Clinical use of a portable electronic device to measure haematocrit.

A small portable device called the blood electrometer (BEM) was developed to assist clinicians to distinguish patients with extreme blood loss from those with normal packed cell volumes. Blood was collected in 5 ml lithium heparin tubes from 80 normal controls and 24 patients in an intensive care unit. BEM and accurate microcentrifugal techniques were compared. Intraclass correlation coefficients between the techniques of r = 0.96 and r = 0.93 were found in the normal controls and patients respectively. Because the BEM operates on the principle of conductivity, changes in some of the biochemical variables which could influence conductivity were investigated in the patients. Mean plasma total protein and albumin concentrations were lower compared with normal reference ranges. Six of the 24 patients were acidotic and 4 alkalotic. Leucocyte counts obtained randomly from 13 patients were elevated. Changes in measurements which could influence conductivity did not affect the BEM reading. We conclude that the portable BEM could be of great value in circumstances where a fixed power source is not available and rapid haematocrit measurements in a large number of patients are required.

Effect of desferrioxamine on reperfusion damage of rat heart mitochondria.

Ischaemia of the myocardium leads to necrosis unless oxygen supply is restored but it has only recently been realised that reperfusion is not without danger. The greatest rate of myocardial damage, as measured by mitochondrial function, occurred during the first 5 minutes of reperfusion in rat hearts subjected to normothermic ischaemic cardiac arrest. Addition of desferrioxamine to the perfusate after 5 minutes of reperfusion did not reverse the mitochondrial damage. It is therefore concluded that desferrioxamine prevents mitochondrial damage caused by ischaemia-reperfusion but does not reverse the damage already present.

Vitamin B-6 nutrition status and cigarette smoking.

We investigated the vitamin B-6 status in smokers, nonsmokers, and exsmokers by measuring both B-6 aldehyde vitamers, pyridoxal-5'-phosphate (PLP) and pyridoxal (PL), in the plasma as well as in the erythrocyte compartment. Two hundred eighty-six healthy, sedentary male workers from a middle-income group were investigated. There were 159 smokers, 59 exsmokers, and 68 nonsmokers. Plasma PLP and PL concentrations were significantly lower in smokers than in the nonsmokers and exsmokers whereas erythrocyte PLP and PL did not differ significantly between groups. Because PLP mainly functions as an intracellular coenzyme, the clinical significance of a depressed plasma PLP concentration alone is uncertain. It is concluded that circulating plasma PLP is labile and not necessarily indicative of intracellular PLP concentrations. The measurement of erythrocyte PLP and/or PL may be more informative about vitamin B-6 status than is plasma PLP alone.

The effect of allopurinol and deferrioxamine on rat heart mitochondrial oxidative phosphorylation after normothermic ischemic cardiac arrest and of reperfusion.

The electron transport chain of the mitochondria is highly sensitive to myocardial ischemia. As free oxygen radicals take part in the damage that occurred during ischemia, this study was undertaken to determine if allopurinol and deferrioxamine had any beneficial effect on mitochondrial function. Our results showed that perfusion with allopurinol did not improve the mitochondrial function, but that reperfusion with allopurinol and deferrioxamine had a beneficial effect. We came to the conclusion that xanthine oxidase, as a generator of superoxide anions, is of minor importance in comparison with the hydroxyl radicals, which are probably formed in the presence of iron in the cell.

Effect of normothermic ischemic cardiac arrest and of reperfusion on the free oxygen radical scavenger enzymes and xanthine oxidase (a generator of superoxide anions).

Recent evidence suggests that free oxygen radicals are produced by ischaemic tissues, accounting for at least part of the damage that results. These free oxygen radicals are produced by xanthine oxidase, amongst others, and removed by scavenger enzymes (catalase, superoxide dismutase and glutathione peroxidase) and anti-oxidants. As mitochondria are oxygen-utilising organelles, they are capable of producing free oxygen radicals. Our results indicate that the removal of free oxygen radicals are not diminished during ischaemia, but the activity of the free oxygen radical generator, xanthine oxidase, is increased. This could lead to an increased superoxide anion concentration.