Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When administered in sufficient amounts, normal saline and Lactated Ringer's Solution are equally effective in maintaining adequate circulatory volumes despite severe blood loss and resultant hypoproteinemia. Arterial pH is maintained within normal limits when either solution is used for resuscitation provided the circulatory volume has been re-expanded to adequate levels for good tissue perfusion and support of aerobic metabolism. The pH of the infused solutions has no effect on blood pH under these circumstances. Fourteen splenectomized dogs were subjected to continuous hemorrhage and simultaneous replacement with either normal saline or Lactated Ringer's Solution. The cumulative replacement volume ratio necessary for equilibration after 61% RBC depletion was 7:1 crystalloid to the whole "undiluted" blood shed, in both groups. Indicators of pulmonary-circulatory physiology remained stable within normal limits. Arterial pH did not exhibit significant changes from normal values after resuscitation with NS or LRS. The group infused with LRS exhibited no change in arterial pH, 7.40 plus or minus .07 initial and 7.40 plus or minus .09 final; in the group with NS replacement a slight decrease from control was noted, 7.40 plus or minus .07 initial and 7.36 plus or minus .06 final. These differences, however, are not statistically significant. Of the 14 subjects, 13 were long-term survivors. The one death was associated with a technical mishap shortly after completion of the experiment. Because banked blood imposes a "net" alkaline metabolic load (sodium citrate), patients expected to be transfused with large volumes of stored blood might be better resuscited with normal salin than with Ringer's Lactate Soultions, to minimize or avert the otherwise resultant metabolic alkalosis.
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PMID:Dilutional re-expansion with crystalloid after massive hemorrahage: saline versus balanced electrolyte solution for maintenance of normal blood volume and arterial pH. 23 99

It has been established that in conditions of intraoperative blood and plasma loss base deficiency is determined not only by hypocarbonatemia, but also by hypoproteinemia, hypophosphatemia and HCO3 metabolism disturbances caused by anemia. Correction of metabolic acidosis in such patients should include infusions of NaHCO3, protein preparations, blood, phosphates. Mellemgaard and Astrup's technique presupposes correction of the deficiency of all buffer bases only with NaHCO3, which dramatically increases its dosage. Thus, it is evident that the technique should be revised. The comparison of the results of metabolic acidosis correction using a conventional and adapted techniques (hydrocarbonate dose in mmol or ml of a 8.4% solution is 24-SB.body weight.0.2%) in statistically homogeneous groups has shown that differentiated "polybuffer" correction of metabolic acidosis with adapted NaHCO3 dose 1.7 times more frequently normalized acid-base balance parameters, reducing the risk of the onset of post-correction metabolic alkalosis to minimum.
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PMID:[Characteristics of the dosage of sodium hydrocarbonate for correction of metabolic acidosis in surgical patients]. 133 43

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.
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PMID:Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis. 267 25

We altered the concentration of plasma proteins in human blood in vitro by adding solutions with [Na+], [K+], and [Cl-] resembling those in normal blood plasma, either protein-free or with a high concentration of human albumin. After equilibrating the samples with a gas containing 5% CO2-12% O2-83% N2 at 37 degrees C, we measured pH, PCO2, and PO2; in separated plasma, we determined the concentrations of total plasma proteins and albumin and of the completely dissociated electrolytes (strong cations Na+, K+, Mg2+ and anions Cl-, citrate3-). With PCO2 nearly constant (mean = 35.5 Torr; coefficient of variation = 0.02), lowering plasma protein concentration produced a metabolic alkalosis, whereas increasing plasma albumin concentration gave rise to a metabolic acidosis. These acid-base disturbances occurred independently of a minor variation in the balance between the sums of strong cations and anions. We quantified the dependence of several acid-base variables in plasma on albumin (or total protein) concentration. Normal plasma proteins are weak nonvolatile acids. Although their concentration is not regulated as part of acid-base homeostasis, hypoproteinemia and hyperalbuminemia per se produce alkalosis and acidosis, respectively.
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PMID:Acid-base effects of altering plasma protein concentration in human blood in vitro. 310 Apr 99

Hypoproteinemia by itself produces a metabolic alkalosis. It is not clear whether a respiratory compensation (hypercapnia) develops with this alkalosis; patients with liver cirrhosis, most of them with hypoproteinemia, are known to hyperventilate. We studied 23 clinically stable patients with hypoproteinemia, with very low albumin-to-globulin ratios (range 0.4 to 1.1), who had either liver cirrhosis (n = 12) or other medical conditions (n = 11). In both groups, there was marked hypocapnia, accompanied by alkalemia (PaCO2 values (mean +/- SD) 31 +/- 2 and 32 +/- 3 torr; pH (mean +/- SD) 7.45 +/- 0.03 and 7.47 +/- 0.03, for the patients with cirrhosis and those without, respectively). Hypoxemia was not the stimulus provoking hyperventilation. The lowering of PaCO2 was proportional to the reduction of serum albumin and total protein concentrations; no detectable difference was seen between the patients with cirrhosis and those without cirrhosis in this apparent dependence of PaCO2 on the concentration of serum proteins. Many of these clinically stable patients with hypoproteinemia, with or without liver cirrhosis, had appreciable concentrations of unidentified anions in plasma (inappropriately high anion gap). Whatever the nonrespiratory acid-base status of the patients with hypoproteinemia, their pulmonary ventilation (hypocapnia) appeared excessive when compared with subjects (presumably) without proteinemia who had similar nonrespiratory acid-base states. The mechanism responsible for the hyperventilation in hypoproteinemia and the nature of the unidentified anions in this condition are obscure.
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PMID:Hyperventilation with hypoproteinemia. 318 88