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)

Beginning 1 wk postpartum, weekly changes of feed and water intake, body weight, milk production, and electrolyte concentrations in serum, saliva, urine, milk, and feces were observed for 8 to 11 wk. Three dietary treatments differing in sodium chloride and sodium bicarbonate supplementation but containing equal sodium concentrations were used. Dietary chloride percents were low .10%, medium .27%, and high .45%. Consistently changes were significant for feed and water intake, body weight, milk production, and electrolyte concentrations in serum, urine, milk, and feces of cows fed the low chloride diet. By wk 8, body weight had declined from 575.0 +/- 56.7 to 476.7 +/- 54.3 kg, and daily milk production decreased from a peak of 27.7 +/- 2.4 to 19.2 +/- 3.9 kg for cows fed the low chloride diet. Serum chloride decreased from 106.0 +/- 2.8 to 75.5 +/- 6.7 meq/liter during the same time. Cows on the low chloride diet developed clinical signs of a deficiency characterized by depraved appetite, lethargy, hypophagia, emaciation, hypogalactiae, constipation, and cardiovascular depression. Metabolic alterations could be summarized as a severe primary hypochloremic, secondary hypokalemic, metabolic alkalosis.
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PMID:Nutritional chloride deficiency in early lactation Holstein cows. 650 51

Our patient's acid-base disturbance may be among the highest recorded in nonfatal cases of metabolic alkalosis. This case also shows that life-threatening alkalemia can be safely and effectively treated by defining and removing the causes of alkalosis and applying aggressive supportive therapy with fluid repletion and potassium and electrolyte replacement. The need for potentially dangerous therapy such as exogenous acid administration, dialysis, or forced mechanical depression of respiration should not routinely be used on the basis of blood pH alone, and it should never replace thoughtful, organized supportive care.
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PMID:Severe metabolic alkalosis. 797 15

The balance between a high filtration rate and high reabsorption rate in the kidney is critical in the maintenance of extracellular fluid volume. One of the mechanisms that maintain this balance is the tubuloglomerular feedback (TGF) mechanism, which operates at the level of the macula densa assessing the load and/or solute concentration coming out of the loop of Henle and controlling this load by adjusting the GFR. This review discusses the potential role of the TGF system with respect to volume homeostasis in various conditions where GFR is maintained, decreased, or increased. In most of the states discussed, the TGF system seems to act appropriately regarding volume control; however, trade-off effects occasionally occur. After acetazolamide administration, during extracellular fluid volume contraction or expansion or acute hyperkalemia, the TGF mechanism responds appropriately with regard to volume balance. After a large reduction of renal mass, the system adjusts to function at a higher level of GFR and distal delivery. In chloride-depletion metabolic alkalosis, glomerulonephritis, diabetes mellitus, and acute renal failure, the adaptation of the TGF system appears to be appropriate with regard to volume control; however, it may lead to trade-off effects, such as maintenance of metabolic alkalosis, glomerular hypertension and sclerosis, or depression of GFR, respectively. Because the TGF mechanism often contributes to compensatory adjustments to or development of disease, it can be appreciated that any in-depth evaluation of the mechanisms responsible for various pathophysiologic conditions should include an assessment of the potential role of the TGF mechanism.
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PMID:Relevance of the tubuloglomerular feedback mechanism in pathophysiology. 813 Mar 53

A total of 34 children with normal renal function underwent either gastrocystoplasty or continent urinary reservoirs with stomach at our institutions. Severe hypochloremic hypokalemic metabolic alkalosis developed in 2 patients, manifested by intractable seizure disorder in 1 and altered mental status with respiratory depression in 1. Symptoms developed at 4 and 6 months, respectively. Despite severe alkalosis, urinary pH was less than 5.0 and fractional excretion of chloride remained high in both patients. Resuscitation with sodium chloride, arginine hydrochloride and potassium chloride restored electrolyte balance in less than 48 hours in both patients. Serum gastrin was slightly elevated in 1 patient (137 pg./ml., normal 0 to 125) who responded to long-term histamine-blocker therapy. The other patient had significant hypergastrinemia (624 pg./ml.) with secondary hyperaldosteronism. Maximum doses of histamine blockers, oral replacement of sodium chloride and potassium chloride, and the proton pump inhibitor omeprazole failed to control recurrent bouts of severe hypochloremic metabolic alkalosis. This patient ultimately underwent removal of three-quarters of the gastric augmentation and replacement with ileum. Postoperatively, serum gastrin levels and electrolytes reverted to normal. The pathophysiology of this potentially lethal complication is further discussed.
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PMID:Metabolic complications of the use of stomach for urinary reconstruction. 832 30

The blood gas and acid-base effects of epidural xylazine were studied in rams. Xylazine at a dose of 0.4 mg kg-1 led to a metabolic alkalosis with a significant increase of pH, plasma bicarbonate and base excess and respiratory depression. Epidural administration of xylazine provided prolonged and very effective analgesia during abdominal and hindlimb surgery in rams.
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PMID:The effect of xylazine epidural anaesthesia on blood gas and acid-base parameters in rams. 855 17

Two Holstein cows from dry lot dairies were evaluated because of clinical signs of depression, anorexia, and decreased milk production. Bilateral abdominal distention and decreased fecal output were found on physical examination. Results of serum biochemical analyses indicated that the cows had severe hypochloremic, hypokalemic metabolic alkalosis. On the basis of physical examination and laboratory findings, an obstruction of the abomasum or cranial portion of the small intestine was suspected in these cows and abdominal exploratory surgery was performed. A mass of gravel was found in the pyloric antrum of the abomasum of 1 cow and the descending duodenum of the other cow. The duodenal obstruction was removed by enterotomy, and the pyloric mass was manually reduced during surgery. The cows were treated with antibiotics and isotonic saline solution (NaCl) supplemented with potassium chloride and recovered quickly after surgery.
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PMID:Gravel obstruction in the abomasum or duodenum of two cows. 883 55

Sodium lactate inhibits ventilation when infused in healthy human subjects. This effect has been attributed to lactate-induced metabolic alkalosis. In order to further delineate the mechanisms responsible for this depression of ventilation, healthy humans were infused with sodium lactate with or without acetazolamide. Sodium lactate increased blood pH from 7.37 +/- 0.02 to 7.47 +/- 0.01 and induced a sustained urinary excretion of bicarbonate. PO2 of arterialized blood decreased by 10.3 +/- 2.1 mmHg, indicating an inhibition of ventilation. Acetazolamide decreased lactate-induced alkalinisation of blood (pH after lactate + acetazolamide 7.42 +/- 0.02), but did not prevent the drop in PO2. Acetazolamide alone tended to stimulate ventilation, as indicated by an increase in PO2. These results indicate that sodium lactate inhibits ventilation independently of changes in systemic blood pH. Alkalinization of the cerebrospinal fluid, or other central effects of lactate, is probably responsible for this ventilatory depression.
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PMID:Effects of sodium lactate on ventilation and acid-base balance in healthy humans. 884 75

Values of blood gas, serum chloride, and potassium were tabulated for 21 dairy cows with coliform mastitis. Severe cases showed marked clinical signs such as loss of appetite and depression of digestive tract motility, and metabolic alkalosis such as an increase in blood pH, hypochloremia and hypokalemia compared with normal and mild cases (p < 0.01). The results showed that metabolic alkalosis can be detected more easily than acidosis in cases of severe coliform mastitis.
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PMID:Metabolic alkalosis in coliform mastitis. 923 24

Esherichia coli endotoxin was administered intravenously to 7 Holstein adult cows, to evaluate the effect of endotoxin on acid-base balance. Endotoxin shock was observed immediately after the administration of endotoxin. A loss of appetite and depression of digestive tract motility continued for about 120 hr after the challenge. Metabolic alkalosis following hypochloremia and hypokalemia were particularly pronounced at 12 to 72 hr after the administration of endotoxin.
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PMID:Evaluation of blood acid-base balance after experimental administration of endotoxin in adult cow. 923 28

This study examined the ventilatory adjustment to chronic metabolic alkalosis induced under controlled conditions in normal human volunteers. Metabolic alkalosis induced by buffers (sodium bicarbonate, trishydroxymethylamine methane) or ethacrynic acid was associated with alveolar hypoventilation, as evidenced by a rise in arterial Pco(2), a fall in arterial Po(2), a reduced resting tidal volume, and a diminished ventilatory response to CO(2) inhalation. Alveolar hypoventilation did not occur when metabolic alkalosis was induced in the same subjects by thiazide diuretics or aldosterone despite comparable elevations of the arterial blood pH and bicarbonate concentration.The different ventilatory responses of the two groups could not be ascribed to differences among individuals comprising each group, pharmacological effects of the alkalinizing agents, differences in the composition of the lumber spinal fluid, changes in extracellular fluid volume, or sodium and chloride balance.The differences in ventilatory adjustments were associated with differences in the patterns of hydrogen and potassium ion balance during the induction of alkalosis. Alveolar hypoventilation occurred when hydrogen ions were buffered (sodium bicarbonate, trishydroxymethylamine methane) or when renal hydrogen ion excretion was increased (ethacrynic acid). Alveolar hypoventilation did not occur when induction of similar degrees of extracellular alkalosis was accompanied by marked potassium loss and no demonstrable increase in external hydrogen loss (thiazides and aldosterone).These observations suggest that respiratory depression does not necessarily accompany extracellular alkalosis but depends on the effect of the mode of induction of the alkalosis on the tissues involved in the control of ventilation.
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PMID:Respiratory adjustment to chronic metabolic alkalosis in man. 1669 40


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