Oxygen consumption, tissue

Rat No. Body weight, e Interval after thyroid- ectomy, month Oxygen consumption Tissue Time after injection, hr. Administered 311 recovered per % of tissues found as ... 

The tiiyroid hormones influence every organ and tissue of tiie body. These hormones are principally concerned with increasing tiie metabolic rate of tissues, which results in increases in tiie heart and respiratory rate, body temperature, cardiac output, oxygen consumption, and the metabolism of fats, proteins, and carbohydrates. The exact mechanisms by which tiie tiiyroid hormones exert their influence 011 body organs and tissues are not well understood. 

In extrahepatic tissues, acetoacetate is activated to acetoacetyl-CoA by succinyl-CoA-acetoacetate CoA transferase. CoA is transferred from succinyl-CoA to form acetoacetyl-CoA (Figure 22-8). The acetoacetyl-CoA is split to acetyl-CoA by thiolase and oxidized in the citric acid cycle. If the blood level is raised, oxidation of ketone bodies increases until, at a concentration of approximately 12 mmol/L, they saturate the oxidative machinery. When this occurs, a large proportion of the oxygen consumption may be accounted for by the oxidation of ketone bodies. 

As metabolism increases, oxygen consumption and carbon dioxide production are enhanced. The concentration of hydrogen ions is also enhanced as more carbonic acid (formed from carbon dioxide) and lactic acid are produced by the working tissue. Furthermore, the concentration of potassium ions in the interstitial fluid is increased. The rate of potassium release from the cells due to repeated action potentials exceeds the rate of potassium... 

Figure 5. Oxygen consumption measurements of tumor lung tissue before and after exposure to an atmospheric Rn-d concentration of 6 WL unirradiated control tissue at the beginning of the...

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. 

In older rats (12-14 weeks), there was a significant increase in relative lung weights as compared to controls following 6 weeks of exposure to 260 ppm hexachloroethane. Oxygen consumption was not measured in these animals, and it is not clear if the tissues were examined histologically (Weeks et al. 1979). 

Exposure to hexachloroethane vapors can cause irritation to the respiratory system. Acute exposure to 260 ppm hexachloroethane had no apparent effect on the lungs and air passages in rats, but acute exposure to a concentration where particulate hexachloroethane was present in the atmosphere caused lung irritation (Weeks et al. 1979). On the other hand, intermediate-duration exposure to 260 ppm hexachloroethane appeared to cause some irritation of the respiratory epithelium, which may have increased susceptibility to respiratory infection. When exposure ceased, the animals recovered, so there were no histopathological indications of tissue damage after a 12-week recovery period. Lesions of the nasal passages, trachea, and bronchi increased mycoplasma infections mucus in the nasal cavities and decreased oxygen consumption were indicators of respiratory tract irritation from repeated episodes of hexachloroethane exposure. 

Low levels of mercuric chloride in polymorphonuclear cells may profoundly alter the cell respiratory burst, measured as chemiluminiscence, oxygen consumption and H2Oz production [171-173], depress phagocytic capacity [172, 173] and enhance release of lysosomal enzymes [ 172] with minimal loss of cell viability. A stimulation of oxygen metabolism in vivo might promote tissue injury, via the local production of free oxygen metabolites, in addition to depression of host defence [173],... 

The flux through the Krebs cycle can be estimated from the oxygen consumption of a cell or tissue. This has been done in a single human muscle during maximum physical... 

From the rate of oxygen consumption of a cell, a tissue or an organ, the rate of generation of ATP can be calculated. 

Unfortunately, it is not always possible to measure oxygen consumption for some cells or tissues in vivo for example, for cells that circulate in blood or in the lymph (e.g. red blood cells, immune cells), for different cells in one organ (e.g. macrophages in liver, glial cells in the brain,... 

The properties are as follows, (i) The activity of the protein (i.e. the inward transport of protons) is inhibited by ATP. (ii) The activity of the protein is increased by the presence of long-chain fatty acids, since they relieve the ATP inhibition, (iii) When mitochondria, isolated from brown adipose tissue, are incubated in the presence of fatty acids, there is a sharp increase in the rates of electron transfer, substrate utilisation and oxygen consumption, whereas the rate of ATP generation remains low. These studies indicate that the rate of proton transport, by the uncoupling protein, depends on the balance between the concentrations of ATP and fatty acids, (iv) In adipocytes isolated from brown adipose tissue, the rate of oxygen consumption (i.e. electron transfer) is increased in the presence of catecholamines. 

The thyroid hormone thyroxine is necessary for the development and function of cells throughout the body. It increases protein synthesis and oxygen consumption in almost all types of body tissue. Excess thyroxine causes hyperthyroidism, with increased heart rate, blood pressure, overactivity, muscular weakness, and loss of weight. 

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