Application of the Bogossian formula for evaluation of the QT interval in pacemaker patients with stimulated left bundle branch block.

BACKGROUND: The presence of left bundle branch block (LBBB) represents a particular challenge in properly measuring the QT interval. Here we demonstrate the applicability of the "Bogossian formula" in pacemaker patients with LBBB due to apical or nonapical right ventricular (RV) pacing and preserved left ventricular function. METHODS: A total of 163 patients with a cardiac one- or two-chamber pacemaker were included in this prospective, multicentre observational study. Twelve-lead ECG recordings were obtained during both intrinsic rhythm and RV pacing with induced LBBB. The QT interval measured during LBBB was corrected using the Bogossian formula to obtain the "modified QT" (QTm). The QTmc interval was calculated with the Bazett formula, and this was compared with the QTc interval during intrinsic rhythm. RESULTS: Eighty-three patients (78 ± 9 years; male n = 83) with apical and eighty patients (71 ± 13 years; male n = 80) with non-apical RV pacing were included in this study. In the apical group the QTmc was determined to be 444 ± 39 ms in paced rhythm and the QTc interval 413 ± 36 ms in intrinsic rhythm. In the non-apical group these values were 430 ± 34 ms in paced and 416 ± 32 ms in intrinsic rhythm. CONCLUSION: The Bogossian formula is a reliable tool for QTc interval evaluation in pacemaker patients with LBBB due to apical or non-apical RV pacing. However, an overestimation of 30 ms should be included in the calculation.

No effect of the cyclooxygenase-2 inhibitor etoricoxib on pre-emptive and post-operative analgesia in visceral surgery: results of a randomized controlled trial.

BACKGROUND: Pre-emptive analgesia in perioperative care has potential benefits for patients. The pre-emptive and postoperative analgesic effects of the cyclooxygenase-2 inhibitor etoricoxib have been investigated using a 2 × 2 factorial trial design. METHODS: According to the 2 × 2 factorial study design, 103 patients scheduled for visceral surgery, were randomly allocated to two groups prior to surgery. Patients could receive either etoricoxib or placebo (to investigate pre-emptive analgesia). Subsequent to surgery, patients randomly received either etoricoxib or placebo, again. It follows, that four treatment modalities (continuous or replaced intervention) result, to investigate postoperative analgesia. Main Outcome Measure was the cumulative morphine use 48 h post-surgery. Other outcomes included pain intensities, pain thresholds and sensory detection. RESULTS: Eighty-six patients (female n = 42; mean age 53.82 ± 13.61 years) were evaluated on the basis of an intention to treat analysis. Pre-emptive administration of 120 mg etoricoxib did not significantly reduce the cumulative morphine dose within the first 48 h after surgery, when compared to the administration of placebo. The analysis of the post-operative treatment groups showed a non-significant 8% reduction in morphine dose during the continuous administration of etoricoxib. There were no changes in sensory perception as detected with QST before and after surgery or between groups. CONCLUSIONS: The effect of administering etoricoxib was not superior to placebo in reducing the morphine dose required for postoperative analgesia. The lack of changes in peripheral nociception suggests that central algetic mechanisms are of higher impact in the development of postoperative pain following abdominal or thoracic surgery.

Placental syncytiotrophoblast maintains a specific type of glycocalyx at the fetomaternal border: the glycocalyx at the fetomaternal interface in healthy women and patients with HELLP syndrome.

Recent studies showed that considerable amounts of glycosaminoglycans are released into maternal blood during normal pregnancy and in hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. Maternal endothelia and the syncytiotrophoblast layer have been discussed as a possible origin of these glycocalyx components. Our study aimed to visualize the glycocalyx on the syncytiotrophoblast by electron microscopy, to analyze its structure and composition by immunohistochemistry, and to determine potential differences between healthy women and women with HELLP syndrome. For electron microscopy, a cotyledon was fixed by perfusion of the intervillous space with a 2% lanthanum-nitrate glutaraldehyde solution followed by immersion fixation in the same fixative. For immunohistochemistry, sections of 16 placentas (HELLP patients/healthy women, n = 8 each) were stained with monoclonal antibodies against the main glycocalyx constituents syndecan 1, hyaluronic acid, and heparan sulfate. Semiquantitative evaluation of staining intensity focused on the apical surface of the syncytiotrophoblast and fetal intravillous endothelia as possible localizations of a placental glycocalyx. Electron microscopy revealed a glycocalyx of approximately 250 nm, covering the syncytiotrophoblast layer. This was found to contain large amounts of syndecan 1, but neither hyaluronic acid nor heparan sulfate as major components. Intravillous fetal endothelium did not express any of the investigated glycosaminoglycans. Healthy women and patients with HELLP showed no differences concerning glycocalyx composition and thickness of the syncytiotrophoblast. The composition of the "placental" glycocalyx differs from the adult and fetal vascular glycocalyx. Obviously, the human placental syncytiotrophoblast maintains a special kind of glycocalyx at the fetomaternal interface.

Increased serum concentrations of circulating glycocalyx components in HELLP syndrome compared to healthy pregnancy: an observational study.

Severe inflammation has been shown to induce a shedding of the endothelial glycocalyx (EGX). Inflammatory cytokines, such as tumor necrosis factor α (TNF-α), impede the thickness of the EGX. While a controlled inflammatory reaction occurs already in normal pregnancy, women with hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome had an exaggerated inflammatory response. This study investigates the shedding of the glycocalyx during normal pregnancy and in women with HELLP syndrome. Glycocalyx components (syndecan 1, heparan sulfate, and hyaluronic acid) were measured in serum of healthy women throughout pregnancy (4 time points, n = 26), in women with HELLP syndrome (n = 17) before delivery and in nonpregnant volunteers (n = 10). Serum concentrations of TNF-α and soluble TNF-α receptors (sTNF-Rs) were assessed once in all 3 groups. Syndecan 1 serum concentrations constantly rose throughout normal pregnancy. Immediately before delivery, a 159-fold increase was measured compared to nonpregnant controls (P < .01). Even higher amounts were observed in patients with HELLP prior to delivery (median 12 252 ng/mL) compared to healthy women matched by gestational age (median 5943 ng/mL; P < .01). Relevantly, increased serum levels of heparan sulfate, hyaluronic acid, and sTNF-Rs were only detected in patients with HELLP (P < .01). These findings suggest that considerable amounts of syndecan 1 are released into maternal blood during uncomplicated pregnancy. The HELLP syndrome is associated with an even more pronounced shedding of glycocalyx components. The maternal vasculature as well as the placenta has to be discussed as a possible origin of circulating glycocalyx components.

Inosine, not adenosine, initiates endothelial glycocalyx degradation in cardiac ischemia and hypoxia.

Ischemia/reperfusion and hypoxia/reoxygenation of the heart both induce shedding of the coronary endothelial glycocalyx. The processes leading from an oxygen deficit to shedding are unknown. An involvement of resident perivascular cardiac mast cells has been proposed. We hypothesized that either adenosine or inosine or both, generated by nucleotide catabolism, attain the concentrations in the interstitial space sufficient to stimulate A3 receptors of mast cells during both myocardial ischemia/reperfusion and hypoxia/reoxygenation. Isolated hearts of guinea pigs were subjected to either normoxic perfusion (hemoglobin-free Krebs-Henseleit buffer equilibrated with 95% oxygen), 20 minutes hypoxic perfusion (buffer equilibrated with 21% oxygen) followed by 20 minutes reoxygenation, or 20 minutes stopped-flow ischemia followed by 20 minutes normoxic reperfusion (n = 7 each). Coronary venous effluent was collected separately from so-called transudate, a mixture of interstitial fluid and lymphatic fluid appearing on the epicardial surface. Adenosine and inosine were determined in both fluid compartments using high-performance liquid chromatography. Damage to the glycocalyx was evident after ischemia/reperfusion and hypoxia/reoxygenation. Adenosine concentrations rose to a level of 1 µM in coronary effluent during hypoxic perfusion, but remained one order of magnitude lower in the interstitial fluid. There was only a small rise in the level during postischemic perfusion. In contrast, inosine peaked at over 10 µM in interstitial fluid during hypoxia and also during reperfusion, while effluent levels remained relatively unchanged at lower levels. We conclude that only inosine attains levels in the interstitial fluid of hypoxic and postischemic hearts that are sufficient to explain the activation of mast cells via stimulation of A3-type receptors.

Shedding of the coronary endothelial glycocalyx: effects of hypoxia/reoxygenation vs ischaemia/reperfusion.

BACKGROUND: Vascular endothelium is covered by a glycocalyx. Damage to the glycocalyx after systemic inflammation or ischaemia/reperfusion contributes to increased vascular permeability and leucocyte adhesion. The underlying mechanisms leading to ischaemia/reperfusion-induced glycocalyx shedding are incompletely understood, in terms of lack of oxygen, absence of flow, or return of oxygen. METHODS: Isolated guinea pig hearts perfused with Krebs-Henseleit buffer at 37°C underwent 20 min of either stopped-flow ischaemia or hypoxic perfusion with subsequent reperfusion/reoxygenation (n = 6 each). Hearts perfused with normoxic buffer served as time controls. Epicardial transudate was collected to assess coronary net fluid filtration, colloid extravasation, and histamine release by mast cells. Syndecan-1 and heparan sulphate were measured in coronary effluent, together with lactate, purines, and the release of mast-cell tryptase ß. Additional hearts were perfusion-fixed to visualize the glycocalyx. RESULTS: Both ischaemia and hypoxia with reperfusion/reoxygenation resulted in significant increases in net fluid filtration (P < 0.05) and release of syndecan-1 and heparan sulphate in coronary effluent. These effects were already seen with the onset of hypoxic perfusion. Histamine was released during hypoxia and reoxygenation and also reperfusion, as was tryptase ß, and high concentrations of adenosine (>1 µmol litre⁻¹, hypoxia group) and inosine (> 7 µmol litre⁻¹, ischaemia group) were measured in effluent (P < 0.05). Damage to the coronary glycocalyx was evident upon electron microscopy. CONCLUSIONS: Both ischaemic and hypoxic hypoxia initiate glycocalyx degradation, promoting an increase in permeability. A contributing mechanism could be purine-mediated degranulation of resident mast cells, with liberated tryptase ß acting as potential 'sheddase'.

Sevoflurane preserves the endothelial glycocalyx against ischaemia-reperfusion injury.

BACKGROUND: Healthy vascular endothelium is coated by the glycocalyx, important in multiple endothelial functions, but destroyed by ischaemia-reperfusion. The impact of volatile anaesthetics on this fragile structure has not been investigated. We evaluated the effect of cardiac pre- and post-conditioning with sevoflurane on integrity of the endothelial glycocalyx in conjunction with coronary vascular function. METHODS: Isolated guinea pig hearts perfused with Krebs-Henseleit buffer underwent 20 min stopped-flow ischaemia (37 degrees C), either without or with 1 MAC sevoflurane. This was applied for 15 min before, for 20 min after, or both before and after ischaemia. Transudate was collected for assessing coronary net fluid extravasation and histamine release by mast cells. Coronary release of syndecan-1 and heparan sulphate was measured. In additional experiments with and without continuous sevoflurane, cathepsin B and tryptase beta-like protease activity were measured in effluent. Hearts were perfusion-fixed to visualize the endothelial glycocalyx. RESULTS: Ischaemia led to a significant (P<0.05) increase by 70% in transudate formation during reperfusion only in hearts without sevoflurane. This was accompanied by significant (P<0.05) increases in heparan sulphate (four-fold) and syndecan release (6.5-fold), with electron microscopy revealing massive degradation of glycocalyx. After ischaemia, histamine was released into transudate, and cathepsin B activity increased in effluent (P<0.05). Sevoflurane application attenuated all these changes, except for histamine release. CONCLUSIONS: Sevoflurane protects the endothelial glycocalyx from ischaemia-reperfusion-induced degradation, with both preconditioning and rapid post-conditioning being successful. The mechanism seems to involve attenuation of lysosomal cathepsin B release and to be independent from tissue mast cell degranulation.

[Hypernatremic alkalosis. Possible counterpart of hyperchloremic acidosis in intensive care patients?]. / Hypernatriämische Alkalose. Pendant zur hyperchlorämischen Acidose in der Intensivmedizin?

BACKGROUND: With broad acceptance of Stewart's acid-base model "hyperchloremic acidosis" is regarded as an independent form of metabolic disorder. It is unknown whether hypernatremia plays a corresponding role with respect to the development of alkalosis. METHODS: A total of 201 artificially ventilated, critically ill patients were monitored for hypernatremic episodes. Inclusion criterion was a serum sodium concentration above 145 mmol/l. RESULTS: In 20 patients a total of 78 periods of elevated plasma sodium levels lasting at least 24 h were observed. In 86% of these cases sodium and chloride concentrations were simultaneously increased. The development of alkalosis correlated with the strong ion difference (r=0.80, p<0.01) but not with the serum sodium concentration (r=-0.031, p=0.78). In cases without accompanying hyperchloremia (13%) metabolic alkalosis regularly occurred and a correlation between serum sodium concentration and base excess could be verified (r=0.66, p=0.03). Alkalosis occurred in 84.8% of cases where the strong on difference exceeded 39 mmol/l. CONCLUSION: From the available data hypernatremic alkalosis could not be defined as an independent metabolic disorder. In would seem more appropriate to use the term "strong ion alkalosis" in this context.

[Methylnaltrexone. A new approach for therapy of opioid-induced obstipation]. / Methylnaltrexon. Ein neuer Ansatz zur Therapie der opioidinduzierten Obstipation.

Chronic pain patients using opioids frequently suffer from constipation which compromises well-being. Such an opioid-induced gastro-intestinal complication can occur regularly in patients in palliative care as well as in analgesic sedated intensive care patients or during prolonged perioperative pain therapy. Discomfort and distress in the affected patients can be so severely pronounced that they would rather suffer from the pain than from the side effect of constipation. Conventional therapy can be insufficient in providing satisfactory relief of constipation, mostly because this opioid-induced bowel hypomotility can be laxative-resistant. Moreover, constipation does not decrease during the course of therapy as do other side effects. It is well known that opioid-induced constipation is mediated via activation of micro-opioid receptors in the gastrointestinal tract. Selective peripheral micro-receptor antagonists (such as methylnaltrexone, Relistor) can effectively treat opioid-induced constipation. An interference with central analgesia does not occur as the molecules cannot pass the blood-brain barrier due to their charged states. A reduction of opioid therapy or the development of withdrawal symptoms can be avoided. Studies have shown that methylnaltrexone is not only safe and efficient for chronically constipated palliative care patients but offers promising therapeutic options for further patient collectives.

Serum heparan sulfate levels are elevated in endotoxemia.

BACKGROUND: Increased vascular permeability is a characteristic feature of sepsis which, in the past, has been ascribed exclusively to a malfunction of endothelial cells. However, recently it has become evident that the endothelial glycocalyx is of considerable importance concerning various aspects of vascular physiology, e.g. the vascular barrier and inflammation. Heparan sulfate, one of its essential components is characteristically traceable in blood, in case the endothelial glycocalyx is damaged or destroyed. METHODS: In 15 pigs we investigated whether the administration of endotoxin from gram-negative bacteria (Escherichia coli) results in increased serum levels of heparan sulfate, signalizing a shedding of the glycocalyx. In addition, markers of inflammation (white blood cell count, platelet count, tumour necrosis factor-α and interleukin-6) were evaluated over an observation period of 6 hours. RESULTS: Serum heparan sulfate concentrations significantly increased over time in the endotoxin group and were significantly elevated in comparison to the control group 6 hours after administration of endotoxin (p<0.001). In the endotoxin group all markers of inflammation significantly changed during the time course. CONCLUSIONS: The administration of bacterial endotoxin induced a significant rise in degradation products of the endothelial glycocalyx.

[Expedition glycocalyx. A newly discovered "Great Barrier Reef"]. / Expedition Glykokalyx. Ein neu entdecktes "Great Barrier Reef."

Healthy vascular endothelium is luminally coated by an endothelial glycocalyx, which interacts with the bloodstream and assumes a filter function on the vascular wall. Although this structure was discovered nearly 70 years ago, its physiological importance has been underestimated for a long time. Recent findings indicate that the glycocalyx is, in addition to the endothelial cells themselves, a main constituent part of the vascular barrier. The existence of different colloid osmotic gradients within and beneath this structure has now led to a modification of the Starling equation. In many vascular beds the interstitial space features a protein concentration similar to that of the plasma. The inwardly directed gradient, which retains water and proteins in the vascular system, is generated beneath the glycocalyx by selective protein filtration over this structure. The endothelial glycocalyx, as an additional competent vascular permeability barrier has, therefore, not only a key role for perioperative fluid and protein shifts into the interstitial space, but it seems to be intimately involved in the pathophysiology of diabetes, arteriosclerosis, sepsis and ischemia/reperfusion, especially with respect to associated vascular dysfunctions. The fragile glycocalyx can be destroyed in the course of surgery, trauma, ischemia/reperfusion and sepsis and by inflammatory mediators such as TNF-alpha, causing leukocyte adhesion, platelet aggregation and edema formation. Recent studies have shown that protecting this structure not only maintains the vascular barrier, but constitutes an important component of a rational perioperative fluid therapy.

Impact of the time window on plasma volume measurement with indocyanine green.

Recent reports have questioned the accuracy of the indocyanine green dilution technique for measuring plasma volume. Our objective was to evaluate the impact of different time windows for monoexponential extrapolation. We retrospectively analysed 31 indocyanine green decay curves to investigate the problem in principle (group 1) and prospectively performed another 21 plasma volume measurements to estimate its practical impact (group 2). To monoexponentially extrapolate back to the specific extinction at the time of dye injection, two different time windows were applied to each decay curve, comparing the plasma volumes resulting from sampling within a short (5 min) period of time. Extrapolating back from the longer period led to a higher apparent plasma volume relative to the shorter period in both groups, the difference being 348 +/- 171 ml (group 1) and 384 +/- 131 ml (group 2; mean +/- SD; p < 0.05 each). This result was due to a reliable monoexponentiality of decay only up to the 5th min after dye injection. Thus, to estimate the initial distribution space of indocyanine green via monoexponential extrapolation, the first linear kinetic of indocyanine green decay should be taken.

Lung injury following thoracic aortic occlusion: comparison of sevoflurane and propofol anaesthesia.

BACKGROUND: Halogenated anaesthetics have been shown to reduce ischaemia-reperfusion injuries in various organs due to pre- and post-conditioning mechanisms. We compared volatile and total intravenous anaesthesia with regard to their effect on remote pulmonary injury after thoracic aortic occlusion and reperfusion. METHODS: Eighteen pigs were randomized after sternotomy and laparotomy (fentanyl-midazolam anaesthesia) to receive either sevoflurane or propofol in an investigator-blinded fashion. Ninety minutes of thoracic aortic occlusion was induced by a balloon catheter. During reperfusion, a goal-directed resuscitation protocol was performed. After 120 min of reperfusion, the anaesthetic regimen was changed to fentanyl-midazolam again for another 180 min. The oxygenation index and intra-pulmonary shunt fractions were calculated. After 5 h of reperfusion, a bronchoalveolar lavage was performed. The total protein content and lactate dehydrogenase activity were measured in epithelial lining fluid (ELF). Alveolar macrophage oxidative burst was analysed. The wet to dry ratio was calculated and tissue injury was graded using a semi-quantitative score. Ten animals (n=5 for each anaesthetic) without aortic occlusion served as time controls. RESULTS: The oxygenation index decreased and the intra-pulmonary shunt fraction increased significantly in both occlusion groups. There were no significant differences between sevoflurane and propofol with respect to the oxygenation index, ELF composition, morphologic lung damage, wet to dry ratio and alveolar macrophage burst activity. Differences were, however, seen in terms of systemic haemodynamic stability, where catecholamine requirements were less pronounced with sevoflurane. CONCLUSION: We conclude that the severity of remote lung injury was not different between sevoflurane and propofol anaesthesia in this porcine model of severe lower-body ischaemia and reperfusion injury.

Blood volume is normal after pre-operative overnight fasting.

BACKGROUND: Pre-operative fasting is assumed to cause a deficit in intravascular blood volume (BV), as a result of ongoing urine production and insensible perspiration. Standard regimes consist of volume loading prior or simultaneous to any anaesthetic procedure to minimise the risk of hypotension. However, fluid overload in the context of major abdominal surgery has been shown to deteriorate patient outcome. Our study aimed to quantify total intravascular BV after fasting by direct measurements and to compare it with calculated normal values in comparable non-fasted patients. METHODS: After 10 h of fasting, total plasma volume (PV) and red cell volume (RCV) were measured via the double-label technique (indocyanine green dilution and erythrocytes labelled with fluorescein, respectively) following induction of general anaesthesia in 53 gynaecological patients suffering from malignoma of the cervix. The corresponding normal values were calculated individually from age, body height and body weight. RESULTS: Measured BV, RCV and PV after fasting were 4123+/-589, 1244+/-196 and 2879+/-496 ml, respectively. The differences to the corresponding calculated normal values were not significant (3882+/-366, 1474+/-134 and 2413+/-232 ml, respectively). The measured haematocrit reflected a slight anaemic state (0.35+/-0.03). CONCLUSION: Our data suggest that even after prolonged pre-operative fasting, cardio-pulmonary healthy patients remain intravascularly normovolaemic. Therefore, hypotension associated with induction of general or neuraxial anaesthesia should perhaps be treated with moderate doses of vasopressors rather than with undifferentiated volume loading.

[Metabolic alkalosis despite hyperlactatemia and hypercapnia. Interpretation and therapy with help of the Stewart concept]. / Metabolische Alkalose trotz ausgeprägter Hyperlaktatämie and Hyperkapnie. Interpretation und Therapie mithilfe des Stewart-Modells.

Acid-base disturbances are commonly found in critically ill patients and are often associated with fatal complications. The basis of a successful treatment is a thorough understanding of the causes of these disorders. The "classical methods" to explain acid-base disorders--pH, base excess and bicarbonate concentration--mostly do not provide a causal correlation to the underlying pathology. An unusual case of a combined respiratory-metabolic disorder with hyperlactatemia and hypercapnia is presented. An acidosis masked by hypochloremic and hypoalbuminemic alkalosis was identified with the help of Stewart's concept and finally permitted a successful therapy. The modern Stewart concept provides enhanced information, enabling an exact diagnosis and causal therapy even in complex cases.

[Determinants of insensible fluid loss. Perspiration, protein shift and endothelial glycocalyx]. / Determinanten des insensiblen Flüssigkeitsverlustes. Perspiratio, Proteinshift und endotheliale Glykokalyx.

Accurate perioperative fluid balance is the basis of a targeted infusion regimen. However, neither the initial status nor perioperative changes of the fluid compartments can be reliably measured in daily routine. In particular, insensible losses are not consistently assessed, so that substitution therapy is generally empirical. The object of this paper is to communicate the scientific data on this topic. Preoperative fasting (10 h) does not per se cause intravascular hypovolemia. In adults, total basal evaporation by way of the skin and airways and of any wounds during major abdominal interventions is usually less than 1 ml/kg/h. An inconstant fluid and protein shift towards the interstitial space perioperatively seems to be associated with hypervolemia, which suggests it should be preventable. The decisive factor in this context seems to be deterioration of the endothelial glycocalyx, whose further patho-physiological impact is currently only partially known. Clinical studies have revealed a link between fluid restriction and improved outcome after major abdominal surgery.

Effects of sevoflurane and propofol on ischaemia-reperfusion injury after thoracic-aortic occlusion in pigs.

BACKGROUND: Thoraco-abdominal-aneurysm surgery predicts high mortality. Propofol and sevoflurane are commonly used anaesthetics for this procedure. Halogenated anaesthetics induce organ protection similar to ischaemic preconditioning. We investigated which anaesthetic regimen would lead to a better protection against ischaemia-reperfusion injury induced by temporary thoracic-aortic occlusion. METHODS: Following initial fentanyl-midazolam anaesthesia for surgical preparation, 18 pigs were randomly assigned to two groups: group one received propofol (n=9) and group two sevoflurane (n=9) before, during, and after lower body ischaemia in an investigator blinded fashion. Ten animals without aortic occlusion served as time controls (propofol, n=5; sevoflurane, n=5). For induction of ischaemia, the thoracic aorta was occluded by a balloon-catheter for 90 min. After 120 min of reperfusion, the study anaesthetics were discontinued and fentanyl-midazolam re-established for an additional 180 min. Goal-directed therapy was performed during reperfusion. Fluid and catecholamine requirements were assessed. Serum samples and intestinal tissue specimens were obtained. RESULTS: Severe declamping shock occurred in both study groups. While norepinephrine requirements in the sevoflurane group were significantly reduced during reperfusion (P<0.05), allowing cessation of catecholamine support in 4/9 animals, all 9/9 animals were still catecholamine dependent at the end of the experiment in the propofol group. Serum activities of lactate dehydrogenase, aspartate transaminase, and alanine aminotransferase were lower with sevoflurane (P<0.05). Small intestine tissue specimens did not differ histologically. CONCLUSIONS: Use of sevoflurane compared with propofol attenuated the haemodynamic sequelae of reperfusion injury in our model. Release of serum markers of cellular injury was also attenuated.