provide the initial data on the neurotoxicity of water-soluble contrast agents at the intraneuronal level.
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PMID:Neurotoxic effects of water-soluble contrast agents on rat hippocampus. 646 24


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