Hepatic Venous Oxygen Saturation Research Articles

Mapping hepatic blood oxygenation by quantitative BOLD (qBOLD) MRI.

Abnormalities in hepatic oxygen delivery and oxygen consumption may serve as a significant indicator of hepatic cellular dysfunction and may predict treatment response. However, conventional and oxygen-enhanced hepatic BOLD MRI can only provide semiquantitative assessment of hepatic oxygenation. A hepatic quantitative BOLD (qBOLD) model was proposed for noninvasive mapping of hepatic venous blood oxygen saturation (Yv ) and deoxygenated blood volume (DBV) in human subjects. The validity and the estimation bias of the proposed model were evaluated by Monte Carlo simulations. Eight healthy subjects were scanned after written consent with institutional review board approval. Monte Carlo simulations demonstrated that the proposed single-compartment hepatic qBOLD model leads to significant deviation of the predicted T2* decay profile from the simulated signal due to high hepatic blood volume fraction. Small relative estimation bias for hepatic Yv and significant overestimation for hepatic DBV were observed, which can be corrected by applying the calibration curves established from simulations. After correction, the mean hepatic Yv in human subjects was 56.8 ± 6.8%, and the mean hepatic DBV was 0.190 ± 0.035, consistent with measurements from other invasive approaches. Except in regions with significant vascular contamination, the maps for hepatic Yv and DBV were relatively homogenous. With estimation bias correction, the hepatic qBOLD approach enables noninvasive mapping of hepatic blood volume and oxygenation in human subjects. The established protocol may be used to quantitatively assess hepatic tissue hypoxia in multiple liver diseases.

Distal Pancreatectomy with En bloc Celiac Axis Resection Performed while Monitoring Hepatic Arterial Flow by using a Transonic Flowmeter during Operation

Pancreatic body cancer often involves the common hepatic artery and/or the celiac axis, and is regarded as an unresectable disease. Hepatic blood flow must be monitored while performing distal pancreatectomy with en bloc celiac axis resection (DP-CAR) for managing the progression of pancreatic body cancer. We first confirmed a safe level of blood flow by monitoring hepatic venous oxygen saturation (ShvO2) to prevent hepatic ischemia caused by occlusion of the common hepatic artery. However, this method is technically difficult and a long period of time is required to insert the catheter. Thus, we monitored hepatic arterial flow by using a transonic flowmeter in the hepatic artery during operation. Between April 1992 and January 2011, 14 patients underwent DP-CAR. In 6 of these 14 patients we measured ShvO2. In 2 of the 14 patients, a transonic flowmeter was used for determining the hepatic arterial flow during operation. There were no complications during this operation. Operation time when the blood flow was monitored using a transonic flowmeter was less than that when ShvO2 was measured. Monitoring the transonic flowmeter hepatic artery is a useful and quick method for real-time evaluation of hepatic circulation during operation.

Biochemical and Morphologic Effects After Extended Liver Resection in Rats: Preliminary Results

After hepatic resection and transplantation with a partial graft, death and regeneration of the hepatocytes coexist in the liver. However, when the functional liver mass is inadequate to ensure a proper balance between regeneration vs functional and metabolic demands, small-for-size syndrome develops. We assessed the early effects of extended hepatic resection on liver function in a rat model. Six male Sprague-Dawley rats underwent 80% resection of the liver, and 6 rats served as a control group. At 6 hours after resection, blood samples were obtained from the hepatic vein for measurement of reduced glutathione (GSH), oxidized glutathione (GSSG), and hepatic venous oxygen saturation (Shv o 2), and for standard liver function tests including determination of concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), γ-glutamyl transpeptidase, and total bilirubin. The remnant lobe was removed for GSH assay and histopathologic analysis. In the resection group, values were significantly higher for ALT ( P = .002), AST ( P = .002), and Shv o 2 ( P = .01), whereas a significant decrease was observed for blood GSH ( P = .009) but not liver GSH. Also in the resection group, we observed characteristic hepatocyte vacuolization with a gradient from periportal acinar zone 1 to the centrolobular area, the presence of hemorrhagic necrosis, and several leukocyte adhesions. The Shv o 2 and GSH data suggest early alteration of oxygen metabolism, as demonstrated by the reduction in oxygen uptake and decreased liver GSH secretion, with preservation of hepatic GSH. Mitochondrial dysfunction and oxidative injury seem to have a crucial role in early onset of liver damage.

Blood lactate and pyruvate levels in the perioperative period of liver resection with pringle maneuver

Bleeding during liver surgery is often routinely controlled by the Pringle maneuver consisting in the temporary clamping of hepatic artery, portal vein, and bile duct. This study aimed at investigating a possible influence of the Pringle maneuver on tissue hypoxia during liver resection. Twenty-five consecutive patients undergoing elective liver resection were prospectively randomized either to be treated with the Pringle maneuver (Pringle group, n = 14) or without clamping (Controls, n = 11). Blood lactate levels, pyruvate levels, and hepatic vein oxygen saturation were monitored perioperatively. Patients were comparable with respect to resection time, intraoperative blood loss, and duration of surgery. The Pringle maneuver induced a significant increase in arterial lactate levels during liver resection when compared to Controls (2.6 +/- 0.3 vs 1.8 +/- 0.2 mmol/l; p < 0.05). Further, the Pringle maneuver significantly increased hepatic venous lactate (3.3 +/- 0.3 vs 1.6 +/- 0.3 mmol/l; p < 0.05) and lactate/pyruvate ratio in hepatic venous blood (43 +/- 8 vs 21 +/- 5; p < 0.05) during surgery. This was paralleled by a temporal decrease in hepatic venous oxygen saturation in the Pringle group (61 +/- 4 vs 73 +/- 4%; p < 0.05). Our findings demonstrate that liver metabolism and tissue oxygenation were markedly affected by occlusion of the liver hilus. Restricting the use of the Pringle maneuver to cases with severe bleeding might therefore be beneficial in patients undergoing liver resection.

Vasopressin decreases intestinal mucosal perfusion: a clinical study on cardiac surgery patients in vasodilatory shock

Low to moderate doses of vasopressin have been used in the treatment of cathecholamine-dependent vasodilatory shock in sepsis or after cardiac surgery. We evaluated the effects of vasopressin on jejunal mucosal perfusion, gastric-arterial pCO2 gradient and the global splanchnic oxygen demand/supply relationship in patients with vasodilatory shock after cardiac surgery. Eight mechanically ventilated patients, dependent on norepinephrine to maintain mean arterial pressure (MAP) > or = 60 mmHg because of septic/post-cardiotomy vasodilatory shock and multiple organ failure after cardiac surgery, were included. Vasopressin was sequentially infused at 1.2, 2.4 and 4.8 U/h for 30-min periods. Norepinephrine was simultaneously decreased to maintain MAP at 75 mmHg. At each infusion rate of vasopressin, data on systemic hemodynamics, jejunal mucosal perfusion, jejunal mucosal hematocrit and red blood cell velocity (laser Doppler flowmetry) as well as gastric-arterial pCO2 gradient (gastric tonometry) and splanchnic oxygen and lactate extraction (hepatic vein catheter) were obtained. The cardiac index, stroke volume index and systemic oxygen delivery decreased and systemic vascular resistance and systemic oxygen extraction increased significantly, while the heart rate or global oxygen consumption did not change with increasing vasopressin dose. Jejunal mucosal perfusion decreased and the arterial-gastric-mucosal pCO2 gradient increased, while splanchnic oxygen or lactate extraction or mixed venous-hepatic venous oxygen saturation gradient were not affected by increasing infusion rates of vasopressin. Infusion of low to moderate doses of vasopressin in patients with norepinephrine-dependent vasodilatory shock after cardiac surgery induces an intestinal and gastric mucosal vasoconstriction.

Increased splanchnic oxygen extraction because of routine nursing procedures*

Multiple organ failure is a common complication of acute circulatory and respiratory failure. We hypothesized that therapeutic interventions used routinely in intensive care can interfere with the perfusion of the gut and the liver, and thereby increase the risk of mismatch between oxygen supply and demand. Prospective, observational study. Interdisciplinary intensive care unit (ICU) of a university hospital. Thirty-six patients on mechanical ventilation with acute respiratory or circulatory failure or severe infection were included. Insertion of a hepatic venous catheter. Daily nursing procedures were recorded. A decrease of >or=5% in hepatic venous oxygen saturation (Sho2) was considered relevant. Observation time was 64 (29-104) hours (median [interquartile range]). The ICU stay was 11 (8-15) days, and hospital mortality was 35%. The number of periods with procedures/patient was 170 (98-268), the number of procedure-related decreases in Sho2 was 29 (13-41), and the number of decreases in Sho2 unrelated to procedures was 9 (4-19). Accordingly, procedure-related Sho2 decreases occurred 11 (7-17) times per day. Median Sho2 decrease during the procedures was 7 (5-10)%, and median increase in the gradient between mixed and hepatic venous oxygen saturation was 6 (4-9)%. Procedures that caused most Sho2 decreases were airway suctioning, assessment of level of sedation, and changing patients' position. Sho2 decreases were associated with small but significant increases in heart rate and intravascular pressures. Maximal Sequential Organ Failure Assessment scores in the ICU correlated with the number of Sho2 decreases (r: .56; p < 0.001) and with the number of procedure-related Sho2 decreases (r: .60; p < 0.001). Patients are exposed to repeated episodes of impaired splanchnic perfusion during routine nursing procedures. More research is needed to examine the correlation, if any, between nursing procedures and hepatic venous desaturation.

Assessment of hepatosplanchnic pathophysiology during thoracoabdominal aortic aneurysm repair using visceral perfusion and shunt☆

Despite the recognition of importance to avoid visceral ischemia during thoracoabdominal aortic aneurysm (TAAA) repair, the methodology of visceral perfusion seems still controversial and its pathophysiology has not been clearly understood. We investigated hepatosplanchnic metabolism during visceral perfusion/shunt in TAAA repair. Seventeen patients (10 male, 64+/-15 years old) who underwent elective TAAA repair using visceral perfusion/shunt under mild hypothermic distal aortic perfusion were retrospectively enrolled. Their aneurysm extension was type I and II in eight patients. In seven patients, four visceral arteries were perfused through a side-arm of distal aortic perfusion, while they were perfused by an independent pump in another five patients. In four of these 12 (two in each technique), visceral perfusion was converted into selective shunt after completion of aortic anastomosis. In the remaining five patients, four branches were initially perfused through a side-arm of distal aortic perfusion, and aortic perfusion was subsequently stopped after completion of aortic anastomosis. Hepatic venous oxygen saturation (ShO(2)), oxygen and lactate extraction ratio (OER, LER), and arterial ketone body ratio (AKBR) were measured at six time points. There was no mortality, liver/renal dysfunction, or spinal cord injury. Two patients required re-exploration for bleeding. Fourteen patients were extubated within 24h postoperatively. Mean intensive care unit stay was 2.3+/-1.7 days. During visceral perfusion, OER raised (31+/-13% to 68+/-21%, p=0.0012) and ShO(2) decreased (67+/-12% to 34+/-24%, p=0.0026) significantly. They recovered to baseline at skin closure. During the same period, LER (41+/-22% to -1+/-34%, p=0.0035) and AKBR (0.47+/-0.13 to 0.20+/-0.08, p=0.0012) significantly decreased. AKBR recovered to baseline at skin closure, but LER did not. ShO(2) (R(2)=0.483, p=0.0257) and LER (R(2)=0.774, p=0.0018) at skin closure and LER after initiation of partial cardiopulmonary bypass (R(2)=0.427, p=0.0211) had significant correlation with postoperative peak serum bilirubin level. AKBR after initiation of partial cardiopulmonary bypass had significant correlation with postoperative peak serum alanine aminotransferase level (R(2)=0.289, p=0.0476). Visceral perfusion/shunt in TAAA repair may avoid critical irreversible hepatosplanchnic ischemia but provide unphysiological blood flow to the liver and thus should be shortened.

Effect of propofol on hepatic blood flow and oxygen balance in rabbits

Propofol has been reported to alter hepatic blood flow and to increase hepatic oxygen consumption. This study was designed to determine the effect of propofol on hepatic blood flow and oxygenation in rabbits, in order to establish its net effect on hepatic oxygen balance. Twenty, adult male, New Zealand white rabbits were randomly divided into two groups: Group P (propofol, 0.6 mg.kg(-1).min(-1)) or Group C (10% intralipid, 0.6 mg.kg(-1).min(-1)). An electromagnetic flowmeter was used to measure hepatic blood flow, and blood, from the carotid artery, the portal vein, and the hepatic vein, was used to determine hepatic oxygenation. After we obtained baseline values, we repeated measurements ten, 30, and 60 min after initiating the infusion. Intralipid did not affect systemic hemodynamics, hepatic blood flow, or oxygenation during the 60 min infusion; however, propofol caused a time-dependent decrease in mean arterial blood pressures and an increase in portal venous flow and total hepatic blood flow. In contrast, hepatic arterial blood flow remained unchanged during the propofol infusion. Hepatic oxygen delivery and consumption increased in a time-dependent manner to maximums of 25% and 21.4% (both, P < 0.05) above baseline, respectively. Hepatic venous oxygen saturation and extraction was unchanged throughout the study period. Propofol increases total hepatic blood flow, primarily by increasing hepatic portal venous flow. The increase in liver oxygen consumption was fully compensated by an increase in oxygen supply to the liver, resulting in a preserved, hepatic oxygen balance.

Significance of intraoperative monitoring of arterial blood flow velocity and hepatic venous oxygen saturation for performing minimally invasive surgery in a patient with multiple calcified pancreaticoduodenal aneurysms with celiac artery occlusion

Even for patients with multiple pancreaticoduodenal aneurysms, successful treatment with noninvasive operative procedures can be employed, if intraoperative devices are considered. A 73-year-old man, without any symptoms, was admitted to our hospital and had computed tomography (CT) scanning to examine his liver for hepatitis C virus (HCV). Selective superior mesenteric artery (SMA) angiography confirmed multiple aneurysms in the anterior inferior pancreaticoduodenal artery (AIPDA), one aneurysm in the posterior inferior mesenteric artery (PIPDA), and another in the occluded celiac trunk, all with severe calcification. All of the aneurysms were thought to communicate with each other. With the celiac artery occlusion, the right hepatic artery (RHA) was revealed to be supplied by collateral arteries from the aneurysms in the AIPDA, and the left hepatic artery was shown to be supplied by collaterals from the left gastric artery. Intraoperative Doppler echography, at the time of the clamping of both IPDAs, demonstrated a marked decrease of blood velocity in all aneurysms (before clamping, >50 cm/s; after, <10 cm/s), although loss of pulsation and a marked decrease of flow in the RHA were inevitable. Therefore, each of these two IPDAs were ligated on the proximal side to the aneurysm, thus preserving the blood flow of the pancreas head fed by the PIPDA; bypass grafting from the AIPDA to the RHA, using the great saphenous vein, was done at the same time. After the creation of an anastomosis, the hepatic venous oxygen saturation (ShvO2) increased from 38% (at the time of ligation of the IPDAs) to 57% under ventilation. The patient's postoperative clinical course was uneventful. We describe and discuss our successful noninvasive operative management of multiple pancreaticoduodenal aneurysms, done while monitoring the blood flow and ShvO2, with some consideration of the literature.

Bench-to-bedside review: Is there a place for epinephrine in septic shock?

The use of epinephrine in septic shock remains controversial. Nevertheless, epinephrine is widely used around the world and the reported morbidity and mortality rates with it are no different from those observed with other vasopressors. In volunteers, epinephrine increases heart rate, mean arterial pressure and cardiac output. Epinephrine also induces hyperglycemia and hyperlactatemia. In hyperkinetic septic shock, epinephrine consistently increases arterial pressure and cardiac output in a dose dependent manner. Epinephrine transiently increases lactate levels through an increase in aerobic glycolysis. Epinephrine has no effect on splanchnic circulation in dopamine-sensitive septic shock. On the other hand, in dopamine-resistant septic shock, epinephrine has no effect on tonometric parameters but decreases fractional splanchnic blood flow with an increase in the gradient of mixed venous oxygen saturation (SVO2) and hepatic venous oxygen saturation (SHO2). In conclusion, epinephrine has predictable effects on systemic hemodynamics and is as efficient as norepinephrine in correcting hemodynamic disturbances of septic shock. Moreover, epinephrine is cheaper than other commonly used catecholamine regimens in septic shock. The clinical impact of the transient hyperlactatemia and of the splanchnic effects are not established.

Influence of Enteral and Parenteral Nutrition on Splanchnic Hemodynamics in Septic Patients

Enteral nutrition is believed to augment splanchnic perfusion, thereby preserving splanchnic integrity, whereas parenteral nutrition does not offer this benefit. In an effort to study this, we compared splanchnic oxygen exchange and blood flow in critically ill, septic patients to normal controls during enteral or total parenteral nutrition. Splanchnic oxygen exchange and hepatic blood flow characteristics in 14 critically ill, septic patients were compared to 19 normal controls while fasting and during nutrient administration. Nutrients were delivered as intraduodenal feedings or parenteral nutrition. Splanchnic hemodynamics were measured at baseline, 90 min, and 210 min during nutrient administration. Hepatic blood flow index (HBFI) by indocyanine green dye (ICG) clearance, splanchnic oxygen consumption index (SplVO(2)I), and hepatic venous oxygen saturation (ShvO(2)) were measured using hepatic venous catheterization. Plasma volume (PV) was measured from the volume of ICG distribution. Results were analyzed using population means (+/-SD) and one-way analysis of variance. There was no statistical change in HBFI, SplVO(2)I, PV or ShvO(2) over the study time interval within any group (p < 0.05), irrespective of whether enteral or parenteral nutrition was the nutrient source. Septic patients, whether fasting or receiving nutrition, demonstrated higher HBFI and SplVO(2)I levels, whereas ShvO(2) levels were uniformly lower throughout the study compared to normal controls. Critically ill patients exhibited a hyperdynamic splanchnic state as indicated by the marked increase in HBFI and SplVO(2)I. However, neither nutrient regimen at clinically relevant rates altered splanchnic hemodynamics over the course of study. Thus, enteral nutrients do not appear to offer hemodynamic protection to the splanchnic system in critically ill patients.

Investigation of muscle pH as an indicator of liver pH and injury from hemorrhagic shock

BackgroundDuring hemorrhagic shock blood flow to vital organs is maintained by the diversion of blood from both the splanchnic organs and skeletal muscle. In this swine study, we tested the hypotheses that (1) liver and muscle pH are correlated during both shock and resuscitation and (2) muscle pH during shock is an indicator of potential liver injury after resuscitation. Materials and methodsHemorrhagic shock was induced over 15 min to lower systolic blood pressure to 40 mm Hg and was maintained for 60 (n = 5) or 90 (n = 5) min. Resuscitation was achieved with shed blood and warm saline to maintain mean pressure >60 mm Hg for 120 min. Liver and muscle pH were measured with microelectrodes throughout the entire shock and resuscitation periods, along with hepatic venous oxygen saturation. Arterial lactate and aspartate aminotransferase were measured at baseline, end of shock, and resuscitation. Correlation between muscle and liver pH was determined. The ability of muscle pH to predict liver injury (40% increase in arterial aspartate aminotransferase) was compared with other predictors: liver pH, arterial lactate, and tonometric-arterial PCO2 gap. ResultspH values and rates of change were similar in both muscle and liver tissue. Liver pH was well correlated with muscle pH during both shock and resuscitation, R2 = 0.84. Muscle pH predicts potential liver injury with the same sensitivity as blood lactate in this swine shock model. ConclusionsMinimally invasive measurement of muscle pH warrants further study as a method to assess splanchnic hypoperfusion and resultant injury.

Regional oxygenation and systemic inflammatory response during cardiopulmonary bypass: Influence of temperature and blood flow variations

Objective: To evaluate the role of target temperature (28° or 34°C) in cardiac surgery on regional oxygenation during hypothermia and rewarming and systemic inflammatory response. Design: Prospective, controlled, and randomized clinical study. Setting: University hospital. Participants: Elderly patients (mean age 70 ± 2 years) with acquired heart disease with an anticipated bypass time exceeding 120 minutes (n = 30). Interventions: The patients were cooled to either 28°C (n = 15) or 34°C (n = 15). At hypothermia, bypass blood flow was reduced twice from full flow (2.4 L/min/m2 body surface area [BSA]) to 2.0 L/min/m2. Measurements and Main Results: Hepatic and jugular venous oxygen tension and saturation were higher at 28°C than at 34°C. In comparison with the preoperative values, at 28°C hepatic venous values were higher; whereas at 34°C, they were lower. The reduction of pump blood flow during hypothermia, from 2.4 to 2.0 L/min/m2was accompanied by reductions of central, jugular, and hepatic oxygenation at both target temperatures. During rewarming, central and regional venous oxygenation decreased irrespective of the preceding temperature. The decrease was most pronounced in hepatic venous blood, with the lowest individual values <10%. Serum concentrations of C3a and IL-6 increased during hypothermia and increased further during rewarming irrespective of the preceding temperature. Conclusion: During cardiopulmonary bypass, hypothermia at 28°C increases regional and central venous oxygenation better than at 34°C. In contrast, venous oxygenation decreases during rewarming irrespective of the preceding temperature. No significant difference in the systemic inflammatory response associated with target temperature was detected. © 2003 Elsevier Inc. All rights reserved.

Hepatic ischemia-reperfusion syndrome after partial liver resection (LR): Hepatic venous oxygen saturation, enzyme pattern, reduced and oxidized glutathione, procalcitonin and interleukin-6

The hepatic ischemia-reperfusion syndrome was investigated in 28 patients undergoing elective partial liver resection with intraoperative occlusion of hepatic inflow (Pringle maneuver) using the technique of liver vein catheterization. Hepatic venous oxygen saturation (ShvO2) was monitored continuously up to 24 hours after surgery. Aspartate aminotransferase, glutamate dehydrogenase, gamma-glutamyl transpeptidase, pseudocholinesterase, alpha-glutathione S-transferase, reduced and oxidized glutathione, procalcitonine, and interleukin-6 were serially measured both before and after Pringle maneuver during the resection and postoperatively in arterial and/or hepatic venous blood. ShvO2 measurement demonstrated that peri- and postoperative management was suitable to maintain an optimal hepatic oxygen supply. As expected, we were able to demonstrate a typical enzyme pattern of postischemic liver injury. There was a distinct decrease of reduced glutathione levels both in arterial and hepatic venous plasma after LR accompanied by a strong increase in oxidized glutathione concentration during the phase of reperfusion. We observed increases in procalcitonin and interleukin-6 levels both in arterial and hepatic venous blood after declamping. Our data support the view that liver resection in man under conditions of inflow occlusion resulted in ischemic lesion of the liver (loss of glutathione synthesizing capacity with disturbance of protection against oxidative stress) and an additional impairment during reperfusion (liberation of reactive oxygen species, local and systemic inflammation reaction with cytokine production). Additionally, we found some evidence for the assumption that the liver has an export function for reduced glutathione into plasma in man.

Impairment of Hepatosplanchnic Oxygenation and Increase of Serum Hyaluronate During Normothermic and Mild Hypothermic Cardiopulmonary Bypass

Hepatic sinusoidal endothelial cells (SECs) are more vulnerable to hypoxia or hypothermia than hepatocytes. To test the hypothesis that hepatic venous desaturation during cardiopulmonary bypass (CPB) leads to impairment of SEC function, we studied the plasma kinetics of endogenous hyaluronate (HA), a sensitive indicator of SEC function, and hepatosplanchnic oxygenation during and after CPB. Twenty-five consecutive patients scheduled for elective coronary artery bypass graft surgery, who underwent normothermic (>35°C;n = 15) or mild hypothermic (32°C;n = 10) CPB participated in this study. A hepatic venous catheter was inserted into each patient to monitor hepatosplanchnic oxygenation and serum levels of HA concentration. Hepatic venous oxygen saturation decreased essentially to a similar degree during normothermic and mild hypothermic CPB. Hepatosplanchnic oxygen consumption and extraction increased during normothermic (P < 0.05), but not mild hypothermic, CPB. Both arterial and hepatic venous HA concentrations showed threefold increases during and after CPB in both groups. A positive correlation was found between hepatosplanchnic oxygen consumption and arterial HA concentrations during CPB, suggesting a role of changes in hepatosplanchnic oxygen metabolism in the mechanisms of increases in serum HA concentrations. The failure of the liver to increase HA extraction to a great degree suggests that a functional impairment of the SEC may contribute to the observed increase of serum HA.

Disturbances in hepatocellular function during cardiopulmonary bypass using propofol anaesthesia

Background and objective Serum hyaluronate is thought to be an indicator of derangement in hepatocellular integrity, and the change in serum hyaluronate is a useful indicator in various liver disorders. We assessed the changes in serum hyaluronate in patients undergoing coronary artery bypass graft surgery. Methods Eleven patients scheduled for elective coronary artery bypass graft surgery were studied. An oximetry oxygen saturation catheter was inserted into the right hepatic vein to permit monitoring of hepatic venous oxygen saturation. Perioperative measurements included: haemodynamic variables; systemic oxygen delivery and uptake; arterial, mixed venous and hepatic venous oxygen saturation; arterial and hepatic venous plasma concentrations of lactate, arterial ketone body ratio (ratio of acetoacetate to 3-hydroxybutyrate); and arterial and hepatic venous hyaluronate were measured. Results Arterial and hepatic venous hyaluronate increased during cardiopulmonary bypass compared with the prebypass period. These increases returned to prebypass values after the cessation of bypass (hepatic venous hyaluronate value at the prebypass period: 26 ± 13 ng mL–1, during bypass: 77 ± 40 ng mL–1; 1 h after bypass: 57 ± 42 ng mL–1; 6 h after bypass: 32 ± 15 ng L–1, 24 h after bypass; 62 ± 21 ng mL–1; mean ± SD, P < 0.05). The arterial and hepatic venous hyaluronate during cardiopulmonary bypass was correlated with total bilirubin and hepatic venous lactate concentrations 6 h after bypass (arterial hyaluronate at cardiopulmonary bypass period vs. total bilirubin at 6 h after bypass;r =0.793, P =0.0036, hepatic venous hyaluronate during bypass vs. that at 6 h after bypass;r =0.795, P =0.0035). Conclusions Hepatocellular integrity might be disturbed during cardiopulmonary bypass when propofol anaesthesia is used.

Decreased splanchnic oxygen uptake and increased systemic oxygen uptake in cirrhosis are normalized after liver transplantation.

The aim of this study is to (1) characterize the impact of orthotopic liver transplantation (OLT) on splanchnic and systemic oxygen uptake (VO(2)) in patients with liver cirrhosis, and (2) investigate possible influencing factors, as well as metabolic consequences, of reduced splanchnic VO(2) in patients with cirrhosis. Therefore, we measured systemic VO(2) (indirect calorimetry), portal pressure (hepatic venous pressure gradient), hepatic blood flow (HBF; primed continuous infusion of indocyanine green), and hepatic turnover (arteriohepatic venous concentration differences multiplied by HBF) of oxygen, glucose, free fatty acids (FFAs), and aromatic amino acids (AAAs) in 52 patients with advanced cirrhosis and 16 patients with a clinically stable long-term course after OLT. Systemic VO(2) was significantly increased in patients with cirrhosis (261 +/- 7 mL/min) and normalized after OLT (216 +/- 8 mL/min; P < .001). Arterial and hepatic venous oxygen saturation and splanchnic oxygen extraction (in percent) were not different between patients with cirrhosis and after OLT. Splanchnic VO(2) was decreased in patients with cirrhosis (41 +/- 3 mL/min, representing 16% +/- 1% of systemic VO(2)) and normalized after OLT (69 +/- 6 mL/min; P < .001, representing 32% +/- 3% of systemic VO(2); P < .001). In patients with cirrhosis, a decrease in HBF was associated with decreased splanchnic VO(2) (r = 0.74; P < .001). Conversely, decreased splanchnic VO(2) reflected a decrease in hepatic glucose production (r = 0.34; P = .01) and hepatic extraction of FFAs (r = 0.40; P < .01) and AAAs (r = 0.30; P < .05). These results show that (1) splanchnic and systemic VO(2) normalize after OLT, indicating correction of hepatic and extrahepatic metabolic derangements; (2) in cirrhosis, HBF becomes limiting for hepatic oxygen supply; and (3) impaired splanchnic VO(2) reflects a decrease in metabolic liver function.

Disturbances in hepatocellular function during cardiopulmonary bypass using propofol anaesthesia.

Serum hyaluronate is thought to be an indicator of derangement in hepatocellular integrity, and the change in serum hyaluronate is a useful indicator in various liver disorders. We assessed the changes in serum hyaluronate in patients undergoing coronary artery bypass graft surgery. Eleven patients scheduled for elective coronary artery bypass graft surgery were studied. An oximetry oxygen saturation catheter was inserted into the right hepatic vein to permit monitoring of hepatic venous oxygen saturation. Perioperative measurements included: haemodynamic variables; systemic oxygen delivery and uptake; arterial, mixed venous and hepatic venous oxygen saturation; arterial and hepatic venous plasma concentrations of lactate, arterial ketone body ratio (ratio of acetoacetate to 3-hydroxybutyrate); and arterial and hepatic venous hyaluronate were measured. Arterial and hepatic venous hyaluronate increased during cardiopulmonary bypass compared with the prebypass period. These increases returned to prebypass values after the cessation of bypass (hepatic venous hyaluronate value at the prebypass period: 26 +/- 13 ng mL(-1), during bypass: 77 +/- 40 ng mL(-1); 1 h after bypass: 57 +/- 42 ng mL(-1); 6 h after bypass: 32 +/- 15 ng L(-1), 24 h after bypass; 62 +/- 21 ng mL(-1); mean +/- SD, P < 0.05). The arterial and hepatic venous hyaluronate during cardiopulmonary bypass was correlated with total bilirubin and hepatic venous lactate concentrations 6 h after bypass (arterial hyaluronate at cardiopulmonary bypass period vs. total bilirubin at 6 h after bypass; r=0.793, P=0.0036, hepatic venous hyaluronate during bypass vs. that at 6 h after bypass; r=0.795, P=0.0035). Hepatocellular integrity might be disturbed during cardiopulmonary bypass when propofol anaesthesia is used.

Hepatosplanchnic oxygenation is better preserved during mild hypothermic than during normothermic cardiopulmonary bypass.

To assess and compare the effects of normothermic and mild hypothermic cardiopulmonary bypass (CPB) on hepatosplanchnic oxygenation. We studied 14 patients scheduled for elective coronary artery bypass graft surgery who underwent normothermic (>35 degrees C; group I, n=7) or mild hypothermic (32 degrees C; group II, n=7) CPB. After induction of anesthesia, a hepatic venous catheter was inserted into the right hepatic vein to monitor hepatic venous oxygen saturation (ShvO(2)) and hepatosplanchnic blood flow by a constant infusion technique that uses indocyanine green. The ShvO(2) decreased from a baseline value in both groups during CPB and was significantly lower at ten minutes and 60 min after the onset of CPB in group I (39.5 +/- 16.2% and 40.1 +/- 9.8%, respectively) than in group II (61.1 +/- 16.2% and 61.0 +/- 17.9%, respectively; P <0.05). During CPB, the hepatosplanchnic oxygen extraction ratio was significantly higher in group I than in group II (44.0 +/- 7.2% vs 28.7 +/- 13.1%; P <0.05). Hepatosplanchnic oxygenation was better preserved during mild hypothermic CPB than during normothermic CPB.

The hepatosplanchnic area is not a common source of lactate in patients with severe sepsis.

To investigate the role of the splanchnic region in the hyperlactatemia of septic patients. Prospective, observational study. Thirty-one-bed mixed medicosurgical intensive care unit. Ninety invasively monitored and mechanically ventilated patients with severe sepsis. Splanchnic lactate balance was measured in all patients. Splanchnic blood flow was determined by using the primed continuous indocyanine green infusion technique in 69 patients. In 71 patients, gastric mucosal Pco2 and the Pco2 gap (the difference between gastric and arterial Pco2) also were determined by using gas tonometry with an automated gas analyzer. In each patient, arterial, mixed-venous, and hepatic venous blood samples were obtained to determine hemoglobin oxygen saturations and lactate concentrations. Arterial and hepatic venous lactate concentrations were determined in triplicate and were averaged, and the arterial hepatic venous difference in lactate and lactate consumption were calculated. The splanchnic region produced lactate in only six of the 90 patients. Mean arterial pressure, cardiac index, arterial lactate, hepatic venous oxygen saturation, and catecholamine use were similar in the six patients with splanchnic lactate production and in the 84 others. The arterial hepatic venous differences in lactate and splanchnic lactate consumption were related directly to arterial lactate concentrations (y = 0.073x + 0.209, r(2) =.06, p <.05, and y = 0.06x + 0.183, r(2) =.08, p <.05, respectively) but were not related to Pco2 gap, to the gradient between mixed-venous and hepatic venous oxygen saturations, or to bilirubin concentrations. Splanchnic lactate release is uncommon in septic patients, even when hyperlactatemia is severe.