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)

Normothermic global ischemia of 7, 10, 15 and 60 min was found to depress oxalate supported calcium uptake rate measured either in unfractionated homogenates or isolated sarcoplasmic reticulum. The degree of depression increased with the duration of ischemia. Comparison of the isolated sarcoplasmic reticulum with unfractionated homogenates showed that the isolated sarcoplasmic reticulum was more damaged by ischemia than the unfractionated homogenate. The cause of this discrepancy was not due to inactivation of sarcoplasmic reticulum during isolation but was due to the discard of greater portions of undamaged sarcoplasmic reticulum as the ischemic period increased. Ischemia preferentially affected that sarcoplasmic reticulum most easily fragmented by homogenization. To determine if the depression of sarcoplasmic reticulum function is uniform throughout the isolated fraction, we compared several properties of the isolated fractions. After 10 min of ischemia, extensive properties such as calcium oxalate uptake rate, calcium ATPase rate, calcium oxalate capacity and steady-state calcium loading were depressed 50, 41, 48 and 24% respectively. In contrast, intensive properties such as permeability, calcium-ATPase turnover rate, and ratio of forward nucleotide flux to reverse nucleotide flux were unaffected by ischemia. However, one intensive property, the coupling ratio, was depressed 20%. We conclude from this difference in the effects of ischemia on extensive and intensive properties that the major effect of ischemia is to inactivate the Ca-ATPase.
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PMID:Effects of ischemia on the isolation and function of canine cardiac sarcoplasmic reticulum. 294 2

Induced precipitation of Ca-oxalate crystals and the possibility of its prevention were studied in dogs. In the first phase of the experiments precipitation of Ca-oxalate crystals in canine renal tubules was induced by intraperitoneal administration of Na-glyoxylate. Preventive medication (lipoic acid, vitamin B1, Milurit), applied in the second phase, resulted in a significant depression of induced precipitation. The successful experiments serve as a basis for clinical research aimed at a preventive medication of recurrent Ca-oxalate stone formation.
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PMID:Induced precipitation of calcium-oxalate crystals and its prevention in laboratory animals. 310 96

Ryanodine was found to initially inhibit calcium uptake by cardiac sarcoplasmic reticulum. This initial depression was followed by a later marked stimulation of calcium uptake. These effects were noted when calcium uptake was measured in the presence or absence of oxalate. The requirement for preincubation with ryanodine was highly dependent on ryanodine concentration and temperature. The mechanism of action of ryanodine clearly was not an effect on oxalate entry or calcium oxalate precipitation because the effects were also observed in the absence of oxalate. Ryanodine also had no effect on passive calcium efflux from actively loaded vesicles. Because ryanodine had no effect on Ca2+-ATPase activity under defined conditions of an ATP-regenerating system and no calcium gradient, we suggest ryanodine does not change the stoichiometry of the pump. Our results are consistent with the hypothesis that ryanodine closes a calcium channel in a subpopulation of the vesicles.
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PMID:Mechanism of action of ryanodine on cardiac sarcoplasmic reticulum. 315 65

The effect of pH on the excitation-contraction coupling system of canine masseter muscle was studied by evaluating the functional integrity of the sarcoplasmic reticulum (SR) and myofibrils. Increasing proton concentration (pH 7.0-5.8) significantly reduced oxalate supported SR calcium uptake velocity, while Ca2+-stimulated, Mg2+-dependent ATPase activity was unaffected by pH. The efficiency ratio of calcium transport, or the coupling ratio (mumoles Ca2+ transported/mumoles ATP hydrolyzed), decreased from 1.094 +/- 0.042 at pH 7.0 to 0.946 +/- 0.036 at pH 6.0 (P less than 0.05) and to 0.780 +/- 0.024 at pH 5.8 (P less than 0.01). Myofibrillar pCa (-log [free Ca2+] )-ATPase activity was unaffected between pH 7.0 and pH 6.5. At pH 6.0, increasing Ca2+ concentration inhibited myofibrillar ATPase activity, and this inhibitory phenomenon was accentuated at pH 5.8. Kinetic analysis of the myofibrillar pCa-ATPase data, utilizing double-reciprocal plots, demonstrated an increase in Km at low pH. It is concluded that acidosis significantly uncouples calcium transport from ATP hydrolysis in the SR of masseter muscle and significantly alters myofibrillar ATPase activity. It is hypothesized that these defects may explain an observed depression in skeletal muscle cell function during ischemia.
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PMID:Characterization of the effect of pH on the excitation-contraction coupling system of canine masseter muscle. 315 68

Ingestion of ethylene glycol was responsible for severe azotemia, acidosis, and abnormal anionic gap value in a pygmy goat. Clinical signs consisted of ataxia, polydipsia, decreased rumen motility, and constipation. Nervous signs included depression, absence of menace response, vertical nystagmus, and terminal convulsions. Four days after onset of clinical signs, antidotal treatment was ineffective. Lesions and oxalate crystals in the kidney were typical of ethylene glycol or plant oxalate toxicosis in other species. Toxicologic analysis revealed ethylene glycol in the rumen content and glycolic acid in urine and ocular fluid.
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PMID:Ethylene glycol toxicosis in a pygmy goat. 319 47

A 63-year-old man with arterial hypertension suffered from depression and suicidal wish after a cerebrovascular accident and transitory left hemiparesis. He was urgently admitted to hospital in severe metabolic acidosis which caused renal failure and coma, ending fatally within two days. At necropsy calcium oxalate crystals were found in the renal tubules and cerebral vessel walls with chemically induced meningoencephalitis. From these findings glycol poisoning was diagnosed. There was a lethal concentration of ethylene glycol in the urine. The toxic effects of ethylene glycol are due to its metabolites. The oxalate crystals are primarily of diagnostic importance.
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PMID:[Ethylene glycol poisoning]. 337 4

Treatment of isolated, working rat hearts with equiactive conditions of buffer containing low Ca2+ (LC), verapamil (Ver), diltiazem (Dil) or nifedipine (Nif) prior to global ischemia (33 min, 37 degrees C) resulted in an equal enhancement in recovery of contractile function, and high energy phosphate (HEP) stores in reperfused hearts. Treatment only during reperfusion did not enhance recovery or HEP stores. Pretreatment with doses which did not depress preischemic contractile function did not afford protection to globally ischemic hearts. In contrast with Dil (2.5 uM), pretreatment with an equiactive concentration of bepridil (Bep) (20 uM) did not preserve contractile function, HEP, or mitochondrial function and did not reduce Ca2+ overload. The Ca2+ was concentrated in mitochondria of hearts receiving no drug or Bep pretreatment (oxalate-pyroantimonate stain). Increasing concentrations of Ver or Dil given before ischemia resulted in a progressive increase in recovery of contractile function which was proportional to depression of preischemic function. The increase in HEP in these hearts was not proportional to drug concentration, preischemic or postischemic function. Pretreatment with Dil reduced lactate production in both normal and K+-arrested ischemic hearts. Energy preservation is only part of the protective mechanisms of Ca2+ antagonists. The Ca2+ antagonists also reduce Ca2+ overload from reperfusion, and may alter Ca2+ compartmentation during ischemia.
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PMID:Protection of ischemic hearts by Ca2+ antagonists. 349 Dec 15

The effects of the following vasoactive drugs: Bencyclan fumarate, Cetiedil citrate, Cinepazide maleate, Dihydroergocristine methane sulphonate, Nafthydrofuril acid oxalate, Papaverine hydrochloride, Piribedil monomethane sulphonate, Raubasine, Thymoxamine hydrochloride and Xanthinol nicotinate, in concentrations ranging between 0.001 - 2 mM, were tested on the compound action potentials led off from human isolated sympathetic ganglions. The experiments, carried out on 50 isolated lumbar ganglion preparations removed from 23 subjects with arteriopathy of the limbs, indicated that all the drugs are able to impair the synaptic transmission, although at different concentrations. These findings are in favour of the hypothesis that the vasodilatatory effects observed after therapeutic treatment of patients with vasoactive drugs are partially produced by the vasodilatation following the depression of the sympathetic nervous transmission.
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PMID:[Effect of various vasoactive drugs on synaptic transmission in the orthosympathetic ganglia in man]. 608 53

It has been proposed that breakdown of the excitation-contraction coupling system plays a pivotal role in myocardial dysfunction during the course of acute ischemia. We tested this hypothesis by characterizing the function of the sarcoplasmic reticulum at pH 7.1 and 6.4 after 7.5, 15, and 30 minutes of canine normothermic global ischemia. At pH 7.1, whole heart homogenate sarcoplasmic reticulum demonstrated a 49% depression of oxalate-supported calcium uptake at 7.5 minutes of ischemia, which progressed to 85% at 30 minutes of ischemia. At pH 6.4, control homogenate calcium uptake rates were significantly depressed, accompanied by a further depression in the ischemic groups. Isolated sarcoplasmic reticulum calcium uptake mirrored the effects of the whole heart homogenate. Calcium-stimulated magnesium-dependent ATPase (calcium-ATPase) activity was significantly depressed by both ischemia and acidosis, with a decrease in the coupling ratio (mumol calcium/mumol ATP) at 15 and 30 minutes of ischemia. Acidosis (pH 6.4) significantly shifted the sarcoplasmic reticulum pCalcium-ATPase curve to the right, increasing 50% activation from pCalcium 6.0 to 5.5 and depressing the maximum velocity (pH 7.1 = 2.06 +/- 0.14; pH 6.4 = 1.41 +/- 0.05 mumol Pi/mg per min; P less than 0.01). With ischemia, there was a progressive decrease in maximal activation of the calcium-ATPase enzyme and a progressive shift in calcium sensitivity to a higher concentration. Steady state calcium uptake, in the absence of oxalate, demonstrated a similar depression after 7.5 and 15 minutes of ischemia at pH 7.1 and 6.4, associated with a significant increase in the passive permeability coefficient for calcium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of cardiac sarcoplasmic reticulum dysfunction during short-term, normothermic, global ischemia. 614 9

Fifteen dogs were given 9.5 ml of ethylene glycol/kg of body weight, orally. Physical examination and clinical laboratory findings were evaluated at 1 and 3 hours after ingestion. Three of these dogs were also evaluated at 6, 9, 12, 24, 48, and 72 hours after ingestion. At 1 and 3 hours, the dogs were depressed, ataxic, and polydipsic with increased urine output and serum osmolality. Plasma bicarbonate and urine osmolality were decreased. The osmolal and anion gaps were increased at 1 and 3 hours, respectively. Calcium oxalate crystalluria was first observed at 6 hours. Diminished renal excretory function was not evident until 48 hours. Depression, ataxia, metabolic acidosis, polydipsia, and polyuria in the presence of serum hyperosmolality were early (1 and 3 hour) findings that indicated ethylene glycol intoxication in dogs.
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PMID:Early clinicopathologic findings in dogs ingesting ethylene glycol. 652 24


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