Effects of hemodilution during controlled hypotension on hepatic, renal, and pancreatic function in humans

Study Objective: To evaluate the effects of hemodilution during controlled hypotension on the hepatic, renal, and pancreatic function in the clinical setting. Design: Randomized, prospective study Setting: Inpatient surgery at Rosai Hospital. Patients: 20 ASA status I and Il; patients scheduled for total hip arthroplasty. Interventions: Hemodilution was carried out after induction of anesthesia, in which drawn blood was replaced with dextran solution, to achieve final hematocrit (Hct) of 31% (Group A = mild hemodilution group, N = 10) or 23% (Group B = moderate hemodilution group, N = 10). In both groups, controlled hypotension was induced with prostaglandin E(1) (PGE(1)) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes. Measurements and Main Results: Measurements included arterial ketone body ratio (AKBR, aceto-acetate/3-hydroxybutyrate) for hepatic cellular function, pancreatic phospholipase A(2) (P-PLA2) for pancreatic cellular function, and urine N-acteyl-beta-D-glucosaminidase (NAG index) for cellular function of the renal tubule. These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, 60 minutes after recovery of normotension, and on the first postoperative day. Neither AKBR nor P-PLA2 showed a significant change throughout the time course of the study in either group. Urine-NAG index showed a significant increase in moderate hemodilution group at 60 minutes after recovery of normotension (+/- 136%) and on the first postoperative day (+/- 149%) compared with prehemodilution value, whereas it showed no significant change in the mild hemodilution group. Blood urea nitrogen and serum creatinine measured postoperatively were within normal range. Conclusions: PGE(1)-induced hypotension combined with moderate hemodilution using dextran, such as 23% of Hct value, maintains hepatic and pancreatic function but causes damage to the renal tubular cells. (C) 1996 by Elsevier Science Inc.