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)

A study of 70 ophthalmologically asymptomatic patients with abnormal hemoglobinopathy (AS, SS, S Thal) is presented. A significant number of SS and S Thal group patients had visual acuity of less than 20/20. Retinal vein dilation and tortuosity was observed in 54% of S Thal and 83% of SS patients. Early stages of proliferative retinopathy were encountered in 7% of SS and S Thal patients in the study. The importance of routine ocular examination including meticulous binocular indirect ophthalmoscopy with scleral depression in asymptomatic patients with abnormal hemoglobin is stressed.
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PMID:Retinopathy in ophthalmologically asymptomatic patients with abnormal hemoglobins. 45 42

Our previous studies have shown that a phagocytic challenge with IgG-coated erythrocytes (EIgG) depressed macrophage triggered H2O2 production in vitro, and in vivo there was a decrease in the survival rate following bacteremia. The phagocytosis of an equal number of IgG-coated erythrocyte ghosts had none of these effects, indicating that the contents of the erythrocytes are important for these effects. The present study evaluated the role of the scavengers of reactive oxygen intermediates within erythrocytes in the depression of H2O2 production triggered with phorbol myristate acetate following a phagocytic challenge with EIgG. Elicited rat peritoneal macrophages (PM) were challenged with EIgG prepared from normal E or E with inactivated catalase, depleted glutathione, hemoglobin converted to methemoglobin, or fixed with formaldehyde. The depression of triggered H2O2 production was similar when equal numbers of normal EIgG and EIgG with inactivated scavengers were phagocytized. When the phagocytic challenge with normal EIgG was carried out in the presence of cytochalasin B, no depression of triggered H2O2 production was observed. Cytochalasin B partially blocked the phagocytosis of EIgG, so that with larger doses of EIgG there was sufficient ingestion of EIgG to depress H2O2 production in untreated PM. These results indicate that the scavengers of reactive oxygen intermediates present in erythrocytes are neither required nor sufficient to depress H2O2 production by macrophages.
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PMID:Scavengers of reactive oxygen intermediates do not mediate the depression of macrophage hydrogen peroxide production caused by erythrocyte phagocytosis. 175 28

During intravenous sedation, the pulse oximeter was applied as a respiratory monitor to 17 patients (Physical status classification of the American Society of Anesthesiologists, Class I-II) who were to have oral surgical operations, and the changes in arterial saturation of oxygen (SaO2) was observed consecutively. SaO2 dropped after administration of sedative agents in each case; there was some individual variation. Respiratory depression during sedation was evaluated from arterial blood gas analysis. The reduction in SaO2 caused by surgical manipulations was also noted. Furthermore, arterial partial pressures of oxygen (PaO2) and saturation calculated from PaO2 (SAT) measured from blood gas analysis were compared with SaO2 measured by the pulse oximeter. Both PaO2 and SAT correlated well with SaO2. The differences between SAT and SaO2 exceeded the range of error (+/- 2%) in many cases after the administration of sedative agents. These results suggest that the pulse oximeter is useful as a respiratory monitor during oral surgery. However, the pulse oximeter gives incorrect SaO2 readings in the presence of abnormal hemoglobin due to medication with nitrites or smoking habit.
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PMID:Usefulness of the pulse oximeter as a respiratory monitor during intravenous sedation. 181 40

Adult female Wistar rats were injected with 125 mg/kg b.w. of human methemoglobin (M-Hb) in order to induce a first episode of hemodynamically-mediated acute renal failure (HMARF). Eleven days after the injection of M-Hb, other groups of rats received another equal dose of the drug in order to induce a second episode of HMARF. Evaluation of renal function, histopathology studies, and determinations of plasma and kidney erythropoietin (Epo) titers by radioimmunoassay in normoxic and hypoxic conditions were performed 1, 2, 3, 5 and 10 days after M-Hb administration. Treatment induced transient increases in plasma urea concentration, fractional sodium excretion, and urine volume, and significant depression in urine osmolality. In every case, the maximal effect of the first injection of M-Hb on the individual parameters was always greater than that of the second injection, and observed on the 5th post-injection day. Histologic sections showed interstitial cellular infiltration, desquamation of the proximal tubular epithelium and collapse or dilation of the tubular lumen. Treatment with M-Hb depressed Epo titers in both kidney homogenates and plasma in normoxic as well as hypoxic rats. Here again, the effect of the first injection of the drug was higher than that of the second one. These observations indicate that there is a negative correlation between kidney tubule injury and Epo production in normoxic and hypoxic conditions. The findings give support to the concept that Epo production is related to proximal tubular function.
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PMID:Depressed plasma erythropoietin levels in rats with hemodynamically-mediated acute renal failure. 209 64

Landfill disposal of a fertilizer manufacturing waste product was associated with a die-off of gulls in New Hanover County, North Carolina. An estimated 250 herring and ring-billed gulls were found dead at the site following the initial disposal of this material. Chemical analyses revealed that the fertilizer waste contained predominately calcium (12.0 to 22.2%) and nitrite (3.0 to 15.2%). Contents of the proventriculi and gizzards of dead gulls also contained calcium (3.0 to 10.9%) and nitrite (1,730 ppm). Fertilizer waste administered orally to 16-day-old domestic turkeys resulted in acute, progressive signs of depression, respiratory distress, pallor, convulsions and death. The mean percentage methemoglobin in blood from convulsing turkeys (90.6) was significantly increased from that of normal control turkeys (3.6). The ante-mortem signs and increased blood methemoglobin concentrations in the experimental turkeys support the conclusion that the toxic principle in the fertilizer waste was nitrite, and that nitrite poisoning was the cause of the die-off of gulls.
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PMID:Nitrite poisoning in herring gulls (Larus argentatus) and ring-billed gulls (Larus delawarensis). 301 49

The pathophysiology, clinical features, and management of cyanide toxicity are reviewed and sources of cyanide are listed. Cyanide is a deadly poison that is found in many foods and household and industrial products, including some that are readily available. Cyanide binds with cytochrome oxidase, the enzyme responsible for oxidative phosphorylation, and paralyzes cellular respiration. Because the tissues cannot use oxygen that is delivered, aerobic metabolism ceases. The signs and symptoms of cyanide poisoning reflect the extent of cellular hypoxia. Manifestations may include respiratory abnormalities (progressing from tachypnea and dyspnea to respiratory depression and apnea), hemodynamic instability, metabolic acidosis, and, possibly, local irritant effects after oral ingestion of cyanide. The mainstays of therapy are 100% oxygen and specific antidotes to cyanide. Sequential treatment with amyl nitrite by inhalation, intravenous sodium nitrite 3%, and intravenous sodium thiosulfate 25% is directed toward decreasing the amount of cyanide available for cellular binding. Nitrites convert hemoglobin to methemoglobin, which reacts with cyanide to form cyanomethemoglobin. Sodium thiosulfate serves as a source of sulfur groups, which are needed for conversion of cyanide to thiocyanate, a compound that is relatively less toxic and is excreted renally. Supportive care also is important. Cobalt EDTA, hydroxocobalamin, and aminophenols have also been used but are not considered standard treatments. Cyanide poisoning is a medical emergency that requires prompt recognition and immediate and aggressive treatment.
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PMID:Clinical features and management of cyanide poisoning. 353 Jun 15

A coincubation system composed of hepatocytes in primary monolayer culture and erythrocytes suspended in the culture medium was developed and used as a model for investigations of mechanisms of cyanide antidote action at the cellular level. Hepatocyte ATP was used as the cytotoxicity indicator. Treatment of rat hepatocytes in the coincubation system with KCN (1.0 mM) for 10 min at 37 degrees C selectively reduced hepatocyte ATP levels to 33 +/- 15% of control (no KCN added) levels. 4-dimethylaminophenol (DMAP), cobalt(II) chloride, sodium nitrite, sodium thiosulfate, or a combination of the last two antidotes added to the KCN-containing medium significantly reversed ATP depression and the response was concentration dependent. The relative effectiveness, on a molar basis, was estimated to be DMAP greater than CoCl2 much greater than NaNO2 congruent to Na2S2O3. NaNO2 and DMAP induced methemoglobin formation in the absence of cyanide and cyanmethemoglobin formation in its presence; erythrocytes were required in the medium for effectiveness. CoCl2 produced neither cyanmethemoglobin nor thiocyanate in appreciable quantities nor required erythrocytes for antagonism. Na2S2O3 converted cyanide to thiocyanate and reversed ATP depression without erythrocytes in the medium. The addition of erythrocytes increased these rates significantly and to a greater extent than albumin. The overall results are consistent with previously proposed modes of action for these antidotes. However, the enhancement in cyanide metabolism and ATP recovery with Na2S2O3 and erythrocytes in the system was unexpected and raises the possibility that erythrocytes may contribute to cyanide disposition and antagonism in vivo when this antidote is administered.
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PMID:Application of a hepatocyte-erythrocyte coincubation system to studies of cyanide antidotal mechanisms. 356 31

Acute acetaminophen intoxication in the cat was studied to characterize the antidotal profile of acetylcysteine. Toxicosis was associated with cyanosis, hyperventilation, depression, and facial edema. Abnormal laboratory findings were methemoglobinemia and elevated serum glutamic-pyruvic transaminase activity. In one trial, each of ten cats was given a 325-mg tablet of acetaminophen, then another after 4 hours. Five of the cats were given antidotal treatment with acetylcysteine (140 mg/kg, per os) at the time of the second dosing with acetaminophen and at 8-hour intervals thereafter for a total of three treatments. All treated cats survived. Two of the untreated cats died. In another trial, doubling each dose of acetaminophen (650 mg) proved fatal in all of four untreated cats. When antidotal therapy was initiated at the time of the second dosing with acetaminophen and repeated at 8- or 4-hour intervals for three treatments, two of four cats in each treatment group survived. Although antidotal therapy was associated with a return of serum glutamic-pyruvic transaminase and methemoglobinemia values toward normal, only the methemoglobin value was a reliable prognostic indicator.
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PMID:Acetylcysteine for treatment of acetaminophen toxicosis in the cat. 740 22

The potential of methyl ethyl ketoxime (MEKO) to produce neurotoxicity following acute and subchronic exposure was studied in rats. A Functional Observational Battery, assessment of motor activity, and neuropathology evaluations were conducted in the context of acute and subchronic toxicity studies. Three independent studies are reported: a pilot time-effect study designed to determine the time course and time to peak effect following a single high dose of MEKO, a single-dose neurotoxicity study, and a subchronic (13-week) repeated-dose neurotoxicity study in rats. An acrylamide-positive control group was included in the acute and subchronic studies for comparison with MEKO. Following an acute oral exposure of MEKO at a dose level of 900 mg/kg, locomotor activity was decreased compared to control with maximum decreases occurring between 30 and 60 min following oral administration. In the acute study, transient treatment-related changes in ease of cage removal, ease of handling, and in posture and gait were observed 1 hr after dosing with 900 mg/kg MEKO, as were significant depressions in motor activity. Following a single 300 mg/kg dose, transient MEKO-related changes in gait and aerial righting reflex were noted 1 hr after dosing. All effects were reversible within 24 hr of dosing. The single 100 mg/kg dose of MEKO was without observable effects. No acrylamide-related behavioral effects were noted following a single 50 mg/kg dose. In the subchronic study, transient treatment-related changes in ease of cage removal, ease of handling, and in posture, gait, and aerial righting were observed at the 400 mg/kg/day dose level when assessments were conducted immediately after dose administration. No consistent behavioral effects were observed prior to daily dose administration even after 13 weeks of exposure, indicating a lack of cumulative behavioral effect. No consistent behavioral changes were noted at doses of 125 mg/kg/day and below. Significant dose-related decreases in red cell mass, and increases in methemoglobin levels, reticulocyte, leukocyte, Heinz body counts, and spleen weights occurred at subchronic MEKO doses of 40 mg/kg/day and higher. No MEKO-related neuropathological changes occurred. Animals receiving acrylamide at 20 mg/kg/day showed expected behavioral and neuropathological changes consistent with peripheral neuropathy. In conclusion, high doses of MEKO can produce transient and reversible changes in neurobehavioral function consistent with central nervous system (CNS) depression. No evidence of cumulative neurotoxicity was detected. The hematopoietic system was effected at doses which did not produce detectable changes in CNS function.
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PMID:Assessing the neurotoxic potential of methyl ethyl ketoxime in rats. 825

During head injuries and hemorrhagic stroke, blood is released into the extravascular space. The pooled erythrocytes get lysed and hemoglobin is released into the intracranial cavities. Therefore, neurons may be exposed to hemoglobin and/or its breakdown products, hemin and iron, for long periods of time. In this study, the electrophysiological actions of these agents on synaptic transmission in rat hippocampal CA1 pyramidal neurons were studied using extracellular field- and whole cell patch-recordings. Previously our laboratory reported that commercially available hemoglobin produced a dose dependent suppression of synaptic transmission in hippocampal CA1 neurons. In the present study, however, we found that this depression was caused by impurities present in the hemoglobin samples. Commercially available hemoglobin and methemoglobin did not have a significant effect on synaptic transmission. Although, reduced-hemoglobin prepared using a method described by Martin et al. [J. Pharm. Exp. Ther. 232 (1985) 708], produced a significant depression of synaptic transients, these effects were due to contamination with bisulfite that was present due to the reducing procedure. Therefore, the technique of Martin et al. was inadequate in removing the reducing agents or their breakdown products. A number of studies in literature used commercial samples of hemoglobin or reduced hemoglobin prepared using the method of Martin et al. Our observations indicate that it would be important to determine if contaminants, rather than hemoglobin, are responsible for the observed effects in these studies. Unlike hemoglobin, its breakdown products, ferrous chloride and hemin, produced an irreversible and significant depression of field excitatory postsynaptic potentials. The relevance of these effects in neurological complications that follow head injuries and hemorrhagic stroke awaits further investigation.
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PMID:Effects of hemoglobin and its breakdown products on synaptic transmission in rat hippocampal CA1 neurons. 1079 81


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