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Biomedical subjects

F Knudsen

Publications and source records attributed to F Knudsen.

At least 91 records · Page 5Linked to original sources
PubMed1985

Protein C activity in renal disease.

Protein C activity was determined in 19 healthy controls and in 52 patients with renal diseases, clinically divided into three groups I) Nephrotic syndrome, II) Renal insufficiency, III) Terminal uremia, requiring maintenance dialysis. In the nephrotic syndrome protein C levels were found to be normal, but in renal insufficiency and terminal uremia the protein C activity was significantly decreased. A correlation between decreasing protein C and progressive renal failure is suggested. The reduced protein C activity may play an important role in the thrombotic tendency seen in renal diseases and uremia.

Adult↗
PubMed1985

Cellular hypoxia during hemodialysis. Demonstration of intradialytic release of purine and pyrimidine metabolites.

Measurement of hypoxanthine/xanthine has been suggested to be a useful indicator of cellular hypoxia. In humans it has been applied for quantitation of asphyxia in the newborn and hypoxic brain damage after cardiac arrest. To investigate if cellular hypoxia occurs during routine hemodialysis we followed leukocyte count, arterial oxygen tension and plasma hypoxanthine/xanthine in 10 stable dialysis patients. Hemodialysis was associated with transitory leukopenia and decrease in oxygen tension. Plasma hypoxanthine/xanthine increased simultaneously with the decrease in leukocyte count and arterial oxygen tension but returned to normal values at the end of treatment. The study demonstrates that routine hemodialysis, even in stable patients, is associated with cellular hypoxia.

Adolescent↗
PubMed1985

Serum angiotensin-converting enzyme increases during hemodialysis. Evidence for injury of the pulmonary vascular endothelium?

In 19 patients hemodialysis was associated with significant decreases in arterial oxygen tension and leukocyte count. After 240 min of dialysis serum angiotensin-converting enzyme (ACE) corrected for hemoconcentration increased 14.3% (p less than 0.001) indicating injury of the vascular endothelium during hemodialysis. It is suggested that the increase in serum ACE is due to a complement-mediated sequestration of leukocytes in the pulmonary vasculature leading to injury of the vascular endothelium with interstitial edema and pulmonary dysfunction. Furthermore, it is suggested that serum ACE analysis may prove a new method to assess biocompatibility of materials used in devices for extracorporeal circulation.

Adult↗
PubMed1985

On the kinetics of complement activation, leucopenia and granulocyte-elastase release induced by haemodialysis.

In order to elucidate the kinetics of haemodialysis-induced activation of complement, leucopenia and release of granulocyte-elastase, 10 patients (three females and seven males; mean age 47.8 years) were extensively studied during a 4 h haemodialysis treatment and for the following 24 h, and further compared with a healthy control group. Prior to dialysis patients had normal leucocyte count, plasma elastase bound to alpha 1-proteinase inhibitor (E-alpha 1P1) and total haemolytic complement, whereas plasma C3d was higher and plasma C5a lower than in controls. Haemodialysis induced initial leucopenia and subsequent rebound phenomenon lasting 24 h post treatment. These alterations were due to almost selective changes in neutrophile count as monocyte and lymphocyte counts, apart from decrease in the first 30 min, were unchanged. Total haemolytic complement decreased initially during dialysis and rose at the end. Generation of C5a within the dialyser was evident by demonstration of high levels of this anaphylatoxin in dialyser effluent plasma; maximal values observed coincided with the nadir of leukopenia. Plasma C3d and E-alpha 1P1 both progressively rose during dialysis. After termination of extracorporeal circulation the disappearance rates (T/2) were approximately 6 h and 2.5 h respectively. Haemodialysis thus induces changes in the complement and leucocyte system resembling an acute inflammation, which out-lasts the treatment period.

Adult↗
PubMed1985

Relationship between urinary concentrating ability, arginine vasopressin in plasma and blood pressure after renal transplantation.

Arginine vasopressin (AVP) and serum osmolality (Sosm) were determined in plasma before and after a 24-h period of water deprivation in 19 patients with post-renal-transplant hypertension (group I), 14 patients with normal blood pressure after renal transplantation (group II), and 16 healthy control subjects (group III). Urine was collected in four periods of 6 h each for measurement of urine volume (V), urine osmolality (Uosm) and tubular capacity for reabsorption of water (Tc water). AVP and Sosm increased significantly in all groups. The AVP levels were the same in groups I and II, but higher in group I than III both before and after water deprivation. In group II, AVP was higher than in group III only after water deprivation; V was significantly reduced in all groups. In groups I and II, V, Tc water and Uosm were the same. In group III, V was significantly lower than in groups I and II in the last three 6-h periods, and in group III, Tc water was higher in the first 6-h period than in groups I and II. There was a significant positive correlation between AVP and Sosm in all groups. In conclusion, renal water excretion cannot be reduced as rapidly and to the same degree in renal transplant recipients as in control subjects because of a decreased renal capacity for reabsorption of water. The higher AVP level in the transplant recipients may be a compensatory phenomenon for the decreased responsiveness of the renal collecting ducts in the transplanted kidneys. The sensitivity of the osmoreceptors to changes in osmotic stimuli was normal.

Adult↗
PubMed1985

Platelets and antithrombin III in uraemia: the acute effect of haemodialysis.

In 14 haemodialysis patients, platelet count, secondary platelet aggregation rate, immunological antithrombin III and antithrombin III activity were lower and plasma beta-thromboglobulin higher than in 14 age- and sex-matched controls. In contrast, primary platelet aggregation, the degree of secondary aggregation and circulating platelet aggregates did not differ. Haemodialysis was associated with signs of platelet damage reflected by increase in plasma beta-thromboglobulin, extraction of platelets in the dialyser and decline in platelet count. Platelets in the dialyser effluent line were less aggregable than platelets in arterial blood. Circulating platelet aggregates and immunological antithrombin III were unchanged during dialysis whereas antithrombin III activity showed a minor rise. In conclusion, uraemics show a decreased rate of secondary platelet aggregation, and haemodialysis confers further platelet injury due to blood/surface interactions during extracorporeal circulation. The defective platelet function and low antithrombin III activity may help to explain the paradoxical occurrence of both haemorrhagic and thrombotic complications in uraemia.

Adenosine Diphosphate↗
PubMed1985

The effect of dialyser membrane material on intradialytic changes in platelet count, platelet aggregation, circulating platelet aggregates and antithrombin III.

Blood surface interaction during hemodialysis leads to impairment of platelet function and decrease in platelet number, which besides heparinization, may cause or exacerbate bleeding in risk patients. Furthermore, antithrombin III has been shown to increase during dialysis, probably due to vascular endothelial injury caused by infusion of activated platelets into the patient. 23 patients were examined during two successive dialyses, using membranes based on regenerated cellulose (RC) and cellulose acetate (CA). In 12 of the patients, platelet aggregation induced by ADP, circulating platelet aggregates and immunological AT III and AT III activity were determined. Irrespective of the membrane used, hemodialysis was associated with deterioration of platelet function, reflected by a decrease in platelet aggregation with return to predialysis values at the end of dialysis. However, the decline in platelet count and the increase in circulating platelet aggregates were membrane dependent, with RC causing greater changes than CA. No changes in threshold concentration of ADP inducing secondary platelet aggregation or in either immunological AT III or AT III activity were seen during dialysis.

Adolescent↗
PubMed1985

Adult respiratory distress-like syndrome during hemodialysis: relationship between activation of complement, leukopenia, and release of granulocyte elastase.

Twelve patients with terminal uremia (8 females and 4 males) treated with chronic maintenance hemodialysis, were extensively studied during two successive dialyses with alternate use of either a Cuprophan (CP) based membrane, or a Polycarbonate (PC) membrane. Arterial plasma levels of total hemolytic complement, complement factors C3d and C5a, and granulocyte derived elastase were determined immediately before dialysis and sequentially during the entire procedure. Effluent line from the hemodialyzer was similarly sampled. Collected samples were centrifuged immediately at the bedside and instantly frozen in liquid nitrogen in order to preserve labile plasma components of complement. Analysis of the overall results shows that initial arterial leukopenia and generation of C5a in the hemodialyzer, as well as maximal values of hemodialysis-induced free plasma C3d and granulocyte elastase are related. Reflecting differences in biocompatibility, CP membranes were shown to induce significantly more leukopenia, increase in plasma free C3d, generation of C5a, and release of granulocyte-derived elastase. These results indicate that activation of complement, leukopenia, and release of granulocyte derived elastase are interlinked pathophysiological mechanisms of importance for acute deterioration of pulmonary function during hemodialysis, and that this condition is closely related to adult respiratory distress syndrome (ARDS).

Adult↗
PubMed1984

Decreased platelet sensitivity to prostacyclin (epoprostenol) during hemodialysis.

Evidence is accumulating that activation of platelets occurs during conventional hemodialysis. In ten uremic patients, the ADP-induced platelet aggregation and the platelet sensitivity to prostacyclin (PGI2) were examined before and after 120 and 240 minutes of dialysis. The ADP-induced aggregation was enhanced during dialysis reaching statistical significance after 240 minutes compared to predialysis values. The platelet sensitivity to PGI2 was significantly diminished during dialysis. Our results are in agreement with the concept of platelet activation during hemodialysis and lend support to the clinical use of PGI2 during hemodialysis.

Adolescent↗
PubMed1983

Nitroglycerin prolongs the bleeding time in healthy males.

Bleeding time was prolonged when measured 6 minutes after the administration of 0.5 mg nitroglycerin (NTG) sublingually in 15 men aged 25-40 years. The prolongation was not caused by a general inhibition of platelet aggregation. 4 g acetylsalicylic acid inhibited the effect of NTG on the bleeding time with a time course similar to the vessel wall cyclooxygenase. This may indicate that the effect of NTG is mediated by prostacyclin.

Adult↗