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Anesth Analg 1999;89:1371
© 1999 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

The Effects of Sodium Nitroprusside-Induced Hypotension on Splanchnic Perfusion and Hepatocellular Integrity

Stefan W. Suttner, MD*, Joachim Boldt, MD*, Christian C. Schmidt, MD*, Swen N. Piper, MD*, Peter Schuster, MD*, and Bernhard Kumle, MD{dagger}

*Department of Anesthesiology and Intensive Care Medicine, and the {dagger}Clinic of Urology, Klinikum der Stadt Ludwigshafen, Akademisches Lehrkrankenhaus der Universität Mainz, Ludwigshafen, Germany

Address correspondence and reprint requests to Joachim Boldt, MD, Department of Anesthesiology and Intensive Care Medicine, Klinikum der Stadt Ludwigshafen, Bremserstr. 79, D-67063 Ludwigshafen, Germany.


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
The purpose of our study was to investigate the effects of sodium nitroprusside-induced hypotension on splanchnic perfusion and hepatocellular integrity. Thirty patients undergoing radical prostatectomy were allocated randomly to a sodium nitroprusside (SNP) or control group (control). Regional pCO2 was measured using gastric tonometry, and the regional to arterial difference in partial pressure of CO2 and intramucosal pH were calculated. The cytosolic liver enzyme {alpha}-glutathione S-transferase and standard liver enzyme markers (alanine aminotransferase, aspartate aminotransferase, and {gamma}-glutamyltransferase) were also measured. Mean arterial pressure in the SNP group was 50 mm Hg for 97 min during surgery. A significant increase from baseline in regional pCO2 (from 40.0 ± 4.2 mm Hg to 45.3 ± 1.3 mm Hg) and regional to arterial difference in partial pressure of CO2 (from 4.1 ± 1.1 mm Hg to 9.7 ± 1.4 mm Hg) was seen at 90 min after skin incision only in the SNP group. Intramucosal pH decreased significantly from 7.40 ± 0.02 to 7.35 ± 0.03 during the same period in this group. Tonometric variables returned to baseline values within 2 h postoperatively. {alpha}-Glutathione S-transferase concentrations increased significantly in the SNP group from baseline to peak concentrations at the end of surgery (SNP: 9.93 ± 4.94 µg/L; control: 5.85 ± 1.86 µg/L). A return to baseline values was seen 24 h postoperatively. No significant changes in standard liver enzyme markers were seen throughout the study period. It is concluded, that splanchnic perfusion was transiently impaired during controlled hypotension. This is supported by significant changes in tonometric data. Increased serum levels of {alpha}-glutathione S-transferase may indicate a disturbance in hepatocellular integrity. SNP: 9.93 ± 4.94 µg/L; control: 5.85 ± 1.86 µg/L). A return to baseline values was seen 24 h postoperatively. No significant changes in standard liver enzyme markers were seen throughout the study period. It is concluded, that splanchnic perfusion was transiently impaired during controlled hypotension. This is supported by significant changes in tonometric data. Increased serum levels of {alpha}-glutathione S-transferase may indicate a disturbance in hepatocellular integrity.

Implications: We studied gastric mucosal tonometry and the cytosolic liver enzyme {alpha}-glutathione S-transferase to evaluate the effects of controlled hypotension induced by sodium nitroprusside on splanchnic perfusion and hepatocellular integrity. Splanchnic perfusion decreased and {alpha}-glutathione S-transferase increased during and after a hypotensive period, but returned to baseline values within the first postoperative day, indicating a transient impairment of splanchnic perfusion and hepatocellular integrity.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Blood loss in patients undergoing radical prostatectomy may be substantial, and many patients need perioperative transfusion with allogeneic blood. Controlled hypotension, using continuous infusion of sodium nitroprusside (SNP), reduces intraoperative blood loss and the transfusion of allogeneic blood (1–4). The relative safety of this technique has been documented in several studies (5–7). These studies were mainly focused on the effects of controlled hypotension on cerebral and coronary circulation, because the brain and the myocardium are presumed to be the most sensitive of all organs to ischemic damage. However, the cerebral and coronary vascular system is characterized by well-functioning autoregulatory mechanisms. Intestinal blood pressure-flow autoregulation is much less effective than the autoregulation of the brain, heart, or the kidneys. Additionally, autoregulation is of little importance for the hepatic arterial pressure–flow relationship. It is achieved, to a great extent, by a reciprocal relationship between portal and hepatic arterial blood flow. Thus, when portal venous flow decreases, hepatic arterial flow increases and vice versa (8). Therefore, controlled hypotension may result in a decreased blood flow to the liver and other splanchnic organs. Additionally, surgical bleeding and manipulation of upper abdominal viscera may lead to a reduced oxygen availability with the risk of global or regional hypoxia in the splanchnic area. Unfortunately, clinical monitoring of splanchnic circulation is extremely difficult, and measurements that are available include gastric mucosal tonometry, as well as invasive and expensive techniques, such as angiography, hepatic vein catheterization, or laser Doppler velocimetry (9).

Gastric mucosal tonometry is a valid and reliable tool for assessing splanchnic circulation (10,11). Measuring the regional gastric CO2 tension (prCO2) and calculating the gastric intramucosal pH (pHi) and arterial-to-intramucosal pCO2 difference (p[r-a]CO2) provide valuable information about splanchnic perfusion (12,13). Liver function is monitored clinically by the measurement of enzymes, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), and {gamma}-glutamyltransferase ({gamma}-GT), which are released into the circulation secondary to hepatocellular damage. However, the measurement of these enzymes lacks specificity, thus limiting its usefulness as an indicator of hepatic damage. Several studies have indicated that the measurement of the cytosolic liver enzyme {alpha}-glutathione S-transferase ({alpha}-GST) may provide a very sensitive indicator of hepatocellular integrity in a variety of clinical and pathological conditions (14–17). The relatively small molecular weight (51 kDa) and the short half-life of the enzyme (<90 min) results in its rapid release after hepatocellular damage, and makes {alpha}-GST an ideal marker for monitoring acute changes in hepatocellular integrity (18). The influence of controlled hypotension on splanchnic perfusion and hepatocellular integrity is still controversial. Thus, our study was designed to assess the effects of SNP-induced hypotension on splanchnic perfusion and hepatocellular integrity using gastric tonometry and {alpha}-GST as a more sensitive marker of hepatocyte injury.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After approval by our local ethics committee, 30 male ASA physical status II and III patients—scheduled for elective retropubic radical prostatectomy with bilateral pelvic lymphadenectomy—gave informed consent to participate in the study. Patients with any history of known liver disease or preexisting liver dysfunction (ALT/AST >40 units/L), renal insufficiency (creatinine >1.5 mg/dL), abuse of alcohol or drugs, unstable angina pectoris, severe uncontrolled hypertension, a history of myocardial infarction within the last 6 mo or stenosis of the carotid arteries were excluded. Administration of paracetamol and corticosteroids was not allowed within 3 days before or during the study. The patients were randomly allocated to the study group (hypotension induced by SNP, n = 15) or the control group without hypotension (control, n = 15, without SNP). All patients received oral ranitidine (150 mg) prior to surgery and were premedicated with lorazepam (1–2 mg) orally 1 h before induction of anesthesia, which was induced by thiopental (5 mg/kg) and fentanyl (2–3 µg/kg). Atracurium (0.5 mg/kg) was administered to achieve muscle relaxation prior to endotracheal intubation. Isoflurane was used for maintenance of anesthesia (end-expiratory concentration of 1.0 ± 0.3 vol%). A constant fresh gas flow of 2 L/min was used during maintenance of anesthesia. Ventilation was performed in both groups with 60% nitrous oxide in oxygen using a semiclosed rebreathing circuit. The ventilation pattern was adjusted to keep SaO2 >95% (continuous oximetry) and to maintain pCO2 and pH in the physiological range. Routine intraoperative monitoring included continuous invasive measurement of mean arterial blood pressure (MAP) and central venous pressure. SNP was initiated at the beginning of bilateral pelvic lymphadenectomy and was completed with wound closure. The SNP doses applied were within a range from 0.5 to 10.0 µg · kg-1 · min-1 and were adjusted to reduce MAP to 50 mm Hg. A threshold of hypotension was defined as a MAP of below 50 mm Hg in the study group and 70 mm Hg in the control group. Hypotensive episodes were treated by increasing the rate of fluid administration and reducing the concentration of isoflurane and/or SNP when necessary. Crystalloids and gelatin were given to maintain central venous pressure at 10–15 mm Hg. Packed red blood cells were given when the hemoglobin concentration was below 8 g/dL. Anesthesia was provided by anesthetists who were not involved in the study. A nasogastric tube (TRIPTM NGS II Catheter, Instrumentarium Corporation, Helsinki, Finland) was inserted in all patients. The correct positioning of the tube was confirmed by aspiration of gastric fluid and auscultation over the stomach. prCO2 and pHi were measured using the TonocapTM monitor (Tonometrics Division Instrumentarium Corporation, Helsinki, Finland). This monitoring device calculates pHi from the arterial pH, the arterial pCO2 entered by the user, and the measured prCO2 using the Henderson-Hasselbalch equation (10). The p(r-a)CO2 is calculated from systemic arterial pCO2 and prCO2. Arterial blood samples were analyzed immediately after sampling for paO2, paCO2, and pH in an automatic blood gas tension analyzer. Measurements were performed at induction of anesthesia (T1), 90 min after skin incision (90 min), at the end of surgery (T2), and 2 h postoperatively (T3). After surgery, all patients were observed in the postanesthesia care unit for the following 2 h. Peripheral venous blood samples for {alpha}-GST and aminotransferase measurements were taken at T1, T2, T3, and 24 h postoperatively (T4). {alpha}-GST concentration in serum was measured using the Enzyme Immunoassay HepkitTM-{alpha}-Human GST-{alpha} (Biotrin, Dublin, Ireland). The test of this quantitative enzyme immunoassay is based on the sequential addition of sample, enzyme conjugate, and substrate to microtiter wells coated with anti-{alpha}-GST immunoglobulin G. The reference range of {alpha}-GST is 0–7.5 µg/L. The intraassay coefficient of variation was 5.85%. Activity of aminotransferases was measured in routine hospital laboratory tests in serum samples. Reference ranges for AST, ALT and {gamma}-GT were 5–19 IU/L, 5–23 IU/L, and 6–28 IU/L, respectively, as specified by the hospital’s department of clinical chemistry.

Data are shown as the means ± standard deviation. Statistical analysis was performed using Fisher’s exact test, paired and unpaired Student’s t-test, and analysis of variance for repeated measures when appropriate. When multiple comparisons were made, the Bonferroni correction was applied. P values <0.05 were considered significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
The patients in both groups were comparable with respect to ASA physical status, preexisting disease, biometric data, as well as duration of anesthesia and surgery (Table 1). Blood loss in the SNP group was significantly less, compared with the control group (P < 0.05), whereas the need for intraoperative-intravascular volume replacement (crystalloids and colloids) was significantly higher in the control group (P < 0.05). During surgery, hemoglobin concentration decreased significantly (P < 0.05) in both groups, without a difference between the groups (Table 2). Transfusion of allogeneic packed red blood cells was required in three patients in the control group (Table 1). MAP in the SNP group was significantly decreased at 90 min after skin incision, compared with the control group (P < 0.05), whereas no difference was seen in other hemodynamic variables (Fig. 1).


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  		Table 1. Patient Demographics and Perioperative Data
 

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  		Table 2. Time Course of Arterial Blood Gas Variables and Hemoglobin Concentration
 


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  		Figure 1. Mean arterial blood pressure (MAP), central venous pressure (CVP), and heart rate (HR). T1 = induction of anesthesia; 90 min = 90 min after skin incision; T2 = end of surgery; T3 = 2 h postoperatively; T4 = 24 h postoperatively; SNP = sodium nitroprusside. Values are means ± standard deviation. * P < 0.05, significantly different from baseline value; {dagger} P < 0.05, significantly different from control.

 
Baseline values of {alpha}-GST concentrations were normal in all patients and comparable between both groups (Fig. 2). {alpha}-GST concentrations were significantly (P < 0.05) higher than baseline at T2 and remained elevated at T3 in the SNP group. Peak concentrations of this enzyme at T2 were significantly (P < 0.05) higher in the SNP group (SNP: 9.93 ± 4.94 µg/L; control: 5.85 ± 1.86 µg/L). A return to baseline values was seen at T4 in both groups. The preoperative levels of ALT, AST, and {gamma}-GT were within normal limits in both groups. There were no significant changes in these enzyme activities throughout the study. No clinical signs or symptoms of hepatic disorders, gastroenterologic problems, or systemic inflammatory disease were observed in any patient.



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  		Figure 2. Concentrations of serum {alpha}-glutathione S-transferase (GST) (µg/L). T1 = induction of anesthesia; T2 = end of surgery; T3 = 2 h postoperatively; T4 = 24 h postoperatively; SNP = sodium nitroprusside. Values are means ± standard deviation. * P < 0.05, significantly different from baseline value; {dagger} P < 0.05, significantly different from control.

 
There were no differences in arterial blood gas values either within the two groups or between the groups (Table 2). Tonometric measurements showed a significant increase from baseline in prCO2 and p(r-a)CO2 at 90 min after skin incision in the SNP group (P < 0.05). pHi was significantly lower, compared with baseline at 90 min after skin incision in the SNP group (P < 0.05). A significant difference between both groups was seen in prCO2 and p(r-a)CO2 at 90 min after skin incision (P < 0.05). At T2 and T3 prCO2, p(r-a)CO2, and pHi returned to baseline values, with no differences between the groups (Fig. 3).



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  		Figure 3. Changes of intramucosal pH (pHi), regional pCO2 (prCO2), and regional-to-arterial pCO2 [p(r-a)CO2]. T1 = induction of anesthesia; 90 min = 90 min after skin incision; T2 = end of surgery; T3 = 2 h postoperatively; SNP = sodium nitroprusside. Values are means ± standard deviation. * P < 0.05, significantly different from baseline value; {dagger} P < 0.05, significantly different from control.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The effects of controlled hypotension on blood flow have been studied in various organ systems (7,19,20). The margin of safety for a lower limit of MAP has been set at 50 mm Hg based on the belief that autoregulatory mechanisms persist in vital organs, such as the brain and the myocardium. This kind of autoregulation exists only to a minor extent in the gastrointestinal tract and in the liver. As a consequence, systemic hypotension may lead to a decreased splanchnic blood flow and, subsequently, to a decreased oxygen delivery to the superficial mucosal lining of the intestine and the liver.

We found significant increases in prCO2 and p(r-a)CO2 during the hypotensive period and a decrease in pHi. Because the prCO2 is influenced directly by abnormalities of systemic arterial pCO2, other factors, such as hypoventilation or disturbance in the systemic acid–base balance, must be considered in the interpretation of high prCO2. Therefore, we calculated p(r-a)CO2, which is considered the most specific variable for detection of gastric mucosal hypoperfusion and ischemia (13,21). Systemic arterial pCO2 as a major source of error was kept constant and within the physiologic range in all patients throughout the observational period.

During a steady-state splanchnic blood flow and appropriate oxygenation, prCO2 reflects the balance between CO2 production by tissue and CO2 removal by circulation (13). Because mucosal pCO2 gradually accumulates due to a stagnant blood flow or increased anaerobic metabolism, an increase in luminal pCO2 can be observed (22). Thus, the increase of the prCO2 and the p(r-a)CO2 can be related to a decreased gastric blood flow with normal aerobic metabolism or a beginning anaerobic production of CO2. These observations are partly in agreement with the results of Fukusaki et al. (23), who studied the combined effects on gastric intramural pH of mild or moderate hemodilution and controlled hypotension with prostaglandin E1. They concluded that moderate hemodilution (hematocrit of 23%) combined with controlled hypotension might impair oxygenation of the gastrointestinal mucosa, whereas the combination of mild hemodilution (hematocrit of 32%) with hypotension did not cause these effects. The latter finding is in contrast with our results, which indicate a mild, but transient impairment of splanchnic perfusion. Because duration of the hypotensive period and MAP were approximately the same, this difference might be attributed to the higher blood loss in our patients, even in the SNP group. Another explanation would be the use of prostaglandin E1 for induction and maintenance of hypotension, because this prostaglandin is known to increase gastric mucosal blood flow. We decided to use SNP because of its relative safety and widespread use for this anesthetic technique (4).

Splanchnic blood flow is regulated by intrinsic and extrinsic mechanisms. The extrinsic control of gut blood flow comprises sympathetic innervation and the release of vasoactive substances in response to hemodynamic changes. In low-flow states, perfusion of the heart and the central nervous system is maintained at the expense of peripheral tissue and the splanchnic region. This is due to a redistribution of blood flow to these vital organs. However, vasoconstriction due to stimulation of this system is transient, and blood flow starts to recover after initial reduction (8,24). The immediate recovery of gastric mucosal perfusion at two hours postoperatively in our patients might be attributed to this phenomenon. Another, more simple, explanation for the restoration of perfusion might be that SNP infusion was discontinued at this time. It has been shown that measurement of prCO2 and the calculation of pHi and p(r-a)CO2 can be used to assess gastrointestinal hypoxia and ischemia, and might be predictive of the outcome of critically ill patients (25–28). Commonly accepted normal or abnormal values for gastric pHi, prCO2, or p(r-a)CO2 have not been established. Perioperative studies have taken a pHi <7.32 as evidence of intramucosal acidosis (11). A pHi value of 7.35 was used in critically ill patients as an index to guide therapeutic interventions (26,27). Gastric pHi in our study population was never below 7.32, and there was no evidence of intestinal barrier dysfunction, such as systemic infections or inflammatory disease. Accepting a pHi of 7.35 as the lower limit of normality, the patients in the SNP group would have been at a threshold to hypoxic tissue injury. Evidence that there might have been at least a transient hypoxic event within the splanchnic area is provided by the {alpha}-GST levels that increased significantly at the end of surgery. Human hepatic {alpha}-GST has been advocated as a superior marker of hepatocellular damage, compared with other static liver function tests, such as measurement of the aminotransferases (AST, ALT, or {gamma}-GT).

{alpha}-GST is a cytosolic enzyme found predominantly in the liver, comprising approximately 5% of the total soluble cytoplasmic protein mass (29). Periportal hepatocytes contain the largest concentration of aminotransferases, but centrilobular hepatocytes, which are relatively deficient in ALT and AST, are most susceptible to damage from hypoxia (30). In contrast to the aminotransferases, {alpha}-GST is equally distributed in both the centrilobular and the periportal regions. Elevated {alpha}-GST levels returned to baseline within 24 hours postoperatively. This might be attributed to the same autoregulatory escape phenomenon as described for gastric mucosal perfusion (8). In contrast to the increase in {alpha}-GST concentrations, no significant overall changes in aminotransferase activities were found throughout the perioperative period. Other studies dealing with the effects of controlled hypotension on human hepatic function have found similar results concerning routine liver function tests (31,32). No changes in aminotransferase activity (ALT and AST) were reported during controlled hypotension for 180 minutes with prostaglandin E1 at a MAP of 55 mm Hg (31). These authors concluded that even a combination of controlled hypotension and moderate hemodilution (hematocrit of 23%) would maintain hepatic function. Elevated serum levels of aminotransferase activity might be suggestive for hepatocellular damage. However, measurement of these enzymes lacks specificity, since a variety of organs other than the liver contain aminotransferases, which limits the usefulness of these enzymes as indicators of mild ischemic liver damage. The finding that there were no manifest signs of gut mucosal ischemia suggests that gastric mucosal hypoperfusion might be an epiphenomenon in the patients undergoing controlled hypotension. This is supported by results of several other studies in patients undergoing major surgery, such as elective cardiac surgery or abdominal aortic surgery, exhibiting at least transient episodes of gastric intramucosal acidosis (8).

We conclude that splanchnic perfusion during controlled hypotension might be transiently impaired. Variables of gastric tonometry (prCO2, p[r-a]CO2, and pHi) showed significant changes during surgery, but returned to baseline within two hours postoperatively. The margin of safety for controlled hypotension, especially for the splanchnic region, remains unclear. A lower limit of 50 mm Hg for MAP might be below a threshold for adequate splanchnic tissue perfusion. This was supported by the increased concentrations of the hepatic enzyme {alpha}-GST, a sensitive marker for even mild impairment of hepatocellular integrity. Further research is needed to identify whether splanchnic hypoperfusion is an epiphenomenon of controlled hypotension, or whether it reflects an initial step toward gut barrier dysfunction.


   References
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 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Sharrock NE, Mineo R, Urquhart B, Salvati EA. The effect of two levels of hypotension on intraoperative blood loss during total hip arthroplasty performed under lumbar epidural anesthesia. Anesth Analg 1993;76:580–4.[Abstract/Free Full Text]
  2. Boldt J, Weber A, Mailer M, et al. Acute normovolaemic hemodilution vs controlled hypotension for reducing the use of allogeneic blood in patients undergoing radical prostatectomy. Br J Anaesth 1999;82:170–4.[Abstract/Free Full Text]
  3. Sood S, Jayalaxmi TS, Vijaraghvan S, Nundy S. Use of sodium nitroprusside induced hypotension for reducing blood loss in patients undergoing lienorenal shunts for portal hypertension. Br J Surg 1987;74:1036–8.[Web of Science][Medline]
  4. Friedrich JA, Butterworth JF. Sodium nitroprusside: twenty years and counting. Anesth Analg 1995;81:152–62.[Abstract]
  5. Thompson GE, Miller RD, Stevens WC, Murray WR. Hypotensive anesthesia for total hip arthroplasty: a study of blood loss and organ function (brain, heart, liver and kidney). Anesthesiology 1978;48:91–6.[Web of Science][Medline]
  6. Bunemann L, Jensen KA, Riisager S, Thomsen LJ. Cerebral blood flow and metabolism during hypotension induced with sodium nitroprusside and metoprolol. Eur J Anaesth 1991;8:197–201.[Web of Science][Medline]
  7. Lessard MR, Trepanier CA. Renal function and hemodynamics during prolonged isoflurane-induced hypotension in humans. Anesthesiology 1991;74:860–5.[Web of Science][Medline]
  8. Takala J. Determinants of splanchnic blood flow. Br J Anaesth 1996;77:50–8.[Free Full Text]
  9. Bastien O, Piriou , Aoufifi A, et al. Effects of dopexamine on blood flow in multiple splanchnic sites measured by laser Doppler velocimetry in rabbits undergoing cardiopulmonary bypass. Br J Anaesth 1999;82:104–9.[Abstract/Free Full Text]
  10. Fiddian-Greene RG. Gastric intramucosal pH, tissue oxygenation and acid-base balance. Anaesth 1995;74:591–606.
  11. Mythen MG, Webb AR. The role of gut mucosal hypoperfusion in the pathogenesis of post-operative organ dysfunction. Intensive Care Med 1994;20:203–9.[Web of Science][Medline]
  12. Mythen MG, Woolf R, Noone RB. Gastric mucosal tonometry: towards new methods and applications. Schmerzther 1998;33:S85–S90.
  13. Russell JA. Gastric tonometry: does it work? Intensive Care Med 1997;23:3–6.[Web of Science][Medline]
  14. Knapen MFCM, Mulder TPJ, Bisseling JGA, et al. Plasma glutathione S-transferase 1-1: a more sensitive marker for hepatocellular damage than serum alanine aminotransferase in hypertensive disorders of pregnancy. Am J Obstet Gynecol 1998;178:161–5.[Web of Science][Medline]
  15. Beckett GJ, Chapman BJ, Dyson EH, Hayes JD. Plasma glutathione S-transferase measurements after paracetamol overdose: evidence for early hepatocellular damage. Gut 1985;26:26–31.[Abstract/Free Full Text]
  16. Trull AK, Facey SP, Rees GW, et al. Serum glutathione S-transferase—A sensitive marker of hepatocellular damage associated with acute liver allograft rejection. Transplantation 1994;58:1345–51.[Web of Science][Medline]
  17. Hayes PC, Hayes JD, Hussey AJ, et al. Changes in plasma glutathione S-transferase B1 after alcohol ingestion in man: a measure of hepatocellular sensitivity to chronic alcohol excess. Clin Chem Enzyme Commun 1990;2:189–94.
  18. Beckett GJ, Hayes JD. Glutathione S-transferases: biomedical applications. Adv Clin Chem 1993;30:281–380.[Web of Science][Medline]
  19. Kick O, Van Aken H, Wouters PF, et al. Vital organ blood flow during deliberate hypotension in dogs. Anesth Analg 1993;77:737–42.[Abstract/Free Full Text]
  20. Moss E. Cerebral blood flow during induced hypotension [editorial]. Br J Anaesth 1995;74:635–7.[Free Full Text]
  21. Kolkmann JJ, Otte JA, Groeneveld ABJ. Gastrointestinal tonometry: methodological considerations with use of fluid and air. Intensivmed Notfallmed Schmerzther 1998;33:S74–7.
  22. Schlichtig R, Bowles SA. Distinguishing between aerobic and anaerobic appearance of dissolved CO2 in intestine during low flow. J Appl Physiol 1974;76:2443–51.[Abstract/Free Full Text]
  23. Fukusaki M, Hara T, Maekawa T, et al. Effect of controlled hypotension combined with hemodilution on gastric intramural pH. Clin Anesth 1998;10:222–7.
  24. Granger DN, Richardson PDI, Kvietys PR, Mortillaro NA. Intestinal blood flow. Gastroenterology 1980;78:837–63.[Web of Science][Medline]
  25. Maynard ND, Bihari DJ, Dalton RN, et al. Liver function and splanchnic ischemia in critically ill patients. Chest 1997;111:180–7.[Abstract/Free Full Text]
  26. Gutierrez G, Palizas F, Doglio G, et al. Gastric intramucosal pH as a therapeutic index of tissue oxygenation in critically ill patients. Lancet 1992;339:195–9.[Web of Science][Medline]
  27. Doglio GR, Pusajo JF, Egurrola MA, et al. Gastric mucosal pH as a prognostic index of mortality in critically ill patients. Care Med 1991;19:1037–40.
  28. Mythen MG, Webb AR. Intraoperative gut mucosal hypoperfusion is associated with increased postoperative complications and cost. Intensive Care Med 1994;20:99–104.[Web of Science][Medline]
  29. Sundberg AGM, Nilsson R, Appelkvist EL, Dallner G. Immunohistochemical localization of alpha and pi class glutathione transferases in human tissue. Pharmacol Toxicol 1993;72:321–31.[Web of Science][Medline]
  30. Redick JA, Jakoby WB, Baron J. Immunohistochemical localisation of glutathione S-transferase in liver of untreated rats. J Biol Chem 1982;257:15200–3.[Abstract/Free Full Text]
  31. Fukusaki M, Maekawa T, Yamaguchi K, et al. Combined effects of prolonged prostaglandin E1-induced hypotension and haemodilution on human hepatic function. Eur J Anaesth 1997;14:157–63.[Web of Science][Medline]
  32. Fukusaki M, Matsumoto M, Yamaguchi K, et al. Effects of hemodilution during controlled hypotension on hepatic, renal, and pancreatic function in humans. J Clin Anesth 1996;8:545–50.[Web of Science][Medline]
Accepted for publication August 4, 1999.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press