Oxygen consumption normal value

Another phenomenon which is difficult to interpret on the ketolysis basis is the finding that the rate of utilization of the ketones rises sharply with increased concentrations in the blood and tissues. The quantities oxidized under such circumstances apparently have no relationship to the carbohydrate utilized. In fact, they may practically exclude the oxidation of other metabolites since they have been reported to account for 90% of the total oxygen consumption at sufficiently high concentrations. However, such levels of ketones are never found normally and possibly a different relationship to carbohydrate occurs at physiological values. Likewise it is not clear whether a similar response would be expected if the natural isomer alone were administered. 

This curve demonstrates the relationship between oxygen delivery (Do2) and oxygen consumption (Vo2). The latter is normally around 200 ml.min-1 and you should demonstrate that it is not affected until delivery falls to below approximately 300 ml.min-1, which is known as critical Do2. When 02 delivery is less than this, consumption becomes supply dependent. Above the critical value, it is termed supply independent. 

Table 1. Tissue responsiveness to thyroid hormone. Effect of thyroid hormone on oxygen consumption and malic enzyme mRNA levels compared to nuclear T3-binding capacity. Data for selected tissues in adult rats were adapted from the cited references. Oxygen consumption (cu.mm./mg wet weight/h) is the ratio in euthyroid versus thyroidectomized (Tx) rats. The fold of induction of malic enzyme mRNAs was calculated from values obtained from tissues of euthyroid rats and rats treated for 10 days with ISpg T3/IOO g b.w. The binding capacity was measured in normal rats.

Vitamin provides the co-enzyme necessary for the pyruvate oxidation. Avitaminous brain tissue has a lowered rate of oxygen consumption, which Peters has shown may be restored to the normal value by addition of vitamin Bj. 

Iron removal Increased iron and ferritin levels are found in approx. 30% of patients with chronic hepatitis B or C. Several studies have shown that the success rate of interferon therapy is reduced in the presence of elevated liver iron values. This is attributed to the fact that iron overload inhibits not only lymphocyte proliferation, but also the function of killer cells and B cells as well as the production of antibodies. Iron plays a role in the formation of free radicals and the occurrence of dangerous lipid peroxidations, (s. pp 68, 401) Furthermore, iron, like oxygen radicals, promotes fibrogenesis. Iron removal leads to an improvement in laboratory parameters and better response to interferon-a therapy. (217, 243) On the other hand, the iron level is reduced as a result of successful IFN therapy. In the case of a higher serum iron status before the initiation of interferon therapy, venesections at one week intervals should be considered, if necessary until normal laboratory values (iron, ferritin, transferrin saturation) have been restored. During interferon therapy, a low-iron diet is advisable, as is the consumption of 2 x 1 cup of black tea (in the morning and at noon) to reduce iron absorption through chelate formation ( cheap, free of side effects and useful )- (s. p. 625) Silymarin also leads to iron mobilization due to chelate formation. 

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