01), HCO3 (P=0.001), and BE (P=0.02; figure 3) were less marked. The NaHCO3 requirement before PKC phosphorylation reperfusion in the non-restricted normal saline group was 200.44±18.21 whereas in the restricted normal saline group this

requirement before reperfusion was 0±0.0 (P=0.001). We observed no significant differences in arterial blood pH (P=0.78), HCO3 (P=0.12), and BE (P=0.59) after reperfusion between the two groups (figure 3). Figure 3 Mean changes in pH, PCO2, NaHCO3 and serum potassium (K) from baseline to reperfusion in the non-restricted normal saline (NRF) and restricted normal saline (RF) groups. Discussion The present study showed that smaller volumes of Inhibitors,research,lifescience,medical normal saline fluid used during OLT anesthesia led to decreased severity of metabolic acidosis and a decrease in the cumulative dose of NaHCO3. During liver transplant surgery one major problem is progressive metabolic acidosis, which starts during

the dissection stage Inhibitors,research,lifescience,medical and accelerates during the anhepatic phase.1 As Ali et al. have shown in their study, due to the complex pathophysiology of end-stage liver disease it is better to consider the effect of the difference between the total concentrations of strong cations Inhibitors,research,lifescience,medical and anions (SID), the total concentration of weak acids, and the PaCO2 amounts on blood pH for diagnosis and management of the acid-base changes during liver transplantation.2 Thus, the current study has confirmed that restricted Inhibitors,research,lifescience,medical normal saline fluid use could decrease SID and prevent progressive metabolic acidosis during the hepatectomy and anhepatic phases of OLT. It must be considered that during general anesthesia (GA), low SVR of end-stage liver disease aggravated by the inherent vasodilating property of anesthetic

agents.13 The resultant profound decrease in SVR, drainage of ascitic fluid and bleeding during hepatectomy will lead to significant hypotension that requires substantial volumes of fluid administration and vasoconstrictor drugs.14,15 Based on a study Inhibitors,research,lifescience,medical by Schroeder et al., administration of large quantities of sodium chloride-containing fluids for maintenance of the hemodynamic decrease the SID, which in turn leads to a lower pH.16 However in our study we have used more colloid fluid instead of a substantial volume of crystalloid fluid in the restricted normal saline fluid group. Therefore at the end of the anhepatic phase, sodium bicarbonate demand was decreased. According to previous studies administration of large quantities of normal saline fluid during OLT can lead to progressive metabolic acidosis.13,17 selleck Therefore sodium bicarbonate use at end of the anhepatic phase is inevitable.16 However, complications exist with the administration of exogenous sodium bicarbonate for correction of metabolic acidosis. Administration of sodium bicarbonate increases the SID which tends to raise the pH because sodium is a strong cation and bicarbonate is not a strong ion. Simultaneously PaCO2 becomes elevated, which tends to cause a lower pH.