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Biomedical subjects

B Truniger

Publications and source records attributed to B Truniger.

At least 73 records · Page 4Linked to original sources
PubMed1976

[Peritoneal dialysis, ultrafiltration and hyperosmolarity].

Observation of a patient who developed serious hypernatremia during peritoneal dialysis with a dialysis fluid containing 135 mval Na+/1 prompted investigation of net water, sodium, potassium and chloride transport during 45 peritoneal fluid exchanges with standard dialysis solutions containing 1.5 and 4.5 g% glucose. With both solutions and an equilibration time of 0 min, net ultrafiltration was observed (89 ml and 230 ml per exchange respectively). In both groups the calculated sodium concentration of the ultrafiltrate was considerably lower than plasma sodium concentrations (27.0 mval/1 and 36.9 mval/1 respectively, resulting in a new sieving coefficient of 0.20 and 0.27 respectively. Therefore, the free water deficit resulting from peritoneal ultrafiltration is directly responsible for the hypernatremia observed during peritoneal dislysis. While the potassium and chloride transport observed in these studies can be explained by diffusion processes along a given concentration gradient, sodium transport and sodium concentrations raise the question of more complex mechanisms. The data are discussed with reference to the relative significance of diffusion processes versus bulk flow and solvent drag.

Biological Transport↗
PubMed1976

[Electrolyte Emergencies. Selected Aspects].

The question of what factors determine the significance of abnormal electrolyte findings is discussed with reference to a number of examples of acute electrolyte emergencies (hyponatremia, hypernatremia, hypokalemia, hyperkalemia, metabolic alkalosis). In addition to the extent of the deviation from normal and the clinical manifestations already present in all cases, it is principally the rate of dysfunction which determines the action of a clinical or laboratory-determined electrolyte deviation.

Adult↗
PubMed1975

[The function of the diseased kidney].

A few years ago the kidney in chronic renal failure was described as a mass of tissue "without significance, vanishing into the disparity of thousands of fantastically altered organs of strange design and anomalous behaviour". In order to refute this opinion, some of the morphological and pathophysiological evidence is summarized which points to the fact that even in chronic renal failure the remaining nephrons that contribute to renal function behave as a rather homogeneous population characterized by appropriate adaptations of glomerular and tubular functions and by a persistent responsiveness to the changing needs of the patient.

Acid-Base Equilibrium↗
PubMed1975

[Water intoxication].

In uncharacteristic clinical symptomatology the excess of water or the water intoxication render themselves conspicuous less by the signs of an increased fluid content than by central-nervous disturbances. Among the results of laboratory examinations the hypoosmolarity measured cryoscopically always, the hyponatraemia in most cases prove the excess of free water. Exceptions are discussed. A decreased capacity of the elimination of water pathogenetically plays a larger role than primarily excessive water supply. Apart from acute and chronic renal insufficiency the various forms of the Schwartz-Bartter-syndrome (inadequate ADH-secretion) play an increasingly more important role. The therapy demands the reduction of every supply of free water, the treatment of the evoking cause and only in cases of exception the administration of hypertonic saline solution, at the most dialysis treatment.

Diabetic Coma↗
PubMed1971

Relationship between renin and intrarenal hemodynamics in hemorrhagic hypotension.

In order to investigate the possible role of the renin-angiotensin system in the regulation of intrarenal hemodynamics in hemorrhagic hypotension (HH), seven mongrel dogs have been studied under the following conditions: (a) Control, (b) HH (mean arterial pressure 70 mm Hg), and (c) HH + alpha adrenergic blockade by phenoxybenzamine (HH + POB). The following parameters were obtained for the right kidney: Intrarenal distribution of blood flow and local blood flow rates ((133)Xe washout technique); total renal blood flow (RBF) on the basis of the clearance and extraction ratio of PAH and the arterial hematocrit; plasma renin concentrations in the renal artery and vein by the method of Boucher and his associates; and renin release into the renal circulation. Alpha adrenergic blockade reverted the typical redistribution of intrarenal blood flow observed under HH. In hemorrhage, arterial and venous renin concentrations increased by a factor of 3.4 and 4.8 respectively. A further small increase was observed during HH + POB with the respective factors increasing to 4.8 and 5.3, as compared with control values. The renin release into the circulation increased by a factor of 1.2 in HH and 4.0 in HH + POB. Whereas in HH there seemed to be a relationship between increased renin concentrations or renin release, and the redistribution of blood flow, no such correlation was found during alpha-adrenergic blockade. From these observations it is concluded that renin alone is unable to maintain the typical redistribution of RBF seen during hemorrhage. Circumstantial evidence points to a permissive role of the renin-angiotensin system in the pathogenesis of the patchy cortical hypoperfusion caused by sympathoadrenergic mechanisms during hemorrhagic hypotension.

Angiotensin II↗