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K N Frayn

Publications and source records attributed to K N Frayn.

At least 199 records · Page 11Linked to original sources
PubMed1980

Measuring the severity of injury.

Attempts have been made to improve the Injury Severity Score (ISS) system of Baker et al. (1974) using plasma lactate data obtained from 277 patients shortly after injury and before treatment. The ISS is based on the Abbreviated Injury Scale (AIS) values of the individual injuries, being the sum of the squares of the values for the three most severely injured regions. Log (plasma lactate concentration) is positively related to ISS over its whole range. It was not possible to vary the AIS values, either on clinical grounds or using a computer, in such a way that the variance of the log (plasma lactate concentration) about its regression line with ISS was significantly reduced. With a score based on the sum of the squares of the AIS values for all the patient's injuries, some improvement to the AIS values could be made but it was not statistically significant. At the present time Baker's ISS method would seem to be the best way of grading injuries for acute studies.

Humans↗
PubMed1980

Skeletal muscle triacylglycerol in the rat: methods for sampling and measurement, and studies of biological variability.

Previously reported concentrations of triacylglycerol in skeletal muscle have shown high coefficients of variation, and there have been large differences between mean concentrations reported in a given muscle. Conditions for sampling and measurement were therefore investigated. Samples were best taken under anesthesia as breakdown of triacylglycerol was rapid after decapitation. Silicic acid was preferable to zeolite for removal of phospholipids although either agent could interfere with the estimation. Even with apparently reliable methods, a high variability was found in any one muscle and there were large differences between muscles. It is unlikely that the variability was due to contamination with adipose tissue. Concentrations of glycogen and phospholipid were much less variable. Although the store of triacylglycerol in skeletal muscle in caloric terms was found to be 2-18 times greater than that of glycogen, the variability found is likely to hamper studies of its metabolic role.

Anesthesia↗
PubMed1980

Protein metabolism after unilateral femoral fracture in the rat, and comparison with sham operation.

Urinary excretion of nitrogen, creatinine and N tau-methylhistidine were measured in the rat after unilateral femoral fracture or sham operation. Increased urinary nitrogen excretion occurred in both groups of rats. Cumulative excretion of both nitrogen and N tau-methylhistidine was slightly greater after femoral fracture than after sham operation and this difference agreed quantitatively with loss of muscle protein from the limb with fracture. Sham operation caused no local effect on muscle-protein content and no differences were seen in muscle-protein content between the uninjured hind limb of rats with femoral fracture and either hind limb of sham-operated rats. It was concluded that bone fracture per se does not contribute significantly to the increased urinary nitrogen excretion seen after femoral fracture in the rat; similar changes are produced by equivalent sham operation and any difference between the effects of the two procedures represents local muscle wasting, probably due to disue of the fractured leg.

Animals↗
PubMed1979

Regulation of protein metabolism by a physiological concentration of insulin in mouse soleus and extensor digitorum longus muscles. Effects of starvation and scald injury.

1. Although high concentrations of insulin affect both synthesis and degradation of skeletal-muscle protein, it is not known to what extent these effects occur with physiological concentrations. The effects of a physiological concentration of insulin (100 mu units/ml) on muscle protein synthesis, measured with [3H]tyrosine, and on muscle protein degradation, measured by tyrosine release in the presence of cycloheximide, were studied in mouse soleus and extensor digitorum longus muscles in vitro. 2. Insulin significantly stimualated protein synthesis in both muscles, but an inhibition of degradation was seen only in the extensor digitorum longus. 3. Starvation for 24 h decreased the rate of protein synthesis and increased the rate of breakdown in the extensor digitorum longus. Sensitivity to insulin-stimulation of proteins synthesis in the soleus was increased by starvation. 4. ;a 20%-surface-area full-skin-thickness dorsal scald injury produced a fall in total protein content in soleus and extensor digitorum muscles, maximal on the third day after injury. Soleus muscles 2 days after injury showed an impairment of protein synthesis; degradation was unaffected and neither synthesis nor degradation in vitro was significantly affected in the extensor digitorum longus. 5. The advantages and limitations of studies of protein metabolism in vitro are discussed.

Amino Acids↗
PubMed1978

Studies on the mechanism of insulin resistance after injury in the mouse.

Acute insulin resistance developed after scald injury in the mouse. After 2h plasma glucose and insulin concentrations were each raised about two-fold. Glucose metabolism was studied in vitro in soleus muscles isolated at this time. Glycolysis and glycogen synthesis, and their stimulation by insulin, were unchanged in muscles from scalded mice, and insulin-stimulated transport of 2-deoxyglucose slightly increased, showing that the insulin resistance seen in vivo is not maintained in isolated tissues. Binding of insulin to liver cell membranes prepared from scalded mice was unaltered, whilst that of glucagon was slightly but significantly reduced, showing that changes in polypeptide-hormone receptors can occur within this short time. It was concluded that the acute loss of sensitivity to insulin after injury does not result from a change in insulin receptor sites and presumably reflects an impairment of glucose metabolism in vivo mediated by circulating hormones.

Animals↗
PubMed1978

Effects of halothane on glucose metabolism after injury in the rat.

The effects of halothane anaesthesia on glucose metabolism have been investigated in rats after a non-lethal scald injury. Anaesthesia was induced about 70 min after injury. Glucose metabolism was studied at two stages: during and shortly after induction, and about 2 h after induction. Comparisons were made with conscious rats at the corresponding times after injury. All rats were in an ambient temperature of 30 degrees C. During and shortly after the induction of anaesthesia, halothane caused a rapid increase in plasma glucose concentration, which by 30 min had begun to return to the values in injured controls; thus glucose production and utilization were increased. Insulin concentrations were increased also. However, after 2 h exposure halothane had decreased glucose production and utilization, as determined with [5-3H]- and [U-14C]-glucose, increased plasma concentrations of insulin and decreased liver concentrations of glycogen, that is it had exacerbated well-known effects of injury in the rat, including insulin resistance. Hyperglycaemia was not increased.

Anesthesia, Inhalation↗
PubMed1977

Rates of glucose utilization and glucogenesis in rats in the basal state induced by halothane anaesthesia.

1. Rates and rate coefficients of glucose utilization and replacement were determined with [5-3H]- and [U-14C]-glucose in rats starved for 24h, either conscious or under halothane anaesthesia, in a thermoneutral environment. Plasma insulin concentrations were also measured. 2. Halothane anaesthesia decreased the turnover rate by 20%, which was similar to previously reported decreases in metabolic rates caused by natural sleep. 3. Fractional recycling of glucose carbon was little affected by halothane. 4. Comparison of values in one rat with those in another, among both conscious rats and those under halothane anaesthesia, showed that rate coefficients were inversely correlated with plasma glucose concentrations. 5. These findings indicated that halothane, in the concentration used (1.25%, v/v), had little specific effect on glucose metabolism. 6. Although equilibrium plasma glucose concentrations in different rats under halothane were widely different (4-8 mmol/l) the rates of utilization were very similar (2.5-3.1 micronmol/min per 100 g), indicating that these rates were determined by the production of glucose from gluconeogenic precursors released by basal metabolism, the rate of which is necessarily similar in different rats. 7. Among rats under halothane anaesthesia plasma insulin concentrations were negatively correlated with rate coefficients, showing that the differences between rate coefficients were mostly accounted for by differences between rats in tissue sensitivities to insulin. Thus in each 24h-starved rat, sleeping or resting, the main regulators of the plasma glucose concentrations were the rate of supply of gluconeogenic substrates from energy metabolism and the intrinsic sensitivity of the tissues to insulin. 8. We found that a commonly used deionization method of purifying glucose for determination of its specific radioactivity was inadequate.

Anesthesia, Inhalation↗
PubMed1977

Glucose turnover in the post-absorptive rat and the effects of halothane anaesthesia.

1. Rates and rate coefficients of glucose utilization and replacement in post-absorptive rats, either conscious or under halothane anaesthesia, were determined in a thermoneutral environment by using [5-3H]- and [U-14C]glucose. Label was not injected into rats under halothane until about 0.5h after anaesthesia was initiated. 2. Comparison with the results for 24h-starved rats in the preceding paper [Heath et al. (1977) Biochem. J. 162, 643-651] showed that insulin concentrations were considerably higher but rate coefficients for glucose utilization were little altered in post-absorptive rats. Sensitivity to insulin was thus considerably increased by a 24h period of starvation in the rat. 3. Fractional recycling of glucose carbon in post-absorptive rats was under one-half of that in starved rats, reflecting the larger contribution of liver glycogenolysis to glucose production in the former. 4. In post-absorptive rats halothane decreased the mean rate of glucose utilization by about 17%. This decrease was associated with an increase in mean plasma insulin concentration, showing that halothane decreased sensitivity to insulin. 5. Recycling was slightly increased by halothane, indicating that the contribution of liver glycogen to the total glucogenic rate was decreased, probably because liver glycogen concentration were about 40% lower throughout the rate determinations in halothane. 6. Comparison of our results with earlier work shows that during and shortly after induction of halothane anaesthesia glucose turnover must have been greatly increased whereas from about 0.5h after induction it was decreased.

Anesthesia, Inhalation↗
PubMed1977

The site of insulin resistance after injury.

Intracellular glucose concentrations in skeletal muscle have been measured in normal and injured rats individually infused with 51Cr-EDTA as an extracellular space marker. In normal rats, even when infused with glucose at a high rate, membrane transport appeared to be the rate-limiting step in glucose utilization by muscle. After injury the concentration of intracellular glucose was increased, and positively correlated with that in plasma, showing that the loss of sensitivity to insulin after injury is due to impairment of an intracellular metabolic step.

Animals↗
PubMed1976

Effects of metformin on insulin resistance after injury in the rat.

Hyperglycaemia and insulin resistance occur after injury. The effects of the antidiabetic biguanide metformin in injured rats have been studied in order to elucidate the cause of these effects. Metformin (120 mg/kg S. C.) produced a significant hypoglycaemic effect after a 20% dorsal scald but did not affect the blood glucose concentration in non-injured rats. The hypoglycaemic effect did not result from increased insulin secretion. It was associated with a reduction in liver glycogen and an increase in blood lactate concentrations, suggesting that the drug acted by promoting peripheral glucose utilization. This was confirmed by measuring the clearance rate coefficient of [5-3H]glucose. This rate coefficient was significantly increased by metformin treatment (140 mg/kg S. C.) in scalded rats, although it was not affected in non-injured rats. Intravenous glucose tolerance in scalded rats was not improved, probably because of the increased lactate concentration. Metformin (120-160 mg/kg) also produced a hypoglycaemic effect in rats after a 4 hrs period of bilateral hind-limb ischaemia, suggesting that similar metabolic changes occur after these two types of injury.

Animals↗
PubMed1976

Disappearance of 125I-labelled and unlabelled insulins from blood in normal and injured rats.

1. The disappearance from blood of either 125I-labelled bovine insulin or unlabelled rat insulin after a single intravenous injection has been studied in rats. 2. The disappearance of the labelled insulin was slower than that of native insulin. 3. Ether anaesthesia produced a significant impairment, and bilateral nephrectomy a very marked impairment, of disappearance of the labelled insulin, suggesting that changes in the removal of this tracer may nevertheless parallel changes in the metabolism of native insulin. 4. Simultaneous intravenous injection of unlabelled bovine insulin (1 unit/kg) did not affect disappearance of the labelled insulin. 5. A 20% full-thickness scald injury, produced 2 h previously, had no significant effect on disappearance of the labelled insulin, either with or without the simultaneous administration of unlabelled bovine insulin. 6. The disappearance of unlabelled rat insulin from plasma was also similar in control and scalded rats. 7. It was concluded that the half-life of plasma insulin in the rat, as estimated by either of the techniques used, is not significantly affected by this severe non-haemorrhagic injury.

Animals↗
PubMed1976

Effects of insulin-free plasma on the charcoal-separation method for radioimmunoassay of insulin.

Radioimmunoassay of insulin in rat plasma using a popular method (Albano, Ekins, Maritz and Turner 1972) involving charcoal-separation of free and antibody-bound insulin was found to be unsatisfactory despite inclusion in standard tubes of insulin-free plasma prepared in either of two ways. Insulin-free plasma and untreated plasma had different effects on adsorption of free insulin to the charcoal. It was concluded that separation with charcoal is very sensitive to any prior treatment of the plasma. Particular care must be taken to ensure that hormone-free plasma is identical in all other respects to untreated plasma.

Animals↗
PubMed1976

Insulin secretion after injuries of differing severity in the rat.

The effects on insulin secretion of injuries of differing severity have been studied in the rat. The injuries used were dorsal scalds to 20% and 40% of the body surface area, and a 4-h period of bilateral hind-limb ischaemia. These injuries resulted in 48 h mortality rates of 0/10, 7/10 and 5/10 respectively. Rats were studied 1-5-2 h after scalding or removal of tourniquets. The blood glucose concentration was markedly raised after all these injuries, and the plasma insulin concentration was also raised, so that the insulin to glucose ratio in any group did not differ significantly from that in non-injured controls. Injection of glucose (0-5 g/kg i.v.) induced a rise in insulin concentration in all groups, although the insulin to glucose ratio after the lethal 40% scald was lower than in control rats. It was concluded that in the rat normal insulin secretion is maintained even after lethal injuries, although some suppression of the insulin response to exogenous glucose may occur. Insulin resistance is more important in the rat than impairment of insulin secretion even at an early stage after injury.

Animals↗
PubMed1975

Effects of burn injury on insulin secretion and on sensitivity to insulin in the rat in vivo.

Both insulin resistance and impairment of insulin secretion are know to occur in man after injury. The relative importance of these effects was studied in rats 2 h after a non-lethal 20 percent dorsal scald. No impairment of insulin secretion was found after this injury. Concentrations of both blood glucose and plasma insulin were elevated in scalded rats. Scalded rats responded to intravenous glucose injection (1-0 g/kg) with a further rise in plasma insulin concentration, which remained normal for the prevailing blood glucose concentration. However, marked impairment of glucose tolerance was observed, indicating the presence of insulin resistance. After intravenous insulin injection (1-0 U/kg) the initial rate coefficient for fall of blood glucose concentration was significantly lower (p less than 0-02) in scalded (mean 3-9 percent min.(-1) than in control rats (mean 6-3 percent min.(-1). The minimum in blood glucose concentration after insulin injection was reached at 10 min. in control rats, but not until 60 min. after injection in scalded rats. This difference was due to a delay in compensation for the hypoglycaemia in the scalded rats, since the rate of disappearance of insulin measured by injection of a tracer of 125I-labelled bovine insulin was not decreased after this injury. It was concluded that the impairment of glucose utilization in scalded rats (Heath and Corney, 1973) is due to decreased sensitivity to insulin rather than to suppression of insulin release.

Animals↗