Impaired peritoneal fluid drainage in nephrogenic ascites

In three chronic hemodialysis patients nephrogenic ascites and in four patients with ascites of other causes the rate of transfer of fluid from peritoneal cavity to plasma was measured by a radio-labelled albumin method. Ascitic fluid removal rate was lowered in the patients with nephrogenic ascites (median 14, range 10 to 21ml/hr) than in those with normal renal function (median 45, range 10 to 73 ml/hr). These results suggest that lymphatic drainage of the peritoneum is impaired in nephrogenic ascites and that this may contributed to the development of the condition and to the propensity of fluid overloaded dialysis patients to develop ascites. A retained substance or one liberated from abnormal kidneys nay be responsible for reversible for reversible depression of lymphatic flow in uremia. (AU)

Leucocyte sodium transport and dietary zinc in protein energy malnutrition

Zinc supplementation of children who were just completing a period of rapid "catch-up" growth during recovery from severe malnutrition was found to stimulate sodium transport in their leucocytes. These results suggest that zinc status should be studied in the large number of serious illness now known or thought to be associated with impaired sodium transport.(AU)

Tracheobronchial function in health and disease: effect of mucolytic substances

The effect of mucolytic and expectorant substances on ciliary beat frequency, mucus transport velocity and mucus production, was investigated in normal and bronchitic rats. The results showed that: (i) N-acetylcysteine and S-carboxymethylcysteine were mildly cilioexcitatory at low and ciliodepressive at higher concentrations in both normal and bronchitic rats. A similar pattern was seen in mucus transport velocity. (ii) Bisolvan enhanced all aspects of muciciliary activity in both groups of animals. Sobrepin was less effective than Bisolvan and more effective than Tachoquilin. (iii) Geleomytrol, Ozothin and prostaglandin E1 were all cilioexcitatory in rats with bronchitis. Mucus transport velocity was similarly stimulated by both Geleomyrtol and Ozothin. (iv) Ammonium chloride and potassium iodide enhanced mucociliary activity in normal and bronchitic rats. (v) All substances stimulated mucus production, however, the most potent was prostaglandins E1. The mechanisms for increased mucociliary activity involve inter alia the probable cleaving of disulphide bridges, decreased mucosal swelling, altered rheological characteristics and stimulation of adenylate cyclase (AU)

The relationship between intracellular and extracellular potassium in normal and malnourished subjects as studied in leukocytes

Leukocyte potassium has been measured in normal subjects and in malnourished children with and without edema both on admission and during recovery. In nonedematous malnourished children the potassium content was low (328mmol/kg dry solids) and took 2-3 weeks of rehabilitation to return to normal (374 mmol/kg dry solids). Leukocytes from edematous children had normal intracellular potassium values. However, 5 days on a maintenance diet reduced the intracellular potassium in the children with kwashiorkor to a value similar to that found in marasmus. Plasma potassium was significantly lower in kwashiorkor (3.43) than in marasmus (4.74). The relationship between external potassium and internal potassium in normal leukocytes was measured (fig.1) and the values found severe malnutrition compared with normal. It was found that in nonedematous malnutrition intracellular potassium was low compared to the predicted value, whereas in kwashiorkor, although the mean values were normal, no relationship between external potassium and intracellular potassium could be demonstrated. It is concluded that in the leukocyte malnutrition alters either the passive permeability of the membrane to potassium or the active transport of potassium of both.(AU)

Leukocyte electrolytes and sodium transport in protein energy malnutrition

Intracellular electrolytes and sodium transport were measured in leukocytes obtained from malnourished children. In the presence of edema, leukocyte sodium and potassium were raised. The total flux and the glycoside-sensitive portion were increased. Loss of edema was associated with reductions in all these measurements. In marasmus, glycoside-sensitive sodium efflux was reduced compared to recovered values. Sodium was increased and potassium reduced. It is concluded that at least two defects in sodium transport may occur in protein energy malnutrition, an increased passive permeability in kwashiorkor and a reduced active transport for sodium in marasmus. (AU)