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Biomedical subjects

G F Merrill

Publications and source records attributed to G F Merrill.

62 records · Page 4Linked to original sources
PubMed1978

Glucose and lactate kinetics in guinea pigs following Escherichia coli endotoxin administration.

Glucose and lactate turnovers were evaluated during the early stages (first three hours) of endotoxin-induced shock in unanesthetized male guinea pigs following the intravenous (IV) administration of 0.1 mg of Escherichia coli endotoxin. Rate of appearance (Ra), rate of disappearance (Rd), and metabolic clearance rate (MCR) of glucose and lactate were determined by the primed-constant infusion of [6-(3)H]-glucose and NA L(+)[U-14C]-lactate. Arterial glucose concentration was moderately elevated, and the Ra and Rd of glucose were increased significantly following endotoxin administration, while the slight increase in MCR was not statistically significant. Arterial lactate concentration was markedly increased and the Ra and Rd of lactate were significantly elevated. The percentage of [14C]-glucose derived from [14C]-lactate increased from 19% (control) to above 50% following endotoxin. From these data we found no evidence of impaired peripheral extraction of glucose. The increased glucose Ra and the higher percentage of [14C]-glucose being derived from [14C]-lactate suggest increased gluconeogenesis during the early stages following endotoxin administration.

Animals↗
PubMed1977

Effects of multiplication stimulating activity (MSA) on AIB transport into myoblast and myotube cultures.

The effects of a somatomedian analog, Temin's multiplication stimulating activity (MSA), on amino acid transport into muscle cells have been characterized in a series of experiments on myoblasts and myotubes in culture. Addition of MSA to serum-starved L6 myoblasts increased the rate of aminoisobutyrate (AIB) uptake 50-150% within five hours. This early effect on transport was followed by increases in cell number, protein content and 3H-thymidine incorporation. Kinetic analyses indicated that MSA increased the maximal velocity of AIB uptake but had no effect on the KM for AIB. When myoblasts were allowed to fuse (and dividing cells eliminated by addition of 10(-4) M cytosine arabinoside) the AIB transport system(s) remained similarly responsive to MSA. In myoblasts and in myotubes, both the basal and MSA-stimulated rate of AIB uptake were sodium-dependent processes; little stimrulation occurred if sodium was absent from the labeling medium. Further suggesting the involvement of cations in response to hormone, MSA stimulated uptake of the potassium analog, 86Rb+, and increase net intracellular potassium in both myoblasts and myotubes. MSA was active at concentrations equivalent to in vivo levels of somatomedins; neither insulin nor growth hormone had any effect at or near physiological concentrations.

Aminoisobutyric Acids↗
PubMed1977

Regional blood flow redistribution during early burn shock in the guinea pig.

The distribution of blood flow was determined with radioactive microspheres following scald injury in guinea pigs. Burn was induced in halothane-anesthetized guinea pigs by a 3-sec immersion to the xiphoid process in 100 degree C water. Cardiac output and fractional blood flow measurements were made at preburn, 15-min postburn, and 75-min post-burn. In the scalded animals cardiac output decreased 58% by 75 min postburn. Three different blood flow responses to burn were noted: a) Brain, heart, hepatic artery, and adrenals received an increased fraction of the cardiac output; b) the fractional distribution of the diaphragm, liver (portal), spleen, gastrointestinal tract, muscle (from burned portion of the body), and bone remained constant; while c) the pancreas, burned skin, nonburned skin, and adipose tissue received a reduced fraction of the cardiac output. Although some regions of the body (i.e., brain and heart) received a greater percentage of the total cardiac output after burn injury, the cardiac output decrease was sufficient to cause a depression in absolute blood flow to all but two sites (adrenals and hepatic artery).

Animals↗
PubMedDate not supplied

Inhibition of adenosine deaminase and administration of adenosine increase hypoxia induced ventricular ectopy.

Eighteen anesthetized, instrumented beagles (both genders, 10.4 +/- 0.5 kg) were used to investigate the effects of administered adenosine (n = 6), erythro-9-(2-hydroxy, 3-nonyl)adenine (EHNA), a potent inhibitor of endogenous adenosine deaminase (n = 6), and saline (n = 6), on the incidence of ventricular arrhythmias caused by systemic hypoxia (5% O2, 95% N2, PaO2 = 21 +/- 3 mmHg). After dogs were instrumented and monitored variables were in the steady-state, the above compounds were infused continuously into the cannulated left anterior descending (LAD) coronary artery for three minutes before, and throughout a four-minute period of hypoxia. After approximately 4 min of hypoxia the rates of ventricular ectopy [(total beats-normal beats)/total beats x 100 = % ectopy] were 73 +/- 9%, 73 +/- 11%, and 35 +/- 8% for the three groups, respectively. The percent ectopy of the adenosine- and EHNA-treated dogs was significantly greater (p < 0.05) than that for the saline-treated controls. These findings suggest that adenosine contributes to the ventricular arrhythmias of experimental systemic hypoxia.

Adenine↗