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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
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↗