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Biomedical subjects

E Enger

Publications and source records attributed to E Enger.

At least 91 records · Page 5Linked to original sources
PubMed1977

Influence of HLA-A, -B, -C, and -D matching on the outcome of clinical kidney transplantation.

The influence of HLA matching has been studied in the Norwegian material of 142 living related and 311 cadaveric transplants. Graft survival corresponded closely to the degree of HLA haplotype disparity between donors and recipients. Furthermore, graft survival was less in combinations being incompatible for the serologically defined HLA-A and -B antigens as compared to compatible combinations. A weak MLC response, indicating a possible sharing of the HLA-D determinants between donor and recipient, was also associated with superior graft survival, even in the presence of HLA-A and -B disparity. Matching for HLA-C in addition to HLA-A and -B did not seem to improve graft survival.

Cadaver↗
PubMed1977

The influence of HLA-A, -B, -C, and -D matching on kidney graft survival.

The influence of HLA matching has been studied in a Norwegian material of 147 living related first transplants, 281 cadaveric first transplants and 48 cadaveric second transplants. Graft survival corresponded closely to HLA antigen disparity and degree of MLC response in combinations transplanted with kidneys from living related donors. In patients transplanted with cadaveric grafts. HLA identical and compatible grafts performed significantly better than imcompatible grafts. Matching for HLA-C in addition to HLA-A and -B did not seem to improve graft survival.

Cadaver↗
PubMed1976

Effect of sodium depletion on plasma renin concentration before and during adrenergic beta-receptor blockade with propranolol in normotensive man.

Plasma renin levels have been used to discriminate between different forms of hypertension, but how to define the normal range of plasma renin levels has not been agreed upon. Sodium depletion stimulates renin release. Evaluation of plasma renin would, therefore seem possible only in relation to sodium balance. Plasma renin concentration and concurrent daily sodium excretion were determined in 33 healthy normotensive subjects (control group) ingesting high, normal and low sodium diets. A well-defined hyperbolic relationship was found between the two variables indicating that the physiologic level of plasma renin concentration depends on the state of sodium balance. An increase in plasma potassium concentration may reduce plasma renin concentration, but this appeared to be overruled by the stimulating effect of sodium depletion. To examine whether beta-adrenergic stimulation contributes to the increase in plasma renin concentration during sodium depletion, the relationship between plasma renin concentration and concurrent sodium excretion was studied during beta-receptor blockade with propranolol. In 20 healthy normotensive subjects in whom beta-receptor blockade was verified by a significant reduction in pulse rate, the same hyperbolic relationship was found between plasma renin concentration and sodium excretion as in the control group showing that sodium depletion stimulates renin release independent of sympathetic nervous activity.

Adrenergic beta-Antagonists↗
PubMed1976

Tissue toxicity of intravenous solutions. A phlebographic and experimental study.

A phlebographic study in 32 children has shown that i.v. infusion of invertose, glucose, Vamine and Intralipid but not saline, damages the tissues as judged from changes in the vessel walls, oedema and disturbances in the venous circulation. The addition of Heparin to the solutions markedly reduced the frequency of these untoward reactions. The toxicity of invertose, glucose, Vamine and Intralipid was studied experimentally in a biologic tissue: the cheek pouch of the hamster. All solutions particularly Vamine caused some damage to the microcirculation. In this study the factor mainly responsible for thrombophlebitis was the toxicity of the solution infused. Other factors such as surgical trauma, site of entry, local infection, temperature of solutions etc. played only a minor role.

Animals↗
PubMed1975

Human skeletal muscle energy metabolism during and after complete tourniquet ischemia.

The extent of cellular metabolic deterioration and its reversibility was studied on human skeletal muscle needle biopsies during operations in bloodless field. The tissue levels of high energy phosphates and glycolytic metabolites were analyzed after various times of tourniquet ischemia and compared to contralateral control extremity levels. In the ischemic extremity the phosphocreatine (CrP) levels decreased by 40% within 30-60 min and after 60-90 min a 60% reduction was found. No significant ATP changes occurred. Lactate levels increased by 225% after 30-60 min and by 300% after 60-90 min. The glucose and G-6-P levels increased slightly and indicated glycogenolysis. The rate of the metabolic changes decreased with ischemia time. In the control leg no significant metabolic changes could be seen. After the release of the tourniquet there was a rapid restoration of the phosphagen content and clearance of lactate in the ischemic leg. Near control levels of these substances were seen already after 5 min. The present results show that clinical tourniquet ischemia of up to 90 min duration produces less pronounced metabolic alterations than those seen in working muscle.

Adenosine Triphosphate↗
PubMed1975

Early effects of endotoxin on tissue phosphagen levels in skeletal muscle and liver of the dog.

The effects of a bolus injection of gram-negative endotoxin (Pseudomonas aeruginosa) on the high energy phosphate and glycogenolytic metabolite levels of skeletal muscle and liver were studied in dogs. After endotoxin injection there was a sharp increase in the G-6-P and lactate levels within 5--15 min, especially in muscle, followed by an additional but much slower increase of these metabolites during the next 2 h. The CrP and ATP levels were also increased in skeletal muscle early after the endotoxin injection and the levels of these high energy phosphate compounds were still, 2 h after endotoxin, higher than those in control animals. In the liver an early gluconeogenetic response was observed. The results indicate that tissue hypoxia and a consequent exhaustion of tissue high energy phosphate compounds do not occur during the initial period of endotoxin shock. The increased high energy phosphate levels are probably partly caused by sympathicoadrenal stimulation but direct endotoxin effects at the cell membrane level may also play an important role.

Adenosine Triphosphate↗
PubMed1975

Cellular potassium transport and ATPase activity in Bartter's syndrome.

The cellular membrane function expressed as ATPase activity and active cellular K+ changes during in vitro incubation has been studied in two siblings with Bartter's syndrome. The K+ content of skeletal muscle was 20% lower than for controls, and the active potassium transport ability of single skeletal muscle cells was also lower than that of controls. The total ATPase activity of red cell membranes was higher, but the ratio of Na+-K+-activated to Mg2+-activated ATPases was lower than for control patients. The results favour the hypothesis that a primary defect causing the Bartter's syndrome could be an inherited generalized membrane dysfunction in the handling of cations.

Adenosine Triphosphatases↗