Abstract
It has been suggested that hepatic urea synthesis, which consumes HCO3/-, plays an important role in acid-base homeostasis. This study measured urea synthesis rate (R(a) urea) directly to assess its role in determining the acid-base status in patients with end-stage cirrhosis and after orthotopic liver transplantation (OLT). Cirrhotic patients were studied before surgery (n = 7) and on the second postoperative day (n = 11), using a 5-h primed-constant infusion of [15N2]urea. Six healthy volunteers served as controls. R(a) urea was 5.05 ± 0.40 (SE) and 3.11 ± 0.51 μmol·kg- 1·min-1, respectively, in controls and patients with cirrhosis (P <0.05). Arterial base excess was 0.6 ± 0.3 meq/l in controls and -1.1 ± 1.3 meq/l in cirrhotic patients (not different). After OLT, R(a) urea was 15.05 ± 1.73 μmol·kg-1 min-1 which accompanied an arterial base excess of 7.0 ± 0.3 meq/l (P <0.001). We conclude that impaired R(a) urea in cirrhotic patients does not produce metabolic alkalosis. Concurrent postoperative metabolic alkalosis and increased R(a) urea indicate that the alkalosis is not caused by impaired R(a) urea. It is consistent with, but does not prove, the concept that the graft liver responds to metabolic alkalosis by augmenting R(a) urea, thus increasing HCO- 3 consumption and moderating the severity of metabolic alkalosis produced elsewhere.
| Original language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Gastrointestinal and Liver Physiology |
| Volume | 276 |
| Issue number | 5 39-5 |
| State | Published - May 1999 |
Fingerprint
Keywords
- Acid-base metabolism
- Ammonia
- Base excess
- Cirrhosis
- Metabolic alkalosis
ASJC Scopus subject areas
- Gastroenterology
- Physiology
- Physiology (medical)
Cite this
Effect of liver disease and transplantation on urea synthesis in humans : Relationship to acid-base status. / Shangraw, Robert; Jahoor, Farook.
In: American Journal of Physiology - Gastrointestinal and Liver Physiology, Vol. 276, No. 5 39-5, 05.1999.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effect of liver disease and transplantation on urea synthesis in humans
T2 - Relationship to acid-base status
AU - Shangraw, Robert
AU - Jahoor, Farook
PY - 1999/5
Y1 - 1999/5
N2 - It has been suggested that hepatic urea synthesis, which consumes HCO3/-, plays an important role in acid-base homeostasis. This study measured urea synthesis rate (R(a) urea) directly to assess its role in determining the acid-base status in patients with end-stage cirrhosis and after orthotopic liver transplantation (OLT). Cirrhotic patients were studied before surgery (n = 7) and on the second postoperative day (n = 11), using a 5-h primed-constant infusion of [15N2]urea. Six healthy volunteers served as controls. R(a) urea was 5.05 ± 0.40 (SE) and 3.11 ± 0.51 μmol·kg- 1·min-1, respectively, in controls and patients with cirrhosis (P <0.05). Arterial base excess was 0.6 ± 0.3 meq/l in controls and -1.1 ± 1.3 meq/l in cirrhotic patients (not different). After OLT, R(a) urea was 15.05 ± 1.73 μmol·kg-1 min-1 which accompanied an arterial base excess of 7.0 ± 0.3 meq/l (P <0.001). We conclude that impaired R(a) urea in cirrhotic patients does not produce metabolic alkalosis. Concurrent postoperative metabolic alkalosis and increased R(a) urea indicate that the alkalosis is not caused by impaired R(a) urea. It is consistent with, but does not prove, the concept that the graft liver responds to metabolic alkalosis by augmenting R(a) urea, thus increasing HCO- 3 consumption and moderating the severity of metabolic alkalosis produced elsewhere.
AB - It has been suggested that hepatic urea synthesis, which consumes HCO3/-, plays an important role in acid-base homeostasis. This study measured urea synthesis rate (R(a) urea) directly to assess its role in determining the acid-base status in patients with end-stage cirrhosis and after orthotopic liver transplantation (OLT). Cirrhotic patients were studied before surgery (n = 7) and on the second postoperative day (n = 11), using a 5-h primed-constant infusion of [15N2]urea. Six healthy volunteers served as controls. R(a) urea was 5.05 ± 0.40 (SE) and 3.11 ± 0.51 μmol·kg- 1·min-1, respectively, in controls and patients with cirrhosis (P <0.05). Arterial base excess was 0.6 ± 0.3 meq/l in controls and -1.1 ± 1.3 meq/l in cirrhotic patients (not different). After OLT, R(a) urea was 15.05 ± 1.73 μmol·kg-1 min-1 which accompanied an arterial base excess of 7.0 ± 0.3 meq/l (P <0.001). We conclude that impaired R(a) urea in cirrhotic patients does not produce metabolic alkalosis. Concurrent postoperative metabolic alkalosis and increased R(a) urea indicate that the alkalosis is not caused by impaired R(a) urea. It is consistent with, but does not prove, the concept that the graft liver responds to metabolic alkalosis by augmenting R(a) urea, thus increasing HCO- 3 consumption and moderating the severity of metabolic alkalosis produced elsewhere.
KW - Acid-base metabolism
KW - Ammonia
KW - Base excess
KW - Cirrhosis
KW - Metabolic alkalosis
UR - http://www.scopus.com/inward/record.url?scp=0033049387&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033049387&partnerID=8YFLogxK
M3 - Article
VL - 276
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
SN - 1931-857X
IS - 5 39-5
ER -