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Biomedical subjects

K Henderson

Publications and source records attributed to K Henderson.

67 records · Page 4Linked to original sources
PubMed1979

Effect of supplemental glucose or sucrose on liver and carcass glycogen metabolism of young chicks.

An experiment was conducted with Leghorn chicks to evaluate the effect of glucose or sucrose on liver and carcass glycogen. Phosphorylase a and synthase a were assayed to learn if glycogen cycle enzymes could be influenced by the early plane of nutrition. Both glucose and sucrose in drinking water increased liver and carcass glycogen in 3-day-old chicks. Groups given sucrose had more liver glycogen than groups given glucose after 5 days. Supplementary glucose given to fed chicks resulted in an increase in glycogen synthase a and a decrease in glycogen phosphorylase a at 4 days of age. By 6 days of age, differences in synthase activity between groups given sucrose or glucose were small. However, glucose solutions decreased phosphorylase a activity. The relationship between synthase a and phosphorylase a also partially regulates glycogen metabolism.

Age Factors↗
PubMed1979

Control of glycogen metabolism in the developing turkey poult.

An experiment was conducted with young turkey poults to evaluate factors controlling glycogen metabolism in the period following hatching. Glucose and sucrose solutions were given along with a standard starter diet. Liver and carcass glycogen were measured on days 1, 4 and 6. Liver glycogen synthetase (EC 2.4.1.21) and phosphorylase (EC 2.4.1.1) were also assayed at these times. The characteristics of active and inactive glycogen synthetase at these times were determined and sensitivity of the active and inactive forms were related to physiological concentrations of glucose-6-phosphate. Supplemental glucose or sucrose increased carcass glycogen in comparison to controls; however, but sucrose was more effective than glucose in promoting liver glycogen synthesis in 4- and 6-day-old poults. There was an age dependent increase in carcass glycogen between days 1 and 6, but a decrease in liver glycogen between days 4 and 6. The activation of liver glycogen synthetase is incomplete in 1 day old poults but activity increases during the 1st week of life. Activation of glycogen synthetase decreased the apparent Ka for glucose-6-phosphate. Phosphorylase inactivation in vitro was not affected by age. Liver glucose-6-phosphate increases rapidly after hatching and the concentration is related to the in vitro Ka derived for both active and inactive synthetases. Both glucose and sucrose increased liver glucose-6-phosphate at days 4 and 6 as well as glycogen synthetase activity. The increase in enzyme activity may be caused indirectly by an allosteric effect of glucose-6-phosphate. Phosphorylase, while not affected by supplemental carbohydrates, did decrease in activity between days 4 and 6. The decrease in activity could affect the phosphorylase a/ synthetase a ratio and change glycogen metabolism.

Aging↗
PubMed1978

Glycogen metabolism in the turkey embryo and poult.

Fertile eggs from Large White turkey hens were classified according to weight at time of incubation. Glycogen was measured in the 21-day-old embryo and one-day-old poult. Liver glycogen was positively correlated with initial egg weight in the 21-day-old embryo and negatively related to initial egg weight in the one-day-old poult. Glycogen recycling was evident in the one-day-old poult. Maximum accumulation of 14C-glucose as glycogen occurred 60 min post injection. Liver phosphorylase a level was higher in the one-day-old poult than the embryo. Total phosphorylase per gram of liver tissue was not different between the two age groups. Liver phosphorylase b was subject to conversion to phosphorylase a in both age groups. Avian phosphorylase exists in both the active and inactive form.

Animals↗
PubMed1978

Glycogen depletion and repletion in the chick.

Carcass glycogen was degraded by chicks at a faster rate than liver glycogen during the first 72 hr of a 120 hr fast. Degradation of both sources of glycogen proceeded at a slower rate during the final 48 hr. Carcass glycogen was repleted at a greater rate than liver glycogen.

Animals↗
PubMed1978

Effect of dietary energy on hepatic glycogen metabolism in the turkey hen.

An experiment was conducted with turkey hens to investigate the effect of substituting 30% of the carbohydrate calories with corn oil, 1,3-butanediol, or glycerol. Birds fed additional corn oil had the lowest liver glycogen concentration. Corn oil increased phosphorylase, a total phosphorylase, and glycogen synthetase I in comparison to the controls. Also, additional corn oil resulted in the highest specific activity of glucose-6-phosphatase. Dietary glycerol caused the highest concentration of liver glycogen. Glycerol increased glycogen synthetase I, but had little effect upon total activity in comparison to butanediol in the diet. Both butanediol and glycerol gave similar phosphorylase a activity, but butanediol increased total activity. The fat-fed and control-fed hens regulated hepatic glycogen concentration through phosphorylase, while glycerol and butanediol-fed hens regulated glycogen through glycogen synthetase. In vitro activation of glycogen synthetase I was deficient in hens fed additional corn oil, indicating a lack of glycogen synthetase phosphatase activity. The order of activation (glycerol greater than butanediol greater than control greater than corn oil) corresponds to the rank of glycogen concentrations

Animals↗
PubMed1977

Muscle protein catabolism in the septic patient as measured by 3-methylhistidine excretion.

Muscle protein catabolism has been evaluated using the excretion of urinary 3-methylhistidine (3-MEH) is six normal male and six normal female subjects and in four surgical patients, two of whom developed febrile episodes during the course of their study. In addition, their nutritional status was also evaluated using percentage body weight losses before hospital admittance, creatinine-height ratios, and, in two patients, serum alkaline ribonuclease levels. The results indicate that: 1) prolonged starvation may produced decreased 3-MEH excretion because of an adaptive diminution of muscle breakdown in sustained starvation, decreased 3-MEH excretion also may simply reflect diminished lean body mass, 3-MEH excretion may be increased above basal levels because of superimposed stresses such as fever, and the acute phases of starvation produce increased levels of 3-MEH excretion until adaptive mechanisms occur; 2) creatinine-height ratios are low in starvation, and increase not only with improved nutrition but in response to fever and stress of operation, even when these are superimposed on malnutrition; and 3) alkaline RNAase levels are elevated in malnutrition and decrease with improved nutrition but in response to fever and stress of operation, even when these are superimposed on malnutrition; and 3) alkaline RNAase levels are elevated in malnutrition and decrease with improved nutrition. The enzyme may also be elevated by the stress of operations.

Adult↗
PubMed1975

Cellular glucose utilization during hemorrhagic shock in the pig.

To clarify the changes in glucose homeostasis which occur following injury, pigs were subjected to hemorrhagic shock. During shock increased levels of free glucose occurred in red blood cells and muscle tissue, suggesting that inhibition of glucose phosphorylation was occurring. Simultaneously systemic plasma glucose levels were noted to be higher than portal plasma glucose levels while levels of free glucose within the liver fell, indicating that the liver was mobilizing glucose. Plasma insulin and phosphate levels were observed to rise throughout the experiment. From this study it was concluded that the hyperglycemia of injury in these animals was caused by a combination of decreased cellular glucose utilization due to diminished phosphorylation and increased mobilization of glucose by the liver.

Animals↗
PubMedDate not supplied

Continuous caudal anesthesia for inguinal hernia repair in former preterm infants.

STUDY OBJECTIVE: To determine the feasibility of continuous caudal anesthesia with 2-chloroprocaine in conscious former preterm infants undergoing inguinal hernia repair. DESIGN: Prospective study. SETTING: University-affiliated children's hospital. PATIENTS: Ten former preterm infants, ASA physical status II and III, who were 35 to 49.5 weeks postconceptional age at the time of surgery. INTERVENTIONS: Caudal anesthesia was administered via an indwelling catheter using a loading dose of 1 ml/kg (30 mg/kg) of 3% 2-chloroprocaine, followed by incremental doses of 0.3 ml/kg (9 mg/kg) to achieve a level of T4 to T2. The block was maintained by a minimum infusion rate of 30 mg/kg/hr (1 ml/kg/hr) of the same local anesthetic solution. MEASUREMENTS AND MAIN RESULTS: The mean cumulative dose of 2-chloroprocaine was 2.8 +/- 1.0 ml/kg/hr (84 +/- 30 mg/kg/hr) infused over a mean duration of 95 +/- 35 minutes. Serum cholinesterase concentration and plasma 2-chloroprocaine concentration were measured in five infants. CONCLUSIONS: Three percent 2-chloroprocaine can be used effectively for continuous caudal anesthesia in conscious, former preterm infants for inguinal hernia and penoscrotal surgical procedures lasting 85 to 170 minutes.

Anesthesia, Caudal↗