All barbiturates metabolism is in the liver. In Barbiturates metabolism , the haemodilution in cardiopulmonary bypass (CPB) causes reduction in total drug concentration and protein binding fraction at the onset of CPB.
This decrease in protein binding is counteracted by the dilution of unbound drug, resulting in a stable unbound concentration throughout CPB.
The inactive metabolites are conjugated with glucuronic acid and are excreted in the urine. In the case of phenobarbitone, however, 25-30% of the dose is excreted unchanged.
For Barbiturates metabolism the thiopental is metabolized in the liver to hydroxythiopental and carboxylic acid derivatives. Metabolites are usually inactive and are more water soluble facilitating its excretion through kidney.
The metabolism of thiopental is almost complete (99%), with the principal sites of metabolism being oxidation of substituents on the number five carbon atom, desulfuration on the number two carbon atom, and hydrolytic opening of the Barbiturates metabolism acid ring.
Unlike oxybarbiturates, thiopentone is also metabolized to a small extent in extrahepatic sites such as the kidneys and brain. The reserve capacity of the liver to carry out oxidation of barbiturates metabolism is large, and hepatic dysfunction must be extreme before a prolonged duration of action of barb iturates as a result of decreased metabolism occurs.
In patients with cirrhosis, thiopental clearance does not change significantly. However, these patients may have a decreased capacity for thiopental metabolism.
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