Carbon dioxide excretion

Pharmacokinetics Sodium bicarbonate in water dissociates to provide sodium and bicarbonate ions. Sodium is the principal cation of extracellular fluid. Bicarbonate is a normal constituent of body fluids and normal plasma level ranges from 24 to 31 mEq/L. Plasma concentration is regulated by the kidney. Bicarbonate anion is considered labile because, at a proper concentration of hydrogen ion, it may be converted to carbonic acid, then to its volatile form, carbon dioxide, excreted by lungs. Normally, a ratio of 1 20 (carbonic acid bicarbonate) is present in extracellular fluid. In a healthy adult with normal kidney function, almost all the glomerular filtered bicarbonate ion is reabsorbed less than 1% is excreted in urine. 

Alikin, Yu.S. (1975). On some regularities of carbon dioxide excretion in Baikal fish during swimming (In Russian). Vestnik Sibirskogo Otdeleniya AN SSSR, Biologicheskie Nauk 15,63-69. 

Disposition in the Body. Readily absorbed after inhalation and also absorbed after ingestion or through the skin the rate of absorption is increased by the concomitant ingestion of alcohol. It is excreted mainly from the lungs as carbon tetrachloride and carbon dioxide excretion in the urine as urea and an unidentified metabolite, and elimination in the faeces also occur. 

The patient s primary means to compensate for metabolic acidosis is to increase carbon dioxide excretion by increasing respiratory rate. This results in a decrease in PaC02. This ventilatory compensation results from stimulation of the respiratory center by changes in cerebral bicarbonate concentration and pH. For every 1 -mEq/L decrease in bicarbonate concentration below the average of 24, the PaC02 decreases by about 1 to 1.5 mm Hg from the normal value of 40 (see Table 51 ). 

As with the metabolic acid-base disturbances, there are two cardinal respiratory acid-base disturbances respiratory acidosis and respiratory alkalosis. These disorders are generated by a primary alteration in carbon dioxide excretion, which changes the concentration of carbon dioxide, and therefore the carbonic acid concentration in body fluids. A primary reduction in PaC02 causes a rise in pH (respiratory alkalosis), and a primary increase in PaC02 causes a decrease in pH (respiratory acidosis). Unlike the metabolic disturbances, for which respiratory compensation is rapid, metabolic compensation for the respiratory disturbances is slow. Hence these disturbances can be further divided into acute disorders, with a duration of minutes to hours that is too short for metabolic compensation to have occurred, and chronic disorders, that have been present long enough for metabolic compensation to be complete. 

When carbon dioxide excretion is severely impaired (PaC02 >80 mm Hg) and/or life-threatening hypoxia is present (Pa02 <40 mm Hg), the immediate therapeutic goal is to provide adequate oxygenation. Under these circumstances, hypoxia, not acidemia, is the principal threat to life. A patent airway needs to be established, which may necessitate intubation. Excessive secretions must be cleared from the airway and oxygen administered to restore adequate oxygenation. Mechanical ventilation is likely to be required. 

F ure 6.8. Partial pressure of carbon dioxide in arterial blood (y-axis) as a function of time (x-axis). At time zero, hypoventilation suddenly supervenes, e.g. as a result of a severe attack of asthma. As indicated, immediately following the onset of hypoventilation, there is a period during which carbon dioxide accumulates in the body. The PCO2 rises exponentially towards a steady state value. When a steady state is established, the rate of carbon dioxide excretion in the lungs equals the rate of production in the tissues. 

B. the amount of carbon dioxide excreted per minute in the expired gas rises ... 

Absorption of mannitol (209), sorbitol (210), and xyfltol (4) from the intestinal tract is relatively slow, compared to that of glucose. In humans, approximately 65% of orally adrninistered mannitol is absorbed in the dose range of 40—100 g. About one-third of the absorbed mannitol is excreted in the urine. The remainder is oxidized to carbon dioxide (211). 

Sutures are required to hold tissues together until the tissues can heal adequately to support the tensions exerted on the wound duting normal activity. Sutures can be used ia skin, muscle, fat, organs, and vessels. Nonabsorbable sutures are designed to remain ia the body for the life of the patient, and are iadicated where permanent wound support is required. Absorbable sutures are designed to lose strength gradually over time by chemical reactions such as hydrolysis. These sutures are ultimately converted to soluble components that are then metabolized and excreted ia urine or feces, or as carbon dioxide ia expired air. Absorbable sutures are iadicated only where temporary wound support is needed. 

Kohlensaure,/. carbonic acid carbon dioxide, -anhydrid, rt. carbonic anhydride (carbon dioxide), -ausscheidung,/. (Physiol.) c Tbon dioxide excretion, -bestimmer, m. apparatus for determining carbon dioxide, -brot, n, aerated bread, -chlorid, n. carbonyl chloride, -entwickelung,/. evolution of carbon dioxide, -ester, m. carbonic ester, -flasche, /. carbon dioxide cylinder, -gas, n, carbonic add gas (carbon dioxide), -gehalt, m. carbon dioxide content. 

The effect on the eyes was more noticeable. A single application of the solution mentioned above produced moderate redness and short and minor swelling of conjunctiva. Radiotracer studies with Hostapur SAS [102] revealed that after oral (up to 50 mg/kg) and dermal application on rats, the product and its metabolites were very quickly excreted either in completely oxidized form as carbon dioxide or in the urine and feces. Residues in organs and tissues after 7 days were well below 1 ppm. 

Alcohol sulfates are easily metabolized by mammals and fishes either by oral or intraperitoneal and intravenous administration. Several labeled 35S and 14C alcohol sulfates have been used to determine their metabolism in experiments with rats [336-340], dogs [339], swines [341], goldfish [342], and humans [339]. From all of these studies it can be concluded that alcohol sulfates are absorbed in the intestine of mammals and readily metabolized by to and p oxidation of the alkyl chain and excreted in the urine and feces, but are also partially exhaled as carbon dioxide. Fishes absorb alcohol sulfates through their gills and metabolize them in a similar way to that of mammals. 

Excretion data show that saturability of trichloroethylene metabolism occurs at lower exposure levels for rats than for mice (Dekant et al. 1986b Prout et al. 1985). In mice receiving a single oral dose of 10, 500, 1,000, or 2,000 mg/kg trichloroethylene, urinary TCA and exhaled carbon dioxide over a 24-hour period were... 

Nitrogen compounds commonly determined are creatinine, urea, and uric acid. Creatinine is an end product of the energy process occurring within the muscles, and is thus related to muscle mass. Creatinine in urine is commonly used as an indicator and correction factor of dilution in urine. Creatinine in serum is an indicator of the filtration capacity of the kidney. Urea is the end product of the nitrogen luea cycle, starting with carbon dioxide and ammonia, and is the bulk compoimd of urine. The production of uric acid is associated with the disease gout. In some cases, it appears that the excess of uric acid is a consequence of impaired renal excretion of this substance. 

Root products, as defined by Uren and Reisenauer (17), represent a wide range of compounds. Only secretions are deemed to have a direct and immediate functional role in the rhizosphere. Carbon dioxide, although labeled an excretion, may play a role in rhizosphere processes such as hyphal elongation of vesicular-arbuscular mycorrhiza (39). Also, root-derived CO2 may have an effect on nonphotosynthetic fixation of CO2 by roots subject to P deficiency and thus contribute to exudation of large amounts of citrate and malate, as observed in white lupins (40). The amounts utilized are very small and, in any case, are extremely difficult to distinguish from endogenous CO2 derived from soil and rhizosphere respiration. 

Hydroxyurea is an oral drug that inhibits ribonucleotide reductase, which converts ribonucleotides into the deoxyribuon-cleotides used in DNA synthesis and repair. The time to peak concentrations of hydroxyurea is 1 to 2 hours after oral administration. Approximately 50% is degraded by the liver to form urea and respiratory carbon dioxide. The remainder is excreted by the kidney. The half-life ranges from 3.5 to 4.5 hours. Hydroxyurea has shown clinical activity in the treatment of chronic myelocytic leukemia, polycythemia vera, and thrombocytosis. The major side effects are myelo-suppression, nausea and vomiting, diarrhea, and constipation. Rash, mucositis, and renal tubular dysfunction occur rarely. 

PGA degrades by hydrolysis to produce carbon dioxide and glycolic acid (Fig. 13.1.2), which is either excreted or enzymatically converted to other metabo-... 

Dost et al. (1966) studied the excretion of [14C] 1,1-dimethylhydrazine administered i.p. to rats. Following a single (0.88 mg/kg) dose, approximately 30% of the test material was metabolized to carbon dioxide within 10 h. After injection of 20 mg/kg or 80 mg/kg, C02 excretion accounted for approximately 15.2% and 7%, respectively, of the administered dose. Approximately 50% of the administered dose was excreted in the urine over a 2-d period. 

The primary metabolites of hexachloroethane are eventually oxidized to form trichloroethanol and trichloroacetic acid. These ultimate metabolites are excreted along with unchanged hexachloroethane, tetrachloroethene, and pentachloroethane. A small amount of the absorbed hexachloroethane is oxidized completely to carbon dioxide. Hexachloroethane and its metabolites are removed from the body in exhaled... 

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