Effects of hemodilution during controlled hypotension of hepatic, renal, and pancreatic function in humans.
OBJECTIVE
To evaluate the effects of hemodilution during controlled hypotension on, the hepatic renal, and pancreatic function in the clinical setting.


METHODS
Randomized, prospective study.


METHODS
Inpatient surgery at Rosai Hospital.


METHODS
20 ASN status I and II patients scheduled for total hip arthroplasty.


METHODS
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 in (PGE1) to maintain mean arterial blood pressure at 55 mm Hg for 80 minutes.


RESULTS
Measurements included arterial ketone body ratio AKBR, aceto-acetate/3-hydroxybutyrate) for hepatic cellular function, pancreatic phospholipase A2 (P-PLA2) for pancreatic cellular function, and urine N-acetyl-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 lay (+ 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
PGE1 induced hypotension combined with moderate hemodilution using dextran, such as 23% of Net value maintains hepatic and pancreatic function but causes damage to the renal tubular cells.
Fukusaki
M
M
Department of Anesthesiology, Nagasaki Rosai Hospital, Japan.
Matsumoto
M
M
Yamaguchi
K
K
Ogata
K
K
Ide
R
R
Sumikawa
K
K
D020155:3-Hydroxybutyric Acid; D000090:Acetoacetates / Q000097:blood; D000118:Acetylglucosaminidase / Q000652:urine; D000368:Aged; D000527:Alprostadil / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D001806:Blood Urea Nitrogen; D003404:Creatinine / Q000097:blood; D003911:Dextrans / Q000627:therapeutic use; D005260:Female; D005500:Follow-Up Studies; D006400:Hematocrit; D006438:Hemodilution; D006622:Hip Prosthesis; D006801:Humans; D006885:Hydroxybutyrates / Q000097:blood; D007023:Hypotension, Controlled; D007657:Ketone Bodies / Q000097:blood; D007668:Kidney / Q000201:enzymology / Q000502:physiology*; D007684:Kidney Tubules / Q000502:physiology; D008099:Liver / Q000502:physiology*; D008875:Middle Aged; D010179:Pancreas / Q000201:enzymology / Q000502:physiology*; D010741:Phospholipases A / Q000097:blood; D054467:Phospholipases A2; D010952:Plasma Substitutes / Q000627:therapeutic use; D011446:Prospective Studies; D014665:Vasodilator Agents / Q000627:therapeutic use
D000090:Acetoacetates; D003911:Dextrans; D006885:Hydroxybutyrates; D007657:Ketone Bodies; D010952:Plasma Substitutes; D014665:Vasodilator Agents; C016635:acetoacetic acid; D003404:Creatinine; D010741:Phospholipases A; D054467:Phospholipases A2; D000118:Acetylglucosaminidase; D000527:Alprostadil; D020155:3-Hydroxybutyric Acid