Anesth Analg 2003;97:1818-1823
© 2003 International Anesthesia Research Society
REGIONAL ANESTHESIA
The Difference Between Intramural and Arterial Partial Pressure of Carbon Dioxide Increases Significantly During Laparoscopic Cholecystectomy: The Effect of Thoracic Epidural Anesthesia
Koichiroh Nandate, MD*,
Masanori Ogata, MD*,
Masahiro Nishimura, MD*,
Takefumi Katsuki, MD ,
Shinichi Kusuda, MD,
Kohji Okamoto, MD,
Naoki Nagata, MD, and
Akio Shigematsu, MD*
Departments of *Anesthesiology and
First Surgery, University of Occupational and Environmental Health, Japan
Address correspondence and reprint requests to Masanori Ogata, MD, Department of Anesthesiology, University of Occupational and Environmental Health, 1–1 Iseigaoka, Yahatanishiku, Kitakyushu 807–8555, Japan. Address email to mogata{at}med.uoeh-u.ac.jp
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Abstract
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We studied the effects of pneumoperitoneum on gastric submucosal perfusion metabolism during elective laparoscopic cholecystectomy (LASC) by measuring the PCO2 gap, defined as the difference between intramucosal PCO2 and arterial PCO2, using gas tonometry in 20 patients. Furthermore, we examined whether thoracic epidural anesthesia (TEA) affects gastric submucosal perfusion metabolism during LASC. Patients were randomly allocated to receive general anesthesia (group G, n = 10) or general anesthesia combined with TEA (group E, n = 10). In both groups, the PCO2 gap increased significantly during pneumoperitoneum and remained at this level until the end of surgery compared with the baseline value. There were no significant differences in PCO2 gap values between the two groups at any time sampled. These results suggested that pneumoperitoneum significantly impaired gastric submucosal perfusion and metabolism and that TEA did not attenuate the impairment of gastric submucosal perfusion during or after pneumoperitoneum.
IMPLICATIONS: We investigated the effect of pneumoperitoneum on gastric submucosal perfusion by measuring PCO2 gap with the use of gas tonometry. PCO2 gap significantly increased during and after the pneumoperitoneum compared with the control level. Thoracic epidural anesthesia did not attenuate this inhibition.
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Introduction
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The use of laparoscopic surgery is increasing because of its advantages, including minimum surgical incisions, less blood loss, and shorter hospital stays as compared with more traditional surgical methods. However, pneumoperitoneum may induce hemodynamic changes, such as increased mean arterial blood pressures (MAP), systemic vascular resistance, and decreased cardiac output, which complicate anesthetic management (1,2). These changes may affect visceral perfusion and metabolism. The gastrointestinal tract is especially vulnerable to ischemia and hypoxia resulting from its unique blood flow distribution. Gastrointestinal tract malfunction is regarded as an important contributor to both the surgical stress response and postoperative complications (3). Gastrointestinal tract hypoperfusion has been reported to be associated with increased mortality in critically ill patients (4). Therefore, it is necessary to explore methods of attenuating the impairment of visceral perfusion and metabolism during pneumoperitoneum.
It is very difficult to measure gastric submucosal perfusion and metabolism directly in a clinical setting. However, we are able to estimate the condition of gastric submucosal perfusion and metabolism indirectly by measuring gastric intramucosal pH (pHi), which reflects the status of gastric submucosal perfusion and metabolism (5,6). However, in two studies, the concept of measuring pHi by gastric tonometry has been called into question for both pathophysiological and technical reasons (7,8). This concept favored monitoring the PCO2 gap, defined as the difference between intramucosal PCO2 (PrCO2) and arterial PCO2 (PaCO2), rather than pHi as a maker of gastric submucosal perfusion and metabolism (9). The results of previous studies of gastric submucosal perfusion and metabolism during pneumoperitoneum by measuring pHi or PrCO2 were varied and inconsistent (10–12). In the present study, we investigated gastric submucosal perfusion and metabolism during laparoscopic cholecystectomy (LASC) by measuring the PCO2 gap.
Kapral et al. (13) reported that thoracic epidural anesthesia (TEA) attenuated the decreases in pHi during major abdominal surgery. There have been no previous studies of the effects of TEA on gastric submucosal perfusion and metabolism during pneumoperitoneum. In this study, we investigated the effects of TEA by comparing the PCO2 gap in patients under general anesthesia with those under general anesthesia combined with TEA.
The PCO2 gap increased significantly during and after pneumoperitoneum, suggesting impairment of gastric submucosal perfusion. Furthermore, TEA did not attenuate gastric submucosal hypoperfusion during or after pneumoperitoneum.
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Methods
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After obtaining the approval of our local research ethics committee and informed written consent, 20 patients (ASA physical status I or II) undergoing elective LASC were enrolled in this study. Patients with a history of respiratory disease, coronary artery disease, coagulopathy, or previous gastric surgery were excluded. Patients were randomly allocated into two groups receiving general anesthesia (group G) or TEA combined with general anesthesia (group E). Each group consisted of 10 patients. All patients were premedicated with 5 mg of bromazepam and 20 mg of famotidine orally. In group E, an epidural catheter was inserted into the epidural space (Th 8/9) through an 18-gauge Tuohy needle with the paramedian method and then 5–7 mL of bupivacaine 2.0% was administered. The level of epidural anesthesia (analgesia between Th4–11) was confirmed by the pinprick method 20 min after bolus bupivacaine injection.
In both groups, anesthesia was induced with propofol (1.0 mg/kg) and tracheal intubation was facilitated with vecuronium (0.1 mg/kg). Patients were mechanically ventilated with 10–12 breaths/min, and end-tidal CO2 was kept between 30 and 40 mm Hg. After induction of anesthesia, a gastric tonometer tube (TRIP® NGS Catheter; Instrumentarium, Helsinki, Finland) was placed into the stomach. After insertion of this gastric tonometer, air and fluids were aspirated as much as possible. The catheter for gastric tonometry was connected to an automated gas analyzer (Tonometrics Tokibo, Tokyo, Japan). After balloon filling with air in a closed circuit, the PrCO2 was automatically measured by infrared spectroscopy after pre-equilibration for 20 min. A radial artery was cannulated for continuous blood pressure monitoring and blood sampling. In group E, anesthesia was maintained with 3–5 mL of bupivacaine 2.0% into the epidural space every 30–45 min and isoflurane up to 1.0% as a supplement, whereas in group G anesthesia was maintained with isoflurane (1.5%–2.0%). During surgery, acetate Ringer’s solution was continuously infused at 3 to 5 mL · kg-1 · h-1 in both groups.
PrCO2 was measured after induction of anesthesia and immediately before pneumoperitoneum (S1), 30 min after commencement of pneumoperitoneum (S2), immediately after the end of pneumoperitoneum (S3), and 5 min after the operation (S4). pHi values were calculated by inserting the values of PrCO2 and the arterial bicarbonate into Henderson-Hasselbach equation. Arterial pH (pHa), arterial PCO2 (PaCO2), arterial bicarbonate (HCO3-) concentration, arterial lactate concentration, arterial base excess (BE), and MAP were measured at the same time points.
LASC was performed using four cannulas with the patients in the approximately 20° head-up position. Intraabdominal pressure was maintained continuously at 6–8 mm Hg with a conventional pressure pneumoperitoneum device.
All clinical data are presented as median (interquartile range). Sequential changes in all variables were compared with baseline levels using the Wilcoxon’s signed rank test. Differences in all variables between group G and group E at individual time points were compared using the Mann-Whitney U-test. Bonferroni’s correction was applied for multiple comparisons. P values < 0.05 were considered significant.
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Results
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There were no significant differences between the two groups in age, height, weight, total pneumatic inflation, operation or anesthesia time (Table 1). Arterial pH, arterial lactate, and arterial BE values were within the respective normal ranges both during and after pneumoperitoneum.
The PCO2 gap increased significantly after abdominal pneumatic inflation and remained significantly increased at the end of surgery (Fig. 1A). At each sampling time point, subgroup data showed no significant differences in PCO2 gap values between the two groups (Fig. 1B).
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Figure 1. A, median, 25th and 75th percentiles, and ranges (vertical bars) of PCO2 gap. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. *P < 0.05 for comparison versus baseline value, corrected for multiple comparisons. B, median, 25th and 75th percentiles, and ranges (vertical bars) of PCO2 gap. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. Data in white and gray boxes are from the groups E (n = 10) and G (n = 10), respectively. *P < 0.05, corrected for multiple comparisons, between the E and G groups.
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In both groups, PrCO2 increased significantly after the establishment of pneumatic inflation and remained significantly increased at the end of surgery (Fig. 2A). Subgroup data showed no significant differences in PrCO2 values between the two groups at any sampling time point (Fig. 2B).
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Figure 2. A, median, 25th and 75th percentiles, and ranges (vertical bars) of PrCO2. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. *P < 0.05 for comparison versus baseline value, corrected for multiple comparisons. B, median, 25th and 75th percentiles, and ranges (vertical bars) of PrCO2. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. Data in white and gray boxes are from the groups E (n = 10) and G (n = 10), respectively. *P < 0.05, corrected for multiple comparisons, between the E and G groups.
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pHi decreased significantly after the establishment of abdominal pneumatic inflation and remained significantly reduced until the end of surgery (Fig. 3A). At each sampling time point, subgroup data showed no significant differences in pHi values between the two groups (Fig. 3B).
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Figure 3. A, median, 25th and 75th percentiles, and ranges (vertical bars) of pHi. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. *P < 0.05 for comparison versus baseline value, corrected for multiple comparisons. B, median, 25th and 75th percentiles, and ranges (vertical bars) of pHi. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. Data in white and gray boxes are from the groups E (n = 10) and G (n = 10), respectively. *P < 0.05, corrected for multiple comparisons, between the E and G groups.
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MAP showed no changes at any sampling time point as compared to the control level (Fig. 4A). However, subgroup analysis showed that MAP was significantly higher in group E as compared to group G after pneumoperitoneum (Fig. 4B).
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Figure 4. A, median, 25th and 75th percentiles, and ranges (vertical bars) of mean arterial blood pressure. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. *P < 0.05 for comparison versus baseline value, corrected for multiple comparisons. B, median, 25th and 75th percentiles, and ranges (vertical bars) of mean arterial blood pressure. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. Data in white and gray boxes are from the groups E (n = 10) and G (n = 10), respectively. *P < 0.05, corrected for multiple comparisons, between the E and G groups.
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Arterial HCO3- showed no changes at any sampling time point as compared to the control level (Fig. 5A). Subgroup analysis demonstrated no significant differences in arterial HCO3- between the two groups throughout the study (Fig. 5B).
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Figure 5. A, median, 25th and 75th percentiles, and ranges (vertical bars) of arterial bicarbonate. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. *P < 0.05 for comparison versus baseline value, corrected for multiple comparisons. B, median, 25th and 75th percentiles, and ranges (vertical bars) of arterial bicarbonate. S1 = after anesthetic induction and just before pneumoperitoneum (baseline), S2 = 30 min after pneumoperitoneum, S3 = immediately after the end of pneumoperitoneum, S4 = 5 min after an operation. Data in white and gray boxes are from the groups E (n = 10) and G (n = 10), respectively. *P < 0.05, corrected for multiple comparisons, between the E and G groups.
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Discussion
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During and after pneumoperitoneum the PCO2 gap was increased significantly as compared with the pre-pneumoperitoneum level, suggesting that pneumoperitoneum induces gastric submucosal hypoperfusion. pHi values decreased significantly during and after pneumoperitoneum as compared with the pre-pneumoperitoneum level. These changes paralleled those in the PCO2 gap. In the present study, no significant differences were observed in the PCO2 gap between patients receiving general anesthesia and those receiving general anesthesia combined with TEA, suggesting that TEA does not attenuate gastric submucosal hypoperfusion during LASC.
The pHi value is calculated from PrCO2 obtained by tonometry and arterial HCO3- concentration as a proxy for tissue HCO3- concentration. This calculation is based on the assumption that tissue bicarbonate concentration equals that of arterial blood. pHi has been suggested to constitute an index of adequacy of gastric submucosal perfusion or oxygenation. Many studies have shown that pHi measurements provide a reliable indication of the adequacy of splanchnic perfusion (5,6). However, another study has questioned the concept of pHi for the following reasons. First, regional ischemia may make the basic assumption that tissue bicarbonate concentration equals that of arterial blood incorrect (14). Second, systemic arterial bicarbonate is influenced by factors other than gastric submucosal hypoperfusion, such as renal dysfunction (15). Third, the PrCO2 value obtained by tonometry is affected by arterial PCO2 (16). Therefore, neither pHi value nor PrCO2 could be used as an indicator of the adequacy of gastric submucosal perfusion, although we took precautions to avoid methodological errors, including systemic H2 receptor blocker administration and the avoidance of enteral feeding for at least 8 hours before surgery. The PCO2 gap has been reported to be a sensitive and specific tonometric variable of gastric submucosal perfusion, independent of systemic, metabolic, and respiratory acidosis, and it is recommended as an alternative to pHi (17,18). We used the PCO2 gap as an indicator of gastric submucosal hypoperfusion. In the present study, monitoring the PCO2 gap was especially novel, not only because the PrCO2 value is easily affected by arterial PCO2 but also because PCO2 tends to increase during pneumoperitoneum (11,16). By measuring the PCO2 gap, we were able to elucidate both the effect of arterial PCO2 on PrCO2 and evaluate the assumption that tissue bicarbonate concentration equals that of arterial blood during pneumoperitoneum.
The effect of pneumoperitoneum on gastric submucosal perfusion and metabolism has been explored by measuring either pHi or PrCO2, but it remains controversial. By measuring pHi, Eleftheriadis et al. (10) concluded that pneumoperitoneum impaired gastric submucosal perfusion. Koivusalo et al. (11) compared pHi and PrCO2 values between the conventional carbon dioxide pressure pneumoperitoneum method (CPP group) and a mechanical retractor method (Retractor group) during LASC. The results showed that the pHi of the CPP group was significantly lower than that of the Retractor group during the laparoscopic procedure and that the PrCO2 of the CPP group was significantly higher than that of the Retractor group after surgery. The results reported in these two papers were consistent with those of the present study. However, based on the results of saline tonometry, Thaler et al. (12) concluded that pneumoperitoneum did not contribute to significant changes in pHi and PrCO2. This discrepancy might be attributable to differences in the equipment used in these studies. Saline measurements are known to be poorly reproducible and have significantly smaller PrCO2 values than air tonometry, which was used in the present study.
Gastric hypoperfusion is probably a result of the hemodynamic changes induced with CO2 pneumoperitoneum. A previous study showed that pneumoperitoneum induced an increase in the systemic vascular index and a decrease in the cardiac index, indicating that there was a major increase of afterload during pneumoperitoneum (19). These hemodynamic changes may induce splanchnic hypoperfusion. This suggested that we use TEA to preserve splanchnic circulation by reducing afterload. The effects of epidural anesthesia on preserving or improving splanchnic blood flow have been described previously. Kapral et al. (13) demonstrated that TEA attenuated decreases in intramucosal pH during major abdominal surgery. Sielenkamper et al. (20) reported that TEA increased mucosal perfusion in the ileum of rats. Another animal experiment showed that the capacitance vessels in the splanchnic circulation were dilated during sympathetic denervation, causing a blood shift from systemic to splanchnic circulation (21). Although these three studies were performed in open (laparotomy) cholecystectomy, the results suggested that TEA attenuated the surgical stress-induced decreases in gastric submucosal hypoperfusion. However, the results of the present study were contrary to our expectations. There were two possible explanations for this discrepancy. First, MAP values during and after pneumoperitoneum were significantly smaller in group E than in group G, but there were no significant differences in either PCO2 gap or pHi between the two groups. This suggests that the positive effect of TEA on cardiac output by decreasing afterloading was counterbalanced by the negative effect of the head-up position on cardiac output during pneumoperitoneum by decreasing the preload. This possibility is supported by the results of a previous study, in which the head-up position during carbon dioxide pneumoperitoneum significantly decreased cardiac index (22). Second, the duration of pneumoperitoneum in the present study might not have been sufficient to demonstrate the preventive effect of TEA on the surgical stress-induced decreases in gastric submucosal hypoperfusion. Kapral et al. (13) showed that the preventive effect of TEA on the decrease in pHi during abdominal surgery was proportional to the duration of the operation. In the case of pneumoperitoneum of longer duration, TEA might improve gastric submucosal hypoperfusion.
Furthermore, a previous study using transesophageal echocardiography indicated that the middle hepatic venous flow was decreased significantly in elderly patients (23). Further studies of the effects of TEA in elderly patients are required.
The results of the present study indicated that pneumoperitoneum induces gastric submucosal hypoperfusion and that TEA showed no attenuation of this effect. The results of the present study indicate that pneumoperitoneum impairs splanchnic perfusion during surgery. Thus, it is necessary to pay close attention to gastric submucosal hypoperfusion during surgery, especially in patients undergoing protracted procedures and in the elderly.
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Acknowledgments
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Supported, in part, by departmental funding and a grant-in-aid for scientific research (C10671453) from the Ministry of Education, and Culture of Japan.
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References
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- Struthers A, Cuschieri A. Cardiovascular consequences of laparoscopic surgery. Lancet 1998; 352: 568–70.[Web of Science][Medline]
- Joris JL, Noirot DP, Legrand MJ, et al. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993; 76: 1067–71.[Abstract/Free Full Text]
- Mythen MG, Webb AR. Intraoperative gut mucosal hypoperfusion is associated with increased post-operative complications and cost. Intensive Care Med 1994; 20: 99–104.[Web of Science][Medline]
- Fink MP. Gastrointestinal mucosal injury in experimental models of shock, trauma, and sepsis. Crit Care Med 1991; 19: 627–41.[Web of Science][Medline]
- Fiddian-Green RG. Gastric intramucosal pH, tissue oxygenation and acid-base balance. Br J Anaesth 1995; 74: 591–606.[Free Full Text]
- Maynard N, Beale R, Smithies M, Bihari D. Gastric intramucosal pH in critically ill patients. Lancet 1992; 339: 550–1.
- Schlichtig R, Stremple JF. Measuring splanchnic oxygenation by gastric tonometry. JAMA 1994; 271: 983–4.[Abstract/Free Full Text]
- Vincent JL, Creteur J. Gastric mucosal pH is definitely obsolete–please tell us more about gastric mucosal PCO2. Crit Care Med 1998; 26: 1479–81.[Web of Science][Medline]
- Schlichtig R, Mehta N, Gayowski TJ. Tissue-arterial PCO2 difference is a better marker of ischemia than intramural pH (pHi) or arterial pH-pHi difference. J Crit Care 1996; 11: 51–6.[Web of Science][Medline]
- Eleftheriadis E, Kotzampassi K, Botsios D, et al. Splanchnic ischemia during laparoscopic cholecystectomy. Surg Endosc 1996; 10: 324–6.[Web of Science][Medline]
- Koivusalo AM, Kellokumpu I, Ristkari S, Lindgren L. Splanchnic and renal deterioration during and after laparoscopic cholecystectomy: a comparison of the carbon dioxide pneumoperitoneum and the abdominal wall lift method. Anesth Analg 1997; 85: 886–91.[Abstract]
- Thaler W, Frey L, Marzoli GP, Messmer KM. Assessment of splanchnic tissue oxygenation by gastric tonometry in patients undergoing laparoscopic and open cholecystectomy. Br J Surg 1996; 83: 620–4.[Web of Science][Medline]
- Kapral S, Gollmann G, Bachmann D, et al. The effects of TEA on intraoperative visceral perfusion and metabolism. Anesth Analg 1999; 88: 402–6.[Abstract/Free Full Text]
- Antonsson JB, Boyle CC 3rd, Kruithoff KL, et al. Validation of tonometric measurement of gut intramural pH during endotoxemia and mesenteric occlusion in pigs. Am J Physiol 259 (4 Pt 1): G519–23, 1990.
- Creteur J, De Backer D, Vincent JL. Does gastric tonometry monitor splanchnic perfusion? Crit Care Med 1999; 27: 2480–4.[Web of Science][Medline]
- Creteur J, De Backer D, Vincent JL. Monitoring gastric mucosal carbon dioxide pressure using gas tonometry: in vitro and in vivo validation studies. Anesthesiology 1997; 87: 504–10.[Web of Science][Medline]
- Chapman MV, Mythen MG, Webb AR, Vincent JL. Report from the meeting: Gastrointestinal Tonometry: State of the Art. Intensive Care Med 2000; 26: 613–22.[Medline]
- Levy B, Gawalkiewicz P, Vallet B, et al. Gastric capnometry with air-automated tonometry predicts outcome in critically ill patients. Crit Care Med 2003; 31: 474–80.[Web of Science][Medline]
- Joris JL, Noirot DP, Legrand MJ, et al. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993; 76: 1067–71.
- Sielenkamper AW, Eicker K, Van Aken H. TEA increases mucosal perfusion in ileum of rats. Anesthesiology 2000; 93: 844–51.[Web of Science][Medline]
- Fujita Y. Splanchnic circulation following coeliac plexus block. Acta Anaesthesiol Scand 1988; 32: 323–7.[Web of Science][Medline]
- Hirvonen EA, Poikolainen EO, Paakkonen ME, Nuutinen LS. The adverse hemodynamic effects of anesthesia, head-up tilt, and carbon dioxide pneumoperitoneum during laparoscopic cholecystectomy. Surg Endosc 2000; 14: 272–7.[Web of Science][Medline]
- Sato K, Kawamura T, Wakusawa R. Hepatic blood flow and function in elderly patients undergoing laparoscopic cholecystectomy. Anesth Analg 2000; 90: 1198–202.[Abstract/Free Full Text]
Accepted for publication July 2, 2003.
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Abstract
Introduction
