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Biomedical subjects

C E King

Publications and source records attributed to C E King.

At least 19 recordsLinked to original sources
PubMed1990

Effect of helium-neon laser auriculotherapy on experimental pain threshold.

This study was conducted to examine the effects of helium-neon laser auriculotherapy on experimental pain threshold. Eighty healthy female and male subjects, aged 18 to 39 years, were assigned randomly to one of two treatment groups. Subjects in the Experimental Group (n = 41) received laser stimulation, and subjects in the Control Group (n = 39) received sham stimulation to appropriate acupuncture points on the left ear. Experimental pain threshold at the ipsilateral wrist was determined with an electrical stimulus immediately before and after treatment. The mean change (posttreatment minus pretreatment) for the Experimental Group was greater than the mean change for the Control Group (p less than .05). The Experimental Group demonstrated a statistically significant (p less than .05) increase in mean pain threshold after treatment, but the Control Group did not. Results indicate that helium-neon laser auriculotherapy can increase experimental pain threshold and suggest a possible alternative for patients intolerant of transcutaneous electrical nerve stimulation.

Adult↗
PubMed1989

Determination of the steady-state turnover rates of the metabolically active pools of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate in human erythrocytes.

When intact human erythrocytes are incubated at metabolic steady state in a chloride-free medium containing [32P]Pi, there is rapid labelling of the gamma-phosphate of ATP, followed by a slower labelling of the monoester phosphate groups of phosphatidylinositol 4-phosphate (PtdIns4P) and phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] [King, Stephens, Hawkins, Guy & Michell (1987) Biochem. J. 244, 209-217]. We have analysed the early kinetics of the labelling of these phosphate groups, in order to determine: (a) the steady-state rates of the interconversions of phosphatidylinositol, PtdIns4P and PtdIns(4,5)P2; and (b) the fractions of the total cellular complement of PtdIns4P and PtdIns(4,5)P2 that participate in this steady-state turnover. The experimental data most closely fit a pattern of PtdIns4P and PtdIns(4,5)P2 turnover in which one-quarter of the total cellular complement of each lipid is in the metabolic pool that participates in rapid metabolic turnover, with rate constants of 0.028 min-1 for the interconversion of PtdIns and PtdIns4P, and of 0.010 min-1 for the PtdIns4P/PtdIns(4,5)P2 cycle. These rate constants represent metabolic fluxes of approx. 2.1 nmol of lipid/h per ml of packed erythrocytes between PtdIns and PtdIns4P and of approx. 5.7 nmol/h per ml of cells between PtdIns4P and PtdIns(4,5)P2.

Adenosine Triphosphate↗
PubMed1988

Comparative evaluation of gastrointestinal intolerance produced by plain and tri-buffered aspirin tablets.

Two multi-investigator, double-blind, randomized, placebo-controlled, crossover trials were conducted to determine whether tri-buffered formulations of both regular strength aspirin and extra strength aspirin would be less likely than plain aspirin to provoke subjective gastrointestinal (GI) intolerance. Each trial was divided into two phases, a qualification phase and a test phase. During the qualification phase, subjects with a history of gastrointestinal intolerance to aspirin were randomized to a double-blind crossover treatment with aspirin and placebo (325 mg aspirin per tablet in study 1 and 500 mg aspirin per tablet in study 2), two tablets four times a day for 3 days or until the occurrence of stomach upset. Subjects who reported gastrointestinal symptoms with aspirin and not with placebo qualified to participate in the test phase of the study. They were rerandomized to participate in a three-way crossover study of plain aspirin, tri-buffered aspirin, and placebo in the test phase. Tri-buffered aspirin was associated with an appreciable reduction in the incidence of gastrointestinal upset relative to plain aspirin, 34 percentage points in study 1 (p less than 0.001) and 33 percentage points in study 2 (p less than 0.001). Similar results were obtained in the evaluation of the reduction of the severity of gastrointestinal symptoms.

Adult↗
PubMed1987

Multiple metabolic pools of phosphoinositides and phosphatidate in human erythrocytes incubated in a medium that permits rapid transmembrane exchange of phosphate.

1. A Hepes-based medium has been devised which allows rapid Pi exchange across the plasma membrane of the human erythrocyte. This allows the metabolically labile phosphate pools of human erythrocytes to come to equilibrium with [32P]Pi in the medium after only 5 h in vitro. 2. After 5-7 h incubation with [32P]Pi in this medium, only three phospholipids, phosphatidic acid (PtdOH), phosphatidylinositol 4-phosphate (PtdIns4P) and phosphatidylinositol 4,5-bisphosphate (PtdIns4,5P2) are radioactively labelled. The concentrations of PtdIns4P and PtdIns4,5P2 remain constant throughout the incubation, so this labelling process is a reflection of the steady-state turnover of their monoester phosphate groups. 3. During such incubations, the specific radioactivities of the monoesterified phosphates of PtdIns4, PtdIns4,5P2 and PtdOH come to a steady value after 5 h that is only 25-30% of the specific radioactivity of the gamma-phosphate of ATP at that time. We suggest that this is a consequence of metabolic heterogeneity. This heterogeneity is not a result of the heterogeneous age distribution of the erythrocytes in human blood. Thus it appears that there is metabolic compartmentation of these lipids within cells, such that within a time-scale of a few hours only 25-30% of these three lipids are actively metabolized. 4. The phosphoinositidase C of intact human erythrocytes, when activated by Ca2+-ionophore treatment, only hydrolyses 50% of the total PtdIns4,5P2 and 50% of 32P-labelled PtdIns4,5P2 present in the cells: this enzyme does not discriminate between the metabolically active and inactive compartments of lipids in the erythrocyte membrane. Hence at least four metabolic pools of PtdIns4P and PtdIns4,5P2 are distinguishable in the human erythrocyte plasma membrane. 5. The mechanisms by which multiple non-mixing metabolic pools of PtdOH, PtdIns4P and PtdIns4,5P2 are sustained over many hours in the plasma membranes of intact erythrocytes are unknown, although some possible explanations are considered.

2,3-Diphosphoglycerate↗
PubMed1987

Peripheral vascular responses to fluorocarbon administration.

To detect the local effect of hyperoxia on skeletal muscle vasculature, 2.5-ml boluses of oxygenated or deoxygenated fluorocarbon emulsion (F-O2 or F-N2) were washed through the hindlimb of anesthetized dogs at prevailing arterial pressure. Instantaneous hematocrit changes at the outflow were registered and stored in digital form with the red cells serving as the nondiffusible tracer in the resulting washout curves. A gamma density function was fitted and the gamma index (1/square root of alpha) was derived as a measure of skewness or perfusion heterogeneity. After recovery from the initial hypotensive reaction to fluorocarbon emulsion, washout curves for F-O2 and F-N2 were registered and blood samples were taken during 40 min of normoxia followed by 40 min of hypoxic hypoxia. The initial reaction to fluorocarbon significantly increased the gamma index so that the experiments began with a high index of perfusion heterogeneity in the limb vasculature. No significant difference was seen between F-O2 and F-N2 in normoxia but F-O2 maintained greater heterogeneity during hypoxia. The increased heterogeneity observed after the fluorocarbon reaction correlated highly with the severity of the hypotensive reaction which was also found to correlate inversely with the ability of the limb musculature to increase the O2 extraction ratio with onset of hypoxia. This blunting of microcirculatory reactivity to hyperoxia and hypoxia was attributed, in part, to the initial transient fluorocarbon reaction, possibly mediated by complement activation.

Animals↗
PubMed1987

Responses of innervated and denervated gut to whole-body hypoxia.

As a significant user of O2 at rest (20% of whole body), the gut may be subject to more severe limitation of O2 supply during global hypoxia than more vital areas because of preferential redistribution of blood flow. Accordingly, its accumulation of O2 deficit during hypoxia and its excess O2 use during normoxic recovery might be altered by extrinsic neural activity. We measured blood flow and O2 uptake in whole body (WB) and gut segments while anesthetized dogs were ventilated with 9% O2-91% N2 for 30 min followed by 30-min normoxic recovery. In six dogs extrinsic innervation to the gut segment was left intact and it was severed in another six animals. O2 deficit and excess were the accumulated differences from the normoxic O2 uptake for both gut and WB corrected for O2 stores changes. The intact gut, although only 4% body wt, incurred 22% of WB O2 deficit but contributed only 8% to WB O2 excess. The imbalance (gut excess was only 44% of gut deficit) implied that O2 using functions were curtailed during hypoxia without obligating an energy stores deficit. Denervation did not alter these quantitative relationships. Blood flow responses to transition between normoxia and hypoxia were only transiently altered. Extrinsic innervation apparently plays no major role in gut responses to WB hypoxia.

Animals↗
PubMed1987

Muscle O2 deficit during hypoxia and two levels of O2 demand.

We have examined the relative deficits in tension development and O2 uptake in contracting skeletal muscle during severe hypoxic hypoxia. Anesthetized mongrel dogs were ventilated to maintain an end-tidal PCO2 between 35 and 40 Torr. Venous outflow from the gastrocnemius muscle was measured using an electromagnetic flow probe. The tendon was cut and attached to a strain gauge. The muscle was stimulated to contract isometrically at 2 or 4 Hz for 20 min. Hypoxia (9% O2 in N2) was then imposed for 30 min, followed by 30 min of normoxia. Blood flow first increased in proportion to the contraction frequency and then increased further a similar amount in both groups during hypoxia. O2 extraction and blood flow reached maximal levels during hypoxia in the 2-Hz group. The further O2 deficit that was accumulated during 4 Hz and hypoxia was, therefore, a result of the greater discrepancy between O2 supply and demand. O2 uptake decreased more in hypoxia than did developed tension. These results are best explained by ATP supplementation from nonaerobic energy sources that was promoted by the free-flow condition of hypoxic hypoxia.

Animals↗
PubMed1987

Regional O2 uptake during hypoxia and recovery in hypermetabolic dogs.

The regional distribution of O2 deficit in muscle and nonmuscle tissues was measured in hypermetabolic dogs ventilated with a low inspired O2 fraction and was compared with excess O2 used in these regions during normoxic recovery. O2 uptake was stimulated by 2,4-dinitrophenol (DNP). Arterial, mixed venous, and muscle venous blood samples were drawn before, during, and after severe hypoxia (9% O2-91% N2) for the calculation of hindlimb O2 uptake and cardiac output. The O2 deficit and excess O2 uptake in recovery were calculated as the cumulative differences between normoxic control and respective hypoxic and recovery O2 uptake values. The DNP data were compared with data previously obtained in our laboratory. A greater whole-body O2 deficit was incurred in the DNP group during hypoxia and was associated with a larger O2 use in recovery. The total O2 deficit was equally distributed between muscle and nonmuscle tissues, but more excess O2 use occurred in nonmuscle tissues. The greater excess O2 used by nonmuscle tissues may have been associated with the restoration of intracellular ion concentrations brought about by the increased activity of energy-using membrane pumps.

2,4-Dinitrophenol↗
PubMed1987

Systemic and intestinal limits of O2 extraction in the dog.

When systemic delivery of O2 (QO2 = QT X CaO2, where QT is cardiac output and CaO2 is arterial O2 content) is reduced by bleeding, the systemic O2 extraction ratio [ER = (CaO2 - CVO2)/CaO2, where CVO2 is venous O2 content] increases until a critical limit is reached below which O2 uptake (VO2) becomes limited by O2 delivery. During hypovolemia, reflex increases in mesenteric arterial tone may preferentially reduce gut blood flow so that the onset of O2 supply dependence occurs in the gut before other regions. We compared the critical O2 delivery (QO2c) and critical extraction ratio (ERc) of whole body and an isolated segment (30-50 g) of small bowel in seven anesthetized paralyzed dogs ventilated with room air. Systemic QO2 was reduced in stages by controlled hemorrhage as arterial O2 content was maintained, and systemic and gut VO2 and QO2 were measured at each stage. Body QO2c was 7.9 +/- 1.9 ml X kg-1 X min-1 (ERc = 0.69 +/- 0.12), whereas gut O2 supply dependency occurred when gut QO2 was 34.3 +/- 11.3 ml X min-1 X kg gut wt-1 (ERc = 0.63 +/- 0.09). O2 supply dependency in the gut occurred at a higher systemic QO2 (9.7 +/- 2.7) than whole-body QO2c (P less than 0.05). The extraction ratio at the final stage (maximal ER) was less in the gut (0.80 +/- 0.05) than whole body (0.87 +/- 0.06). Thus during reductions in systemic QO2, gut VO2 was maintained by increases in gut extraction of O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

O2 delivery to contracting muscle during hypoxic or CO hypoxia.

The consequences of a decreased O2 supply to a contracting canine gastrocnemius muscle preparation were investigated during two forms of hypoxia: hypoxic hypoxia (HH) (n = 6) and CO hypoxia (COH) (n = 6). Muscle O2 uptake, blood flow, O2 extraction, and developed tension were measured at rest and at 1 twitch/s isometric contractions in normoxia and in hypoxia. No differences were observed between the two groups at rest. During contractions and hypoxia, however, O2 uptake decreased from the normoxic level in the COH group but not in the HH group. Blood flow increased in both groups during hypoxia, but more so in the COH group. O2 extraction increased further with hypoxia (P less than 0.05) during concentrations in the HH group but actually fell (P less than 0.05) in the COH group. The O2 uptake limitation during COH and contractions was associated with a lesser O2 extraction. The leftward shift in the oxyhemoglobin dissociation curve during COH may have impeded tissue O2 extraction. Other factors, however, such as decreased myoglobin function or perfusion heterogeneity must have contributed to the inability to utilize the O2 reserve more fully.

Animals↗