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)

Subcellular fractions in hearts from rats with severe acute uremia (24 hours after total nephrectomy) and moderate chronic uremia (2 weeks after five sixths nephrectomy) were studied and compared with preparations from acute and chronic sham-operated rats, respectively. Calcium- and magnesium-sensitive actomyosin adenosine triphosphatase (ATPase) activities were normal in both groups. Acute uremia was associated with a significant depression of sarcolemmal Na+,K+ ATPase activity. Calcium transport by fragmented sarcoplasmic reticulum was also depressed in the presence and absence of oxalate in acute uremia. Mitochondrial calcium transport and adenosine triphosphate (ATP) and creatine phosphate (CP) concentrations were normal in these animals. Chronic uremic animals showed no abnormal subcellular mechanisms. These data suggest a direct effect of acute uremia on some membrane functions in myocardial cells. The discrepancies observed between acute and chronic uremic groups may be due to a different degree of uremic state. The observation of depressed calcium transport by fragmented sarcoplasmic reticulum (FSR) in acute uremic hearts which were previously shown to have increased contractile reserve suggests that studies of calcium transport in FSR may not always truly reflect the contractile capacity of the heart.
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PMID:Studies of subcellular control factors in hearts of uremic rats. 13 36

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

Investigation of multiple serum and urinary factors in 44 patients with calcium urinary stone disease confirmed a number of defects that have been described previously: elevation of mean serum calcium and uric acid above normal, and depression of mean serum magnesium. Urinary excretion of calcium and uric acid was increased and was increased and was probably related to food ingestion. Urinary magnesium also increased after eating but less than calcium, with the result that for most patients the magnesium to calcium x 100 ratio approached levels observed in stone formation. Urinary oxalate excretion was constant during the entire observation period and apparently was not affected by ingestion of a defined diet. Nine additional patients had persistent hypercalcemia owing to hyperparathyroidism (5 confirmed, 1 suspected), malignancy (2) and drug ingestion (1). Metabolic evaluation of patients with calcium urinary calculi continues to contribute to decisions regarding their best therapeutic regimen.
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PMID:Contribution to therapeutic decisions of ratios, absolute values and other measures of calcium, magnesium, urate or oxalate balance in stone formers. 95 3

Randall described a pre-calculus lesion of the renal papilla in the 1930s and this was substantiated by others during the next decade and then largely ignored. This insignificant subepithelial calcification of the renal papilla. Randall's plaque type I, becomes the nucleus of at least 15% of calcium oxalate calculi, as demonstrated by apatite nuclei existing in papillary depression on the external stone surface. Cross section study of the stone demonstrates the peripheral nucleus with eccentric lamination postulating a mural origin. Contrariwise, study of the stone developing upon a nucleus originating in the papillary ducts (without producing obstruction) or out in the calix demonstrates a central nucleus surrounded by concentric laminations or lack of a mural origin, the more common type of calcium oxalate stone structure. Obstruction of the papillary ducts by hyperexcretion of stone salt may result in anemic infarction and sloughing of the apex of the papilla. Data concerning the prevalence of Randall's plaques in the population have been reviewed. Evidence of the incidence of calcium oxalate calculi that have developed upon Randall's plaques has been presented. A plea for further study of the pathology of the renal papilla has been voiced.
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PMID:The riddle of Randall's plaques. 123 69

The effect of perfusate [Ca2+] on the function of cardiac sarcoplasmic reticulum (CSR) was assessed by the oxalate-supported Ca2+ uptake rate of ventricular homogenates of isolated rat hearts maintained in a modified Langendorff preparation. The total Ca2+ pumping activity of the CSR was determined by using 20 microM ruthenium red or 625 microM ryanodine to close the CSR Ca2+ release channel. The homogenate Ca2+ uptake rate in the absence of ruthenium red or ryanodine decreased progressively with increasing perfusate [Ca2+] (25.7 +/- 1.2, 21.4 +/- 1.5, 17.2 +/- 1.1, and 16.3 +/- 1.2 [mean +/- SEM] nmol Ca2+.min-1.mg-1 for hearts perfused for 5 minutes with 0.2, 1.4, 2.8, and 5.6 mM Ca2+, respectively; p = 0.0001; n = 8). This depression was not observed when Ca2+ uptake was assayed in the presence of ryanodine or ruthenium red. Since the Ca2+ uptake in the presence of ryanodine or ruthenium red is determined by the Ca(2+)-ATPase, this result suggests that perfusion with varying [Ca2+] did not affect the Ca(2+)-ATPase. The observed decrease in Ca2+ uptake in the absence of ryanodine or ruthenium red is caused by an increased efflux through the ryanodine-sensitive Ca2+ release channel. When hearts perfused for 5 minutes with 0.2 or 5.6 mM Ca2+ were reperfused for 10 minutes with 1.4 mM Ca2+, homogenate Ca2+ uptake rates were restored to near control levels. These effects of perfusate Ca2+ were not direct effects, because changes in the [Ca2+] of the homogenization medium did not alter the homogenate Ca2+ uptake activity in either the presence or absence of ryanodine. The homogenate Ca2+ uptake rates were unaffected by prior active loading of the CSR with Ca2+. These results suggest a regulatory role of perfusate Ca2+ in increasing the open state of the ryanodine-sensitive Ca2+ release channel that is distinct from the beat-to-beat regulation of Ca2+ release from the CSR by Ca2+ (Ca(2+)-induced Ca2+ release).
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PMID:Effect of perfusate [Ca2+] on cardiac sarcoplasmic reticulum Ca2+ release channel in isolated rat hearts. 138 83

The effect of normothermic ischemia and ischemia/reperfusion on the function of cardiac sarcoplasmic reticulum (CSR) was investigated using a modified Langendorff perfusion of isolated rat hearts. The function of the CSR was assessed by the oxalate-supported Ca2+ uptake rate of ventricular homogenates. The contribution of the ryanodine-sensitive portion of the CSR was determined by using 20 microM ruthenium red or 625 microM ryanodine to close the CSR Ca2+ release channel. The Ca2+ uptake rate of the CSR decreased progressively with increasing duration of ischemia, but this depression was much less when uptake was assayed in the presence of ryanodine. The depression in CSR Ca2+ uptake preceded ischemic contracture. Ryanodine and ruthenium red stimulated uptake almost equally in control hearts, but ruthenium red was much less effective than ryanodine after ischemia. This difference could not be overcome by increasing the ruthenium red concentration. These results confirm the suggestion that the Ca2+ release channel is inappropriately opened after ischemia. The CSR uptake rates were almost completely restored at 15 minutes of reperfusion after 5 and 10 minutes of ischemia but were only partially restored after 15 minutes of ischemia. At reperfusion, mechanical function (end-diastolic pressure and peak systolic developed pressure) was markedly depressed after only 15 minutes of ischemia. The degree of "stunning" correlated well with the depression of CSR function in individual hearts. The decreased Ca2+ uptake of the CSR was not due to a buildup of ADP in the homogenates.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversibility of the effects of normothermic global ischemia on the ryanodine-sensitive and ryanodine-insensitive calcium uptake of cardiac sarcoplasmic reticulum. 172 84

The effect of ischemia on the function of cardiac sarcoplasmic reticulum (SR) was assessed by the calcium uptake rate of rat whole-heart homogenates in the presence of 10 mM oxalate. Previous studies have shown that this uptake is restricted to the SR. The contribution of the ryanodine-sensitive fractions of the SR to the total homogenate uptake was assessed by using 20 microM ruthenium red and 625 microM ryanodine to close the SR calcium release channel under previously established optimal conditions. Global ischemia of 10, 15, 30, and 60 minutes depressed homogenate calcium uptake rate 19 +/- 2%, 50 +/- 6%, 65 +/- 3%, and 81 +/- 5%, respectively. This decrease was not observed when the uptake rates were measured after closure of the calcium channel with ryanodine or ruthenium red. Similar results were obtained with a Langendorff in vitro perfusion preparation, in which calcium uptake was decreased 35 +/- 5%, 37 +/- 8%, 58 +/- 7%, and 64 +/- 4% after 10, 15, 30, and 60 minutes of ischemia, but no significant decrease was observed when homogenate uptake rates were measured in the presence of ryanodine. Thus, ischemia caused a depression in the calcium uptake rate of cardiac SR only when this activity was measured in the absence of SR calcium channel blockers. Reperfusion of ischemic hearts in a Langendorff preparation resulted in recovery of homogenate calcium uptake activity that correlated well with the return to sinus rhythm of the reperfused hearts. These reperfused hearts showed no change in the calcium uptake rate measured in the presence of ryanodine. These results suggest that the decrease in homogenate calcium uptake caused by ischemia is not due to a defect in calcium pumping capabilities but is due to an increased efflux through the ryanodine-sensitive calcium release channel of cardiac SR.
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PMID:Differential effect of global ischemia on the ryanodine-sensitive and ryanodine-insensitive calcium uptake of cardiac sarcoplasmic reticulum. 247 12

Transient ischemia does not induce myocardial necrosis but may be associated with prolonged contractile dysfunction ("stunned" myocardium). It has been suggested that alteration of the excitation-contraction coupling system (sarcoplasmic reticulum) could be responsible for this phenomenon. We tested this hypothesis by characterizing sarcoplasmic reticulum (SR) function in an isolated rat heart model of "stunned" myocardium (hearts reperfused after 10 min of normothermic global ischemia). At the end of the ischemic period oxalate-supported Ca-uptake was depressed either in the whole homogenate or in isolated SR (to 47% and 22% of control values, respectively). During reperfusion Ca-uptake of the whole heart homogenate recovered almost completely whereas slight but significant depression persisted in isolated SR (48 +/- 2 vs 67 +/- 4 nmol/min x mg, P less than 0.01). In the presence of ruthenium red or ryanodine, two inhibitors of SR Ca-release channels, Ca-uptake was stimulated. Both in the whole heart homogenate and in isolated SR, such stimulation was remarkably smaller after reperfusion than in control conditions (P less than 0.001) suggesting reduced conductivity state of the SR Ca-release channels. Ca-stimulated, magnesium-dependent ATPase activity was remarkably reduced during ischemia and postischemic reperfusion induced only incomplete recovery (93 +/- 18 vs 169 +/- 14 nmol ATP/min x mg protein, P less than 0.05). We conclude that complex modifications of SR function occur in the "stunned" myocardium and could contribute to the contractile impairment found in this condition.
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PMID:Sarcoplasmic reticulum function in the "stunned" myocardium. 247 59

This study examined the possibility that the postischemic mechanical depression observed in the "stunned" myocardium is a result of an alteration in the control of intracellular calcium. Regional myocardial stunning was produced in five open-chest dogs by eight to twelve 5-minute occlusions of the left anterior descending coronary artery, alternated with 10-minute reflow periods and followed by a final 60-minute period of reperfusion. Systolic segment shortening in the postischemic zone, measured by sonomicrometry, fell from 14.9% at baseline to -1.1% at the end of reperfusion. Sarcoplasmic reticulum isolated from stunned myocardium demonstrated a 17% reduction in oxalate-supported 45Ca2+ transport compared with sarcoplasmic reticulum from normal myocardium (0.93 vs. 1.12 mumol Ca2+/mg protein/min, p less than 0.005). There was also a 20% decrease in the maximal activation by Ca2+ of the sarcoplasmic reticulum Ca2+, Mg2+-ATPase (2.46 vs. 1.96 mumol Pi/mg protein/min, p less than 0.005), and a downward shift in the Ca2+-activation curve of the Ca2+, Mg2+-ATPase. These results indicate that myocardial stunning is associated with damage to the calcium-transport system of the sarcoplasmic reticulum. Altered intracellular control may contribute to the inability of the stunned heart to maintain normal mechanical function.
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PMID:Alterations in cardiac sarcoplasmic reticulum calcium transport in the postischemic "stunned" myocardium. 275 55

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


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