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Biomedical subjects

M Sohtell

Publications and source records attributed to M Sohtell.

27 records · Page 2Linked to original sources
PubMed1978

Electrochemical forces for chloride transport in the proximal tubules of the rat kidney.

The electrochemical forces for chloride transport in the proximal tubule of the rat kidney were studied using micropuncture techniques. Electrical transmembrane potentials were recorded in randomly punctured tubules with Ling-Gerhard electrodes. Chloride activities in the luminal, cellular and interstitial compartments were measured with ion selective micro-electrodes. Electrical potential measurements between cell to interstitium and lumen to interstitium were -72.1 +/- 2.6 mV and +0.5 +/- 1.4 mV (mean +/- S.D.) respectively. The calculated chloride concentrations for lumen, cell and interstitium were 133.0 +/- 10.3 mM, 8.5 +/- 1.0 mM and 99.1 +/- 3.2 mM (mean +/- S.D.) respectively. The net electrochemical forces, qualitatively, offer a passive chloride ion pathway through the tubular wall and a chloride equilibrium over the luminal membrane seems to exist.

Animals↗
PubMed1976

In vivo micropuncture PCO2 measurements.

An electrode is presented which permits in vivo PCO2 measurements using a micropuncture technique. The tip diameter of the electrode is only a few microns, the tip is specially designed for measuring PCO2 in small tissue compartements.

Animals↗
PubMed1976

A short duration renal acidification test.

As earlier investigations of renal acidification capacity were poorly standardized it was considered important to develop a clinically useful method. The ability of the kidneys to acidify urine was studied in 19 normal persons by short ammonium chloride loading. Ammonium chloride was given in a dose of 150 mmol/m2 body surface in one of four different ways: whole tablets, crushed tablets, capsules and in solution. The degree of acidosis developed in each subject was measured in arterialized capillary blood samples. Urine was analysed for pH, titratable acid, ammonium ions (TA and NH4+) and phosphate. The excretion of TA, NH4+ and phosphate increased with the degree of acidosis in blood whilst urine pH decreased. The critical level appeared to lie around a base excess of -6 mmol/l below which all subjects could acidify their urine to a pH below 5.0. For clinical applications a frame of reference with tolerance limits is given for acidification capacity related to the degree of acidosis expressed as base excess.

Acidosis, Renal Tubular↗
PubMed1976

Urine acidification capacity in renal stone formers.

A short ammonium chloride loading test was used in the investigation of renal acidification capacity of 51 patients with idiopathic recurrent renal stones containing calcium. Many of these patients had suffered from prolonged and severe stone disease. In 31% of the patients an impaired acidification with varying degrees of severity was found. Eight patients had defects suggesting distal renal tubular acidosis (RTA). One case with the complete and two cases with the incomplete form of RTA were found. A further five patients, who were all able to acidify their urine to an acid pH, had milder defects in the excretion of titratable acid and/or ammonium ions which may indicate an early stage of distal tubular acidosis. Six patients were suspected of having a proximal acidification defect, as they showed delayed responses to the ammonium chloride induced acidosis.

Acidosis↗
PubMed1976

Bicarbonate re-absorption in renal stone patients with acidification defects.

A pathological renal response to ammonium chloride loading was found to be common in renal stone formers. In order to elicit further information about the impaired acidification capacity eight patients were investigated by bicarbonate loading. One patient with a mild acidification defect had normal tubular re-absorption of bicarbonate. Five of these eight patients with suspected proximal acidification defect and two patients with impaired distal acidification were found to have a low bicarbonate threshold and an increased, fractionated, bicarbonate excretion at a normal plasma bicarbonate level. Four of the patients with suspected, proximal, acidification defect reached a maximal re-absorption of bicarbonate (Tm) that was low, while three patients did not reach a Tm. These three factors indicate increased bicarbonate wastage from the kidneys. A constantly alkaline urine, such as exists in patients with proximal acidification defect may give rise to an increased risk of the precipitation of renal stones - primarily calcium-phosphate stones.

Acidosis, Renal Tubular↗
PubMed1976

Urinary excretion of beta2-microglobulin in renal stone patients under normal conditions and during acidosis and alkalosis.

The urinary excretion of beta2-microglobulin was studied under normal conditions and during acidosis and alkalosis in 65 patients with renal stones. Eleven patients were studied under two of these conditions. Four out of 51 patients examined under normal conditions had an increased excretion of beta2-microglobulin in their urine. Four out of five patients with distal acidification defects were found to have an increased excretion of beta2-microglobulin during induced acidosis. During alkalosis, four out of eight patients with acidification defects increased their excretion of the protein. The tubular proteinuria that could be provoked during acute acidosis and alkalosis was considered to be secondary to changes in the acid-base status and may indicate a renal tubular defect.

Acidosis↗