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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects were investigated of a 25-minute inhalation of halothane with oxygen on three to four months old pigs of the Large White breed. Symptoms of malignant hyperthermia did not occur. The actual total anesthesia, which causes slight hypoproteinemia, hypoglycemia and hypocholesterolemia without significant changes in the content of non-esterified fatty acids (NEFA) and urea, induced only a slight increase of circulating 11-hydroxycorticosteroids (11-OHCS). The combination of anesthesia with castration of gilts or barrows significantly increased the concentration of 11-OHCS but did not reach the level recorded after the application of ACTH. The higher levels of 11-OHCS were accompanied by higher concentrations of NEFA and glucose. The treatment of the animals lasting half an hour prior to inhalation of halothane at maximum doses or one hour in the control unanesthetized pigs produced an effect, mainly on the 11-OHCS concentration and on the activity of creatine kinase in the plasma. The results indicate that the adrenocortical response to the effect of halothane is not stronger than the response to simple handling connected with excitement and muscular activity of the animals. Therefore there is no reason of considering halothane anesthesia as a factor causing great stress and pigs which in its course do not respond with malignant hyperthermia as animals insensitive to stress. The aptness of denotation of clinical manifestations of genetically defective muscles in pigs is discussed.
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PMID:[The effect of halothane anesthesia on the function of the adrenal cortex and some metabolites in the blood plasma of pigs not susceptible to malignant hyperthermia]. 22 19

The authors presented their own material of years 1974-1977. During this period 8788 children were born, in it 737 (8,3%) with low birth weight (below 2500 g). Retrolental fibroplasia was diagnosed in 4 children, it was 0,5% of newborns with low birth weight, and 0,04% of the all live-borns. The retrolental fibroplasia was diagnosed in: 1) the child born in 27 week of pregnancy with 1000 g of body weight, 2) in two children born in 32-33 week of pregnancy with 1450 g and 1350 g of body weight, 3) in a child born in 31 week of pregnancy with 1600 g of body weight. The infants were nursed in incubators with about 30% of oxygen during 36 to 46 days. Contemporary hypoglycemia, hypoproteinemia, atelectasia of lungs with respiratory insufficiency were diagnosed. In the discussion the authors underlined the role of immaturity and hypoxia of the premature baby, which play the role in the secondary injury of vessel's walls of retina. The disturbancy of carbohydrate and protein metabolism were certainly secondary pathogenic agent sin retrolental fibroplasia. There exists the necessity of oxygen therapy of premature baby, but to take cre of the infant in the incubator does not mean the necessity of oxygen therapy . Even with controlled oxygen dosage in incubator the retrolental fibroplasia may occur as a result of relative hyperoxydation induced by the constriction of retina vessels. The authors underlined the necessity of repeated ophthalmologic examination of premature babies in about every 2 weeks, what makes very early diagnosis possible.
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PMID:[Risk of damage to the organ of vision in low birth weight infants]. 26 40

The approach to fluid resuscitation in burn shock continues to be refined in step with improved knowledge of the complex fluid, electrolyte, and protein shifts that characterize this form of shock. Local burn tissue and generalized nonburn tissue edema occur initially after injury because of the release of histamine, which causes increased microvascular permeability. Subsequent edema formation in burned and nonburned tissue occurs according to distinctly different mechanisms. Burn tissue edema forms because of direct thermal injury to endothelial cells and increased burn tissue osmolarity. Nonburn tissue edema is attributed to severe hypoproteinemia caused by protein flux into burn-injured tissue. Interstitial protein depletion in nonburn tissue also increases the ease of water transport into the interstitial space. Cell damage occurs with ischemia caused by decreased perfusion. More cell damage can occur with reperfusion and the subsequent formation of oxygen radicals. Fluid therapy is designed to support the patient's cardiovascular system so as to restore and maintain tissue perfusion. General formulas serve as guidelines for the amount of fluid to infuse; however, fluid therapy should be tailored to the individual patient's needs based on factors such as extensiveness of burns, extremes of age, inhalation injury, pre-existing cardiopulmonary disease, and delayed fluid resuscitation. Ringer's lactate solution is the most common fluid used in the early postburn period. The addition of colloid to resuscitation efforts should begin as microvascular permeability is restored or immediately if the patient presents in frank shock. Continuous monitoring is necessary to judge the adequacy of fluid replacement.
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PMID:Burn shock. 235 24

Animal studies have indicated that volume resuscitation is successful with salt-containing crystalloid solutions as well as colloid solutions. Hyperosmolar salt solutions appear to have benefits over isosmolar solutions. Both, however, produce hypoproteinemia, which can lead to edema formation due to changes in the transcapillary oncotic gradient and possibly by changing the interstitial matrix. The lung appears to be much more resistant to edema formation than the soft tissues. Except for the dog, the lung does not appear to be significantly altered from shock with no substantial increase in protein permeability being evident in most studies. Colloid therapy, either proteins or dextran, effectively restores cardiovascular stability after hypovolemia and also prevents the increased transcapillary fluid flux seen in the lung and soft tissues, the former not appearing to be of much clinical significance, while the latter may lead to significant tissue edema. Blood replacement is necessary to restore adequate oxygen delivery to the tissues. The ideal hematocrit appears to be around 30-35.
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PMID:Animal research on hypovolemic shock and resuscitation: an update. 618 28

Blood has a number of rheological properties which partially determine flow, especially at capillary level, and its capacity to deliver oxygen. It is non-Newtonian, pseudoplastic, thixotropic and viscoelastic. Viscosity can be studied with different types of viscosimeters (coaxial cylinder or capillary viscosimeters). It can be defined by the ratio of stress of deformation to rate of deformation. Viscosity depends on macrorheological parameters: hematocrit, serum proteins, especially fibrinogen and globulins, and also on microrheological parameters: degree of aggregation and red blood cell deformability. Viscosity rises when the temperature falls and decreases with the radius of the tube through which the blood flows (Fahraeus-Linqvist effects). Blood viscosity is studied clinically at different temperatures, and, above all, at different rates of deformation by carefully recording the hematocrit. Plasma viscosity, fibrinogen, albumia and immunoglobulin levels, the viscosity of blood cell suspensions in normal saline must also be taken into consideration. Special investigations (rheoscopy, filtrability) provide information about red cell aggregation and deformability. Hyperviscosity syndromes are observed with: --raised hematocrit (polycythemia and pseudopolycythemia), --conditions with raised serum proteins or changes in their composition (especially hyperfibrinogenemia, raised immunoglobulins, low albumin levels); inflammatory syndromes, dysglobulinemias (Fahey's syndrome of plasma hyperviscosity), --low temperature (hypothermia), --increased red cell aggregability (shock, fat embolism), --reduced red cell deformability due to various congenital and acquired conditions (sickle cell anemia, renal failure, hyperlipoproteinemia, thrombosis, diabetes). Conversely, hypoviscosity may occur with a low hematocrit, hypoproteinemia, hypofibrinogenemia, and hyperthermia. Increased viscosity results in a slowing of blood flow, stagnation of its constituents and in ischemia. Therapeutic interventions may be considered on the different components of the hyperviscosity syndrome: hemodilation, plasmapheresis, dispersion of aggregants, agents acting on red cell deformability.
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PMID:[Blood hyperviscosity syndromes. Classification and physiopathological understanding. Therapeutic deductions]. 636 7

Pulmonary edema is an important feature of many newborn lung diseases, including respiratory distress from severe perinatal asphyxia, heart failure, hyaline membrane disease, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often results from increased filtration pressure in the microcirculation of the lungs. This occurs during sustained hypoxia, in left ventricular failure associated with congenital heart disease or myocardial dysfunction, following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution, and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema) or fibrosis (long-standing lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the lungs and its relationship to neonatal respiratory distress. 657 79

Pulmonary edema is an important cause of respiratory distress in newborn infants. It occurs with severe perinatal asphyxia, heart failure, hyaline membrane disease, persistent patency of the ductus arteriosus, pneumonitis from group B beta-hemolytic streptococcus, and chronic lung disease (bronchopulmonary dysplasia). Neonatal pulmonary edema often develops from increased pressure in the microcirculation of the lungs. This may occur in conjunction with sustained hypoxia; left ventricular failure associated with congenital heart disease or myocardial dysfunction; following excessive intravascular infusions of blood, colloid, fat, or electrolyte solution and in conditions that increase pulmonary blood flow. Low intravascular protein osmotic pressure from hypoproteinemia may predispose infants to pulmonary edema. Hypoproteinemia is common in infants who are born prematurely. Large intravascular infusions of protein-free fluid further decrease the concentration of protein in plasma and thereby facilitate edema formation. Lymphatic obstruction by air (pulmonary interstitial emphysema of fibrosis (chronic lung disease) also may contribute to the development of edema. Bacteremia, endotoxemia, and prolonged oxygen-breathing injure the pulmonary microvascular endothelium and cause protein-rich fluid to accumulate in the lungs. Epithelial protein leaks may develop when the transpulmonary pressure needed to inflate the lungs increases because of high surface tension at the air-liquid interface. Fibrin clots from in some of the air spaces, which in combination with atelectasis and edema constitute the pathologic features of hyaline membrane disease. The risk of neonatal pulmonary edema can be reduced by several therapeutic measures designed to lessen fluid filtration pressure, increase plasma protein osmotic pressure, and prevent or reduce the severity of lung injury.
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PMID:Edema formation in the newborn lung. 676 Oct 39

Several studies indicate the pathophysiological importance of reactive oxygen species in rats with nephrotic syndrome induced by puromycin aminonucleoside, an experimental model of the human minimal change disease. The role of reactive oxygen species in these rats was further evaluated, examining the effect of dietary deficiency and supplementation of antioxidants (vitamin E and selenium) on biochemical and renal ultrastructural alterations induced by puromycin aminonucleoside. Male Wistar rats, weaned at 3 weeks, were placed on diets normal, deficient or supplemented in vitamin E and selenium for 4 weeks. At the end of this period, rats were divided in two groups: control (sacrificed without any further treatment) and nephrotic (injected with puromycin aminonucleoside and sacrificed 7 and 22 days later). In control rats, the dietary deficiency or supplementation of antioxidants resulted in no significative differences in renal function, proteinuria or kidney ultrastructure. However, kidney lipoperoxidation, kidney glutathione peroxidase activity and circulating levels of vitamin E changed according to the amount of antioxidants in the diet. Seven days after the injection of puromycin aminonucleoside, rats fed normal, deficient or supplemented diets, developed nephrotic syndrome. However, proteinuria, hypoproteinemia, renal dysfunction and ultrastructural alterations were higher in rats fed a deficient diet. In contrast, proteinuria and kidney ultrastructural alterations were lower in rats fed a supplemented diet. Kidney lipoperoxidation and glutathione peroxidase activity increased on day 7 in rats fed a normal or a deficient diet, but not in rats fed a supplemented diet. This study shows that nephrotic syndrome induced by puromycin aminonucleoside in rats is modified by dietary antioxidants (vitamin E and selenium). Dietary supplementation ameliorates it and dietary deficiency exacerbates it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary antioxidants on puromycin aminonucleoside nephrotic syndrome. 764 24

Acute hemorrhage is a main cause of reduction of blood oxygen capacity. The main aim of correction of sequels of acute hemorrhage is to maintain effective gas exchange by restoring central circulation and microcirculation, the rate of diuresis, by normalizing water-salt exchange, to eliminate anemia, hypoproteinemia, and acute blood coagulability disorders. The values of oxygen budget with calculated oxygen delivery and consumption and those of hemoglobin and hematocrit which are of great value only after recovery of circulating blood volume are considered to be major indications for hemotransfusion. A relationship is established between the extraction and uptake of oxygen and its delivery. The concept of the critical level of oxygen delivery is considered, ways of correcting oxygen indebtedness are presented. Alternatives to the use of hemotransfusions by employing the solutions of modified hemoglobulin and perfluorocarbon-containing emulsions are under consideration. A possible algorithm of aid rendering in acute hemorrhage is given.
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PMID:[Acute hemorrhage. View on the problem]. 1261 Nov 47

Metabolic changes after surgery, trauma, or serious illness have a complex pathophysiology. The early posttraumatic stress response is physiologic and associated with a state of hyperinflammation, increased oxygen consumption, and increased energy expenditure. These are part of a systemic reaction that encompasses a wide range of endocrinological, immunologic, and hematological effects. Surgery initiates changes in metabolism that can affect virtually all organs and tissues; the metabolic response results in hormone-mediated mobilization of endogenous substrates that leads to stress catabolism. Hypercatabolism has been associated with severe complications related to hyperglycemia, hypoproteinemia, and immunosuppression. Proper metabolic support is essential to restore homeostasis and ensure survival.
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PMID:Metabolic considerations in management of surgical patients. 2162 91


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