Control of pH during hypothermic liver storage. Role of the storage solution.
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Adenosine Triphosphate↗
Biomedical subjects
A L Busza
Publications and source records attributed to A L Busza.
Glucose-containing organ preservation solutions and intracellular acidosis.
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Adenosine↗
Spectral resolution in clinical magnetic resonance spectroscopy.
We observe linewidths of 0.1-0.4 ppm in 31P spectra of human muscle, liver, and brain. T2 measurements of muscle phosphocreatine, together with previous brain studies, indicate that further improvements in linewidth to 0.02-0.05 ppm might often be achieved, but in some lesions magnetic susceptibility variations may limit spectral resolution.
Brain↗
Evidence for negative cooperativity in human erythrocyte sugar transport.
1. When D-glucose exchange influx is measure over a wide range of concentrations then two affinity constants (2.27 and 26.0 mM) are evident. This is consistent with a transport model (the allosteric pore model) in which there is negative cooperativity between subunits of the transport protein. 2. The equations for the allosteric pore model interacting with two substrates (or a substrate and an inhibitor) have been derived and have been used to analyse data from exchange inhibition and for mixed infinite-trans uptake experiments. 3. The exchange inhibition of tracer 3-O-methyl-D-glucose, D-xylose and D-fructose uptake by D-glucose also shows evidence for negative cooperativity and for two inhibition constants which are approximately equal to the D-glucose equilibrium exchange affinity constants. 4. The uptake of D-glucose into infinite-trans D-glucose or 3-O-methyl-D-glucose gives Km values of 2.6 and 2.33 mM, respectively. The uptake of 3-O-methyl-D-glucose into infinite-trans D-glucose or 3-O-methyl-D-glucose gives Km values of 6.0 and 4.6 mM, respectively. V values are slightly higher when the internal sugar is 3-O-methyl-D-glucose. 5. In cells that are treated with fluorodinitrobenzene the apparent Ki value for D-glucose inhibition of tracer D-fructose uptake is lowered. It is proposed that this is due to a partially selective effect of FDNB on the internal subunit interface stability constant (the internal pore gate).
Biological Transport, Active↗
Brain metabolism and blood flow in acute cerebral hypoxia studied by NMR spectroscopy and hydrogen clearance.
We have developed a reliable, reproducible model of hypoxia in the gerbil. 1H and 31P NMR spectroscopy demonstrates that cerebral energy metabolism is very resistant to hypoxia. Cerebral blood flow (measured by hydrogen clearance) began to increase when the arterial oxygen tension (paO2) was reduced to 40-50 mm Hg, and there was no change in phosphorus metabolites or lactate until paO2 was below 40 mm Hg. In 50% of the animals lactate increased prior to any change in the phosphorus metabolites or intracellular pH, suggesting that 1H NMR may be more sensitive than 31P NMR at detecting hypoxic or ischaemic changes. The calculated rate of oxygen delivery at a time when phosphorus energy metabolism becomes impaired is similar in both hypoxia and ischaemia (ca 4mL/100 g/min). We suggest that the critical factor in ischaemia is the reduction in oxygen supply, rather than the accumulation of toxic metabolites, such as lactate.
Animals↗
Controllable graded cerebral ischaemia in the gerbil: studies of cerebral blood flow and energy metabolism by hydrogen clearance and 31P NMR spectroscopy.
A technique for remotely controlling the degree of carotid artery occlusion in the gerbil model of cerebral ischaemia has been developed. The technique relies on manually adjustable nylon snares around the carotid arteries, in conjunction with a computer-based monitoring system, to control the degree of occlusion. This has allowed us to determine the dependence of energy metabolism (as assessed by 31P NMR spectroscopy) on blood flow in greater detail than was possible in our previous studies. Data obtained show that energy changes first appear at flows of 25-30 mL/100 g/min, while at flows below 20 mL/100 g/min there is a major derangement of energy metabolism. The model was used to determine the sensitivity of cerebral energy metabolism to reduced cerebral blood flow under normothermic conditions and in mild hypothermia (30 degrees C). Hypothermia had a protective effect in that energy metabolites were maintained at flows significantly below the normothermic threshold.
Adenosine Triphosphate↗