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Results for “HYPOPROTEINEMIA”

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At least 19 recordsLinked to original sources
PubMed1986

Effects of hypoproteinemia on lung microvascular protein sieving and lung lymph flow.

Experiments were conducted on five chronically instrumented unanesthetized sheep to determine the effects of sustained hypoproteinemia on lung fluid balance. Plasma total protein concentration was decreased from a control value of 6.17 +/- 0.019 to 3.97 +/- 0.17 g/dl (mean +/- SE) by acute plasmapheresis and maintained at this level by chronic thoracic lymph duct drainage. We measured pulmonary arterial pressure, left atrial pressure, aortic pressure, central venous pressure, cardiac output, oncotic pressures of both plasma and lung lymph, lung lymph flow rate, and lung lymph-to-plasma ratio of total proteins and six protein fractions for both control base-line conditions and hypoproteinemia base-line conditions. Moreover, we estimated the average osmotic reflection coefficient for total proteins and the solvent drag reflection coefficients for the six protein fractions during hypoproteinemia. Hypoproteinemia caused significant decreases in lung lymph total protein concentration, lung lymph-to-plasma total protein concentration ratio, and oncotic pressures of plasma and lung lymph. There were no significant alterations in the vascular pressures, lung lymph flow rate, cardiac output, or oncotic pressure gradient. The osmotic reflection coefficient for total proteins was found to be 0.900 +/- 0.004 for hypoproteinemia conditions, which is equal to that found in a previous investigation for sheep with a normal plasma protein concentration. Our results suggest that hypoproteinemia does not alter the lung filtration coefficient nor the reflection coefficients for plasma proteins. Possible explanations for the reported increase in the lung filtration coefficient during hypoproteinemia by other investigators are also made.

Animals↗
PubMed1989

Effect of hypoproteinemia on blood volume recovery after moderate hemorrhage in conscious splenectomized dogs.

Hypoproteinemia is generally considered to form a threat to blood volume homeostasis. In conscious splenectomized dogs we studied whether severe hypoproteinemia, in the presence or absence of edema, would compromise the early recovery of blood volume after moderate hemorrhage (congruent to 25%). Hypoproteinemia, achieved by 10 days of repeated plasma exchange and a low-protein diet, did not induce a fall in steady-state blood volume. The interstitial colloid osmotic pressure decreased, an adaptive response probably playing a major role in this maintenance of blood volume. Within the first 2 hr after hemorrhage blood volume recovered by about 30% of the hemorrhaged volume. This early recovery of blood volume was enhanced rather than impaired in hypoproteinemia, in particular in the presence of edema. Since circulating protein did not increase within this 2-hr period, acute fluid attraction occurred through transcapillary influx of interstitial fluid. Chronic hypoproteinemia apparently enhances this fluid attraction. This may be explained by the low interstitial fluid oncotic pressure and fluid expansion, thus by those very factors directed to maintain blood volume in hypoproteinemia.

Animals↗
PubMed1988

Hyperventilation with hypoproteinemia.

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.

Acid-Base Equilibrium↗
PubMed1992

A simplified two-pore filtration model explains the effects of hypoproteinemia on lung and soft tissue lymph flux in awake sheep.

We used a simplified two-pore filtration model to examine the effects of hypoproteinemia on lung and soft tissue lymph flux in awake sheep (n = 7). To induce hypoproteinemia, we subjected each animal to 3 days of batch plasmapheresis (6 units per day). Data were collected in near steady-state conditions, 15-18 hr following completion of the last plasmapheresis episode. At this time, plasma protein concentration had fallen by 34%, while lung and soft tissue lymph protein concentrations had fallen by 55 and 62%, respectively. Lung and soft tissue lymph flows increased 52 and 87%, respectively. The plasma-to-lymph osmotic pressure gradients for lung and soft tissue lymph were unchanged by protein depletion (soft tissue, 7.7 mm Hg; lung, 4.8 mm Hg). We applied these results to a heteropore model of the microvascular barrier that consisted of two types of pores: those which plasma proteins could not cross (sigma = 1) and those which proteins could cross without restriction (sigma = 0). We varied the proportion of small pores to large pores until the measured data fit a model in which the calculated microvascular hydrostatic pressures in normal and hypoproteinemic conditions were equal. This was based on the assumption that microvascular hydrostatic pressure did not change with plasma protein depletion. These conditions could be satisfied when the small pores accounted for 90% of total barrier porosity. According to the model, lymph flow increased in hypoproteinemia because of an increase in protein-free liquid flux through the large percentage of small pores; protein flux through the small percentage of large pores remained unchanged. The net result was an increase in lymph flow and a decrease in the lymph protein concentration. The model reproduced these changes even though the plasma-to-lymph osmotic pressure gradients were unchanged. We conclude that a simplified heteropore model can explain the effects of hypoproteinemia on lung and soft tissue lymph flux.

Animals↗
PubMed1995

Gigantic ameloblastoma of the mandible complicating hypoproteinemia: case report.

A case of gigantic ameloblastoma of the mandible complicating hypoproteinemia is reported. The patient, a 73-year-old male, had refused a surgical procedure on an ameloblastoma for 13 years. By the time the tumor had increased in size and fistulas from it had formed, hypoproteinemia and generalized edema had occurred. The tumor was removed when the serum total protein level had recovered to about 5 g/dl following the administration of a plasma protein preparation. After the operation, hypoproteinemia and edema clearly improved. Hypoproteinemia is thought to be caused by leakage of plasma or occasional bleeding through the oral fistulas of ameloblastoma, and in this patient's case, poor nutrition because of his masticatory and swallowing difficulties.

Aged↗
PubMed2003

[Pre-operation application of recombinant human growth hormone for liver cirrhosis with portal hypertension and hypoproteinemia].

OBJECTIVE: To evaluate the effectiveness of pre-operation use of recombinant human growth Sixty patients with hormone (rhGH) for liver cirrhosis with portal hypertension and hypoproteinemia. METHODS: Sixty patients with liver cirrhosis and portal hypertension and hypoproteinemia (child's class B) were randomly divided into control group (n = 30) and rhGH group (n = 30). The patients in the rhGH group were given subcutaneously growth hormone at a dose of 4 i.u. per day for five days before operation. All patients were given the same parenteral nutrition before operation. The levels of albumin, globulin, prealbumin, and blood sugar were measured before and 3, 4, and 5 days after given the hormone. Results The prealbumin increased 3 days after given the hormone (P < 0.05), while the albumin increased 5 days after given the hormone (P < 0.05). The general condition and the quality of life of the patients receiving the hormone improved. No side effects had been found. The blood sugar and globulin did not change over time in both groups. CONCLUSION: The pre-operation use of the recombinant human growth hormone may benefit to the alleviation of hypoproteinemia and to the improvement of the quality of life of the patients with liver cirrhosis and portal hypertension and hypoproteinemia when combined with the use of parenteral nutrition.

Adult↗
PubMed1984

Role of thermal injury-induced hypoproteinemia on fluid flux and protein permeability in burned and nonburned tissue.

We studied the role of hypoproteinemia, induced by a major burn injury, on the edema process in burned and nonburned tissues including the lung in the adult sheep. We used lymph flow (QL) and the lymph-plasma (L/P) protein ratio as indicators of the rate of fluid and protein flux across the microcirculation and into the interstitium. We compared the response after a full-thickness burn to 30% of total body surface plus resuscitation by means of lactated Ringer's solution (n = 8) with a comparable degree of hypoproteinemia produced by plasmapheresis with vascular hydrostatic pressure and cardiac output kept constant. We measured lung QL and soft tissue (prefemoral) QL from both the burned and nonburned areas. A twofold increase in QL and a decrease in the L/P ratio was seen in both lung and nonburned tissue in both burn and plasmapheresis animals, indicating the postburn response to be due to hypoproteinemia with no increase in protein permeability. The QL in burned tissue was increased five to ten times with an increase in the L/P ratio. Four burned sheep were resuscitated with pooled plasma. Restoration of plasma proteins eliminated the increase in QL in lung and nonburned tissue but had no effect on the burn response. In summary, burn-induced hypoproteinemia plays a major role in the edema process in nonburned tissues and is corrected by restoration of plasma proteins. Edema in burned tissue does not appear to be related to this process.

Animals↗
PubMed1989

Hypoproteinemia-induced mucosal albumin leakage. Influence of luminal nutrients.

Previous studies indicate that a peptide enteral formula significantly attenuates the intestinal water and albumin loss in volume-expanded rats with acute hypoproteinemia. The purpose of this study was to determine the relative abilities of the fat, carbohydrate, and protein components of the peptide enteral formula to stimulate water absorption and attenuate albumin turnover in intact jejunal segments during hypoproteinemia induced by intravenous infusion of Tyrode's solution (2.5 ml/min/kg) in Sprague-Dawley rats. Radio iodinated albumin movement from blood to lumen was used to estimate mucosal albumin clearance. Net transmucosal water was measured using a volume recovery method. When compared to luminal perfusion with Tyrode's solution (control animals), protein (as a protein hydrolysate) or protein combined with fat significantly enhanced fluid absorption (P less than 0.05) before and during volume expansion. This did not occur with carbohydrates or when carbohydrate was combined with the protein hydrolysate. However, the hypoproteinemia-induced increase in mucosal albumin clearance was significantly (P less than 0.05) attenuated by all solutions containing the carbohydrate component of the diet. These findings indicate that the protein component of the enteral formula is responsible for the enhanced net transmucosal water movement in hypoproteinemic animals. However, the carbohydrate component is largely responsible for the decrease in intestinal albumin clearance.

Albumins↗
PubMed1998

Hypoproteinemia caused by tricuspid regurgitation: report of a case.

A case of tricuspid regurgitation (TR) complicated by severe hypoproteinemia is presented herein. A 68-year-old man who had undergone coronary artery bypass grafting (CABG) for postinfarction angina suffered repeated inferior myocardial infarction due to obstruction of the proximal right coronary artery, 3 years after which he developed systemic edema. Investigations revealed TR associated with hypoproteinemia; however, treatment consisting of aggressive diuretic therapy and albumin administration proved ineffective. The hypoproteinemia manifested as protein-losing enteropathy clinically, and the tricuspid valve was replaced to eliminate high venous pressure. The serum protein levels became normalized after the operation. Although TR is generally well tolerated in the absence of pulmonary hypertension, surgical management is recommended for patients with severe protein deficiency resistant to medical treatment.

Aged↗
PubMed2002

Hypoproteinemia in severe childhood atopic dermatitis: a serious complication.

As a complication of atopic dermatitis (AD), the incidence of hypoproteinemia is increasing among infants with severe AD in Japan. It can be a life-threatening condition owing to hypovolemic shock as a result of hypoproteinemia and vascular infarction as a result of thrombocythemia. However, the pathophysiology of this condition remains unclear. The objectives of the present study were two-fold. The first objective was to determine the main route of protein loss, i.e. through the damaged skin or the gastrointestinal tract, or as a result of insufficient food intake. The second objective was to identify whether allergy or infection was the cause of severe skin inflammation. Fifteen patients with AD were enrolled who had serum protein levels of 3.2-5.8 g/dl. Specific immunoglobulin E (IgE) and skin test to allergens, stool eosinophils, alpha1-antitrypsin clearance, skin Staphylococcus aureus colonization and superantigens (SAgs) produced by the organism, serum SAg-specific IgE antibodies, serum interleukin (IL)-5, IL-6, IL-12, and interferon-gamma (IFN-gamma) were evaluated. Prominent serous skin discharge was seen in all of the patients and was found to have almost the same protein concentration as serum. Marked thrombocytosis, with a maximum of 1,060 x 103/ml, was seen. Skin culture revealed S. aureus colonization in all patients. SAg-producing S. aureus were found in 84.6% of the patients. The concentration of serum IL-5 was significantly increased and correlated well with the blood eosinophil count. Hence, the main route of protein loss was believed to be through damaged skin. The cause of severe inflammation was thought to be a combination of allergic inflammation and skin colonization by SAg-producing S. aureus. Serum cytokines showed a T helper 2 (Th2) T-cell-mediated pattern. To prevent hypovolemic shock, vascular occlusion, and growth retardation, it is of vital importance to diagnose hypoproteinemia at an early stage and start appropriate therapy.

Adolescent↗