Reperfusion Of Liver Graft Research Articles

Postreperfusion Syndrome in Patients Receiving Vasoactive Drugs During Liver Graft Reperfusion.

The most widely used definition of postreperfusion syndrome in liver transplant is a 30% decrease in mean arterial pressure during the first 5 minutes after vascular unclamping. With these criteria, increased postoperative morbidity has been reported. Vasoactivedrugs couldpreventthis syndrome.Themain objective of our study was to determine the incidence and complications associated with postreperfusion syndrome inpatientswho receivedvasoactive support. We studied 246 patients who received norepinephrine infusions to maintain mean arterial pressure ≥60 mm Hg and who were monitored with a Swan-Ganz catheter. Patients received a bolus of adrenaline after vascular unclamping in cases of insufficient response to norepinephrine. Among the study patients, 57 (23.17%) developed postreperfusion syndrome. Patients who developed postreperfusion syndrome did not present with morepostoperative complications interms ofrenal dysfunction (P = .69), repeat surgery (P = .15), graft rejection (P = .69), transplant replacement surgery (P = .76), hospital stay (P = .70), or survival (P = .17) compared with patients without postreperfusion syndrome. In patients who underwent orthotopic liver transplant, in whom vasoactive drugs were administered, a diagnosis of self-limited postreperfusion syndrome during the first 5 minutes after unclamping may not be associated with postoperative complications. The administration of vasoconstrictors may have a preventive effect on the postoperative complications associated with postreperfusion syndrome or they may mask the real incidence of postreperfusion syndrome. A broader definition of postreperfusion syndrome should be accepted.

Impact of graft reperfusion on cardiac function assessed by transesophageal echocardiography during liver transplantation: an observational retrospective study

Cardiovascular instability is common during the reperfusion phase of orthotopic liver transplantation (OLT), and some patients experience a postreperfusion syndrome (PRS). However, there are no reports comparing the cardiac dysfunction between patients with PRS and those without. Thus, the aim of this study was to evaluate cardiac dysfunction in patients exhibiting PRS. This observational retrospective study included 34 patients who underwent OLT and were monitored with transesophageal echocardiography (TEE). The right ventricular/left ventricular (RV/LV) end diastolic area, tricuspid annular plane systolic excursion (TAPSE), left ventricular ejection fraction (LVEF) by Simpson method, pulsed Doppler of the mitral valve, and tissue Doppler motion of the mitral annulus were determined. Echocardiographic measurements were registered at the beginning of surgery and at 1 and 30 min after vascular unclamping. Patients with PRS (PRS group) were identified, and their echocardiographic parameters of ventricular function were compared with those in patients without PRS (non-PRS group). To check the evolution of diastolic-systolic dysfunction, general linear model-repeated measures were estimated. No patient presented systolic/diastolic dysfunction on the basal echocardiogram. One minute after vascular unclamping, the incidence of RV dilation was 4.5 times greater in patients with PRS (Cramer´s V > 0.6), and the incidence of RV systolic dysfunction was 62.5% in patients with PRS compared to 15.40% in patients without PRS (Cramer´s V = 0.45). The incidence of LV systolic dysfunction was 25% in patients with PRS compared to 0% in those without (Cramer´s V = 0.45), and left ventricular diastolic dysfunction was 4.8 times greater in patients with PRS (Cramer´s V = 0.45). No patient presented diastolic dysfunction type III. There were significant differences between groups in the evolutionary pattern at 1 and 30 min after unclamping for RV dilation (p = 0.008) and for TAPSE (p = 0.014). Liver graft reperfusion may alter cardiac function. Cardiac dysfunction was more frequent in patients with PRS. These patients exhibited temporary dysfunction of the RV associated with a varying degree of LV diastolic-systolic dysfunction. Trial registration: clinicaltrials.gov (NCT05175534). January 03, 2022; “retrospectively registered”.

Interleukin-6 Levels During Normothermic Machine Perfusion Impact Postreperfusion Hemodynamics of Liver Graft Recipients: A Prospective Single-center Observational Study.

Hemodynamic instability after liver graft reperfusion increases recipient morbidity after liver transplantation. The etiologies of hemodynamic disturbances appear to be multifactorial and are poorly understood. Normothermic machine perfusion (NMP) provides an opportunity to analyze graft quality prior to transplantation. In the present study, we aim to investigate the influence of interleukin-6 (IL-6) levels during NMP on postreperfusion hemodynamics of the recipient. Consecutive NMP-liver transplants at a single-center were prospectively analyzed. Perfusate samples were collected at the beginning, after 6 h, and at the end of perfusion and analyzed for IL-6 levels. Mean arterial pressure (MAP) and catecholamine consumption during surgery were recorded. IL-6 levels at the end of NMP were correlated to donor and perfusion characteristics as well as changes in MAP and catecholamine requirements during the anhepatic and reperfusion phase. IL-6 perfusate measurements were assessed in 77 livers undergoing NMP and transplantation. Donor age, sex, cold ischemic time, and NMP time did not correlate with IL-6 levels. Perfusates of donation after circulatory death grafts showed higher IL-6 levels at the end of NMP than donation after brain death grafts. However, IL-6 levels at the end of NMP correlated with catecholamine requirements and MAP in the reperfusion phase. Per log10 increase in IL-6 levels, an increase of 42% points in administered catecholamine dose was observed, despite MAP being decreased by 3.6% points compared to baseline values. IL-6 levels may be a predictor for recipient hemodynamic instability during liver reperfusion. Larger studies are needed to confirm this finding.

Role of Transesophageal Echocardiography in the Diagnosis of Multi-chamber Intracardiac Thrombosis During Liver Transplantation: A Case Series.

Intra-cardiac thrombosis is one of the most devastating complications during liver transplantation. In the majority of cases, ICT, followed by massive pulmonary embolism, is commonly occurring shortly after liver graft reperfusion, but it has been reported to occur at any stage of the surgery. We present a series of 3 cases of intra-cardiac thrombosis during orthotopic liver transplantation surgery, including a case of four-chamber intra-cardiac clot formation during the pre-anhepatic stage. This article represents a single-centre 14 year-long experience. Intra-operative TEE is the gold standard to diagnose intra-cardiac thrombosis, monitoring its size, location and dynamics, as well as myocardial performance and the effects of resuscitation efforts.

Effects of liver ischemia-reperfusion injury on respiratory mechanics and driving pressure during orthotopic liver transplantation.

During orthotopic liver transplantation (OLT), liver graft ischemia-reperfusion injury (IRI) triggers a cytokine-mediated systemic inflammatory response, which impairs graft function and disrupts distal organ homeostasis. The objective of this prospective, observational trial was to assess the effects of IRI on lung and chest wall mechanics in the intraoperative period of patients undergoing OLT. In 26 patients undergoing OLT, we measured elastance of the respiratory system (ERS), partitioned into lung (EL) and chest wall (ECW), hemodynamics, and fluid and blood product intake before laparotomy (T1), after portal/caval surgical clamp (T2), and immediately (T3) and, at 90 and 180 minutes post-reperfusion (T4 and T5, respectively). Interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1), IL-1β and tumor necrosis factor-α plasma concentrations were assessed at T1, T4 and T5. EL significantly decreased from T1 to T2 (13.5±4.4 vs 9.7±4.8 cmH2O/L, P<0.05), remained stable at T3, while at T4 (12.3±4.4 cmH2O/L, P<0.05) was well above levels recorded at T2, reaching its highest value at T5 (15±3.9 cmH2O/L, P<0.05). Variations in ERS, EL, driving pressure (∆P) and trans-pulmonary pressure (∆PL) significantly correlated with changes in IL-6 and MCP-1 plasma concentrations, but not with changes in wedge pressure, fluid amounts, and red blood cells and platelets administered. No correlation was found between changes in cytokine concentrations and ECW. We found that EL, ECW, ∆P and ∆PL underwent significant variations during the OLT procedure. Further, we documented a significant association between the respiratory mechanics changes and the inflammatory response following liver graft reperfusion.

The photoplethysmographic amplitude to pulse pressure ratio can track sudden changes in vascular compliance and resistance during liver graft reperfusion: A beat-to-beat analysis.

During liver transplantation, the thermodilution cardiac output (CO) technique cannot respond to sudden hemodynamic changes associated with postreperfusion syndrome. Photoplethysmography (PPG) can reflect changes in intravascular volume and thus can be used to assess vasomotor tone and arterial stiffness on the pressure–volume relation. We investigated whether a beat-to-beat analysis of the arterial pressure–PPG relationship can estimate dynamic changes in vascular characteristics immediately after liver graft reperfusion.In 10 recipients, arterial blood pressure and PPG waveforms recorded simultaneously were analyzed from the beginning of fall to nadir in systolic blood pressure immediately after reperfusion. On a beat-to-beat basis, we compared the ratio of the amplitude of PPG to arterial pulse pressure (PPGamp/PP, as relative vascular compliance) to total peripheral resistance (TPR) and Windkessel compliance (Cwk) obtained from the Modelflow CO algorithm.Following graft reperfusion, PPGamp/PP and Cwk increased (median 41.5%; P = .005 and 42.0%; P < .001, respectively), whereas TPR decreased (median −46.4%; P < .001). Beat-to-beat PPGamp/PP was negatively correlated with TPR (median r = –0.80 [95% CI –0.85 to –0.76] on linear regression and r2 = 0.84 [95% CI 0.73–0.92] on curvilinear regression), and was positively correlated with Cwk (median r = 0.86 [95% CI 0.81–0.91] on linear regression and r2 = 0.88 [95% CI 0.75–0.96] on curvilinear regression).Our results suggest that relative compliance, obtained from beat-to-beat analysis of PPG and arterial pressure waveforms, can track abrupt changes in vascular characteristics associated with postreperfusion syndrome. This simple index would contribute to differential diagnoses of sudden hypotension.

Fibrinolysis after reperfusion of liver graft

From September 2012 to March 2013, a total of 63 adult-to-adult living donor liver transplantations were performed at our institution. All the patients were monitored for their coagulation functions using rotation thromboelastometry (ROTEM, Tem Innovations GmbH) during the procedure at the following points: preoperative baseline, 5 minutes, 30 minutes, and 120 minutes, respectively, after reperfusion of the liver graft. A total of 84.13% of cases (n = 53) revealed fibrinolysis after reperfusion of the graft and the condition was reversed after 30 minutes without any need for additional treatment. No significant coagulopathy was observed during this period in all of the cases. The result of the ROTEM finding must correlate with the clinical situation before instituting any management to avoid the risk of thrombosis of the hepatic artery.

Hemodynamic recovery following postreperfusion syndrome in liver transplantation.

The authors' current understanding of the phenomenon of significant and sustained decrease in arterial pressure following liver graft reperfusion (postreperfusion syndrome [PRS]), is derived from relatively small observational reports, and no large scale analysis of PRS exists up to date. This study investigated its incidence, risk factors, temporal course of hemodynamic recovery, and its impact on functional graft outcome. Retrospective observational study of 1,024 electronic records of orthotopic liver transplant recipients. Major transplant center. Out of 1,024, 715 records satisfied the inclusion criteria. Data were analyzed by multivariable Cox's proportional hazard model to identify risk factors for PRS. Hemodynamic recovery patterns and functional graft outcomes were compared between the cohorts of interest (intraoperative PRS) and control (no intraoperative PRS) after propensity score-matching. Association between donor risk index and hemodynamic recovery after hepatic artery reperfusion was analyzed by a multivariable regression model. The overall incidence of PRS was 31.6% with associated mortality of 0.3%. Independent risk factors for PRS included older donor age, higher donor risk index, and lower central venous pressure at reperfusion. Hemodynamic recovery after PRS following portal vein reperfusion was delayed until hepatic artery reperfusion. The slope of hemodynamic recovery, expressed as %MAP/min, correlated negatively with donor risk index (p=0.014). Immediate and 1-year graft survival rates were similar in both cohorts. Host hemodynamic response to graft reperfusion appeared to be phasic: initial abrupt hypotension after portal vein reperfusion was followed by a period of gradual decline of blood pressure until hepatic artery reperfusion, and sustained hemodynamic recovery afterwards. The slope of hemodynamic recovery correlated negatively with the donor risk index. PRS was not associated with deterioration of post-transplant graft survival and function.

Stroke Volume Response to Liver Graft Reperfusion Stress in Cirrhotic Patients

In patients with advanced cirrhosis, stressful stimuli may reveal a silent reduced cardiac performance. During liver transplantation (LT), graft reperfusion strongly stresses the heart and may unmask latent myocardial dysfunction. The objective of this study was to assess heart response to acutely increased preload after liver graft reperfusion and correlate this response with preoperative data and outcome. Preoperative clinical, echocardiographic, and hemodynamic data, and patient outcome were retrospectively recorded for 235 liver recipients who had no known cardiac disease. Myocardial dysfunction was defined as less than 10 % increase of stroke volume after graft reperfusion (non-responder). We found 84 (35.7 %) non-responder patients. The non-responders showed higher Model for end-stage liver disease scores (p = 0.046), left atrial diameter (LAD) (p = 0.040), hepatic vein pressure gradient (p = 0.055), and hyperdynamic state than responders. The percentages of patients with hyponatremia (p = 0.048) and alcohol etiology (p = 0.025) were also higher among non-responders. Independent predictors of inadequate cardiac response in the multivariate analysis were low preoperative systemic vascular resistance (SVRI) [odds ratio (OR) 3.09, 95 % CI 1.15-4.82; p = 0.027] and enlargement of LAD (OR 2.08, 95 % CI 1.49-2.74; p = 0.044). Non-response was associated with higher rates of early cardiovascular events [hazard ratio (HR) 2.84, 95 % CI 1.09-4.22; p = 0.039] and higher length of intensive care unit stay (p = 0.038). No differences were found in 1-year survival rates. Latent cardiac dysfunction among LT recipients, considered to be abnormal stroke volume response to unclamping of portal vein, is very prevalent. SVRI and LAD were independent predictors of inadequate responses. This condition deserves special attention since it may aggravate the early postoperative course of LT.

Controlled Oxygenated Rewarming of Cold Stored Liver Grafts by Thermally Graduated Machine Perfusion Prior to Reperfusion

The quality of cold-stored livers declines with the extension of ischemic time, increasing the risk of primary dys or nonfunction. A new concept to rescue preserved marginal liver grafts by gentle oxygenated warming-up prior to blood reperfusion was investigated. Porcine livers were preserved by cold storage (CS) in modified HTK-solution for 18 h. Some grafts were subsequently subjected to 90 min of controlled oxygenated rewarming (COR) by machine perfusion with gradual increase of perfusate temperature up to 20°C or simple oxygenated machine perfusion in hypothermia (HMP) or subnormothermia (SNP). Graft viability was assessed thereafter by 4 h of normothermic blood reperfusion ex vivo. Endischemic tissue energetics were significantly improved by COR or SNP and to a notably lesser extent by HMP. COR significantly reduced cellular enzyme loss, gene expression and perfusate activities of TNF-alpha, radical mediated lipid peroxidation (LPO) and increase of portal vascular perfusion resistance upon reperfusion, while HMP or SNP were less protective. Only COR resulted in significantly more bile production than after CS. Histological injury score and caspase 3-activation were significantly lower after COR than after CS. Oxygenated rewarming prior to reperfusion seems to be a promising technique to improve subsequent organ recovery upon reperfusion of long preserved liver grafts.

Reperfusion of liver graft during transplantation: techniques used in transplant centres within Eurotransplant and meta-analysis of the literature

It remains unclear which liver graft reperfusion technique leads to the best outcome following transplantation. An online survey was sent to all transplant centres (n=37) within Eurotransplant (ET) to collect information on their technique used for reperfusion of liver grafts. Furthermore, a systematic review of all literature was performed and a meta-analysis was conducted based on patients' mortality, number of retransplantations and incidence of biliary complications, depending on the technique used. Of the 28 evaluated centres, 11 (39%) reported performing simultaneous reperfusion (SIMR), 13 (46%) perform initial portal vein reperfusion (IPR), 1 (4%) performs an initial hepatic artery reperfusion (IAR) and 3 (11%) perform retrograde reperfusion (RETR). In 21 centres (75%), one reperfusion technique is used as a standard, but in only one centre is this decision based on available literature. Twenty centres (71%) said they would agree to participate in randomized controlled trials (RCT) if required. For meta-analysis, IAR vs. IPR, SIMR vs. IPR and RETR vs. IPR were compared. There was no difference between any of the techniques compared. There is no consensus on a preferable reperfusion technique. Available evidence does not help in the decision-making process. There is thus an urgent need for multicentric RCTs.

Association between plasma cyclic guanosine monophosphate levels and hemodynamic instability during liver transplantation

The activation of cyclic guanosine monophosphate (cGMP) production in patients with end-stage liver disease (ESLD) has been associated with hemodynamic instability during orthotopic liver transplantation (OLT). The aim of this prospective, observational study was to investigate the involvement of cGMP in the mediation of profound hypotension during liver graft reperfusion. An additional objective was to determine whether preoperative cGMP levels are associated with intraoperative hemodynamic instability. Forty-four consecutive patients undergoing OLT were included in the study. Blood samples for cGMP analysis were obtained from (1) the radial artery before the surgical incision; (2) the radial artery, portal vein, and flush blood during the anhepatic phase; and (3) the radial artery 20 minutes after liver graft reperfusion. On the basis of a statistical analysis, the patients were divided into 2 groups: group 1 (preoperative cGMP level ≥ 0.05 μmol/L) and group 2 (preoperative cGMP level < 0.05 μmol/L). We demonstrated a significant correlation between the preoperative levels of cGMP and the amount of catecholamine required to maintain hemodynamic stability during reperfusion (r = 0.52, P < 0.001), the length of the hospital stay (r = 0.38, P = 0.01), and the length of the intensive care unit (ICU) stay (r = 0.44, P = 0.004). We also demonstrated a significantly higher intraoperative catecholamine requirement (P < 0.001) and a prolonged postoperative ICU stay (P = 0.02) in group 1 patients versus group 2 patients. In conclusion, this study demonstrates increased baseline cGMP production in patients with ESLD, which is significantly associated with severe hypotension during OLT. We suggest that preoperative levels of cGMP correlate with hemodynamic instability during liver graft reperfusion.

Impaired stroke volume response after liver graft reperfusion as a predictor of early major cardiovascular events and outcome in cirrhotic patient undergoing liver transplantation

Cubas Quiroga, M. G.; De Vargas, I.; Rivas, E.; Martin, N.; Blasi, A.; Taura, P. Author Information

Selective Expansion of Allogeneic Regulatory T Cells by Hepatic Stellate Cells: Role of Endotoxin and Implications for Allograft Tolerance

Hepatic stellate cells (HSCs) may play an important role in hepatic immune regulation by producing numerous cytokines/chemokines and expressing Ag-presenting and T cell coregulatory molecules. Due to disruption of the endothelial barrier during cold-ischemic storage and reperfusion of liver grafts, HSCs can interact directly with cells of the immune system. Endotoxin (LPS), levels of which increase in liver diseases and transplantation, stimulates the synthesis of many mediators by HSCs. We hypothesized that LPS-stimulated HSCs might promote hepatic tolerogenicity by influencing naturally occurring immunosuppressive CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs). Following their portal venous infusion, allogeneic CD4(+) T cells, including Tregs, were found closely associated with HSCs, and this association increased in LPS-treated livers. In vitro, both unstimulated and LPS-stimulated HSCs upregulated Fas (CD95) expression on conventional CD4(+) T cells and induced their apoptosis in a Fas/Fas ligand-dependent manner. By contrast, HSCs induced Treg proliferation, which required cell-cell contact and was MHC class II-dependent. This effect was augmented when HSCs were pretreated with LPS. LPS increased the expression of MHC class II, CD80, and CD86 and stimulated the production of IL-1α, IL-1β, IL-6, IL-10 and TNF-α by HSCs. Interestingly, production of IL-1α, IL-1β, IL-6, and TNF-α was strongly inhibited, but that of IL-10 enhanced in LPS-pretreated HSC/Treg cocultures. Adoptively transferred allogeneic HSCs migrated to the secondary lymphoid tissues and induced Treg expansion in lymph nodes. These data implicate endotoxin-stimulated HSCs as important immune regulators in liver transplantation by inducing selective expansion of tolerance-promoting Tregs and reducing inflammation and alloimmunity.

Intraoperative Calcium-Related Risk Factors for Biochemical Acute Pancreatitis After Living-Donor Liver Transplantation

Laboratory-based biochemical acute pancreatitis (BAP) is considered to be a benign but common complication after liver transplantation (LT), which to compensate for transfusion-related hypocalcemia, usually demands a large quantity of exogenous calcium which may be associated with pancreatic injury. We sought to investigate the relationship between intraoperative calcium–related factors and BAP occurrence after living-donor LT. Perioperative data, including intraoperative calcium chloride administration and serum calcium levels, were reviewed from 217 patients who underwent living-donor LT. Hyperamylasemia (≥458 U/L) was used to define posttransplantation BAP according to previous reports. Posttransplantation BAP was identified among 37 patients (17.3%), who showed a greater death rate than those in the non-BAP group (21.6% vs 8.6%; P = .013). Compared to with calcium-related parameters, the 2 groups showed differences in the amount of calcium chloride administered during the preanhepatic phase, the serum calcium surge during the initial 2 h after the liver graft reperfusion, the last serum calcium level, and the amount of transfused pack red blood cells ( P < .05). However, after multivariate adjustment, only the amount of administered calcium chloride during the preanhepatic phase (odds ratios, 2.11–5.87, depending an amount) and the serum calcium surge during the initial 2 hours after liver graft reperfusion (odds ratio, 2.34) were selected as risk factors for posttransplantation BAP. The risk ratio of posttransplantation BAP increased in proportion to the administered amount of calcium chloride. In conclusion, limiting excessive calcium administration during the preanhepatic phase and close monitoring of the serum calcium surge after reperfusion may be required to prevent posttransplantation BAP in living-donor LT.

Perfusion Using Oxygenated Buffer Containing Prostaglandin E 1 before Cold Preservation Prevents Warm Ischemia-Reperfusion Injury in Liver Grafts from Non-Heart-Beating Donors

We have previously reported that perfusion using warm oxygenated buffer before cold preservation (preperfusion) improved the viability of liver grafts from non-heart-beating donors. We demonstrated that adenosine triphosphate content was restored and apoptosis was reduced. The objective of the present study was to evaluate mitochondrial functions after this preperfusion and the effects of addition of prostaglandin E 1 (PGE 1) to the preperfusion buffer. Preperfusion improved portal flow, bile production, and mitochondrial function, and reduced alanine aminotransferase levels in the perfusate. Addition of PGE 1 significantly increased bile production and suppressed alanine aminotransferase and tumor necrosis factor-α levels. PGE 1 minimized mitochondrial membrane damage and ischemic injury after liver graft reperfusion. Release of mitochondrial cytochrome c was suppressed by addition of PGE 1. In conclusion, perfusion using oxygenated buffer containing PGE 1 before cold preservation significantly prevented cellular damage, protected mitochondrial function, and suppressed the release of mitochondrial cytochrome c in livers undergoing warm ischemia-reperfusion injury. This method shows promise for reducing cellular damage in non-heart-beating donor liver grafts.

Comparison of central and mixed venous saturation during liver transplantation in cirrhotic patients: a pilot study

Liver transplantation is associated with important haemodynamic variations requiring cardiac output and oximetric data monitoring. The mixed venous saturation (SvO2) integrates parameters combining information about oxygen consumption, cardiac output and haemoglobin concentration. Central venous saturation (ScvO2) can be directly measured from blood drawn in the superior venous system via a central venous catheter. ScvO2 has been proposed as an alternative to SvO2 for intraoperative haemodynamic monitoring. The aim of the present study was to examine the level of agreement between SvO2 and ScvO2 during the preanhepatic and the neohepatic stage of liver transplantation in cirrhotic patients. After agreement from the regulatory authorities for medical research and having obtained informed consent, 30 patients with cirrhosis undergoing liver transplantation were prospectively included. Blood gas samples were simultaneously drawn from the arterial line, the right atrium port and the pulmonary artery port of the catheter: during the preanhepatic stage (two times) and two times 30-40 min after graft revascularization. Arterial saturation (SaO2), haemoglobin concentration, cardiac index, SvO2, ScvO2 and oxygen consumption, delivery and extraction (VO2, DO2 and EO2, respectively) were measured. A Bland-Altman test was used to determine bias and limits of agreement between SvO2 and ScvO2. Both parameters were considered to be equivalent if limits of agreement were within +/-5%. Bland-Altman analysis revealed a bias (limit of agreement) of -1.2% (-9.1 to 6.6%), -0.3% (-4.8 to 4%) and -2.1% (-12 to 7.8%) for the overall measurements and preanhepatic and postgraft reperfusion measurements, respectively. SvO2 decreased significantly between hepatectomy and reperfusion, whereas cardiac index, VO2, DO2 and EO2 showed significantly higher values after reperfusion. ScvO2 and SaO2 levels did not display different values between the two periods. Measurements of SvO2 and ScvO2 showed a good level of agreement during the preanhepatic stage, whereas the level of agreement was low after liver graft reperfusion. The increase of VO2 associated with the decrease of SvO2 and the stability of ScvO2 between the two periods suggest an incomplete mixing of splanchnic venous blood into the right atrium. In addition, our samples were taken from the right atrium, which is not possible using a conventional central venous catheter, as the tip must lie in the superior vena cava and not in the right atrium. ScvO2 cannot be considered equivalent to SvO2 for the haemodynamic monitoring of patients with cirrhosis undergoing liver transplantation.

Is It Possible to Distinguish Between Vasoplegic Syndrome and Postreperfusion Syndrome During Liver Graft Reperfusion?

In Response: In the case we reported,1 the patient's arterial blood pressure remained at approximately 60/40 mm Hg for about 40 minutes and responded poorly to norepinephrine and phenylephrine. The cardiac output was increased (8.0 L/min) and the systemic vascular resistance (SVR) was low (369 dynes · s · cm−5), with a heart rate of >100 bpm. Hemoglobin-oxygen saturation, temperature, electrolytes, and acid-base status were normal. Thus, our patient's hemodynamics were typical of the vasoplegic syndrome (severe and persistent hypotension, tachycardia, normal or increased cardiac output, decreased SVR, and poorly responsive to volume infusions and vasoconstrictive drugs)2,3 and differed from postreperfusion syndrome (PRS) in etiology, symptoms, and treatment (Table 1).Table 1: Differences Between VS and PRSWe accept that vasoplegic syndrome is related to ischemia reperfusion injury of intestine and graft liver, which is why we cited articles related to ischemia reperfusion injury. Further studies are needed to explore the precise mechanism of vasoplegic syndrome during liver transplantation. Patients with vasoplegic syndrome tend to have increased morbidity and mortality.4,5 The conventional treatment, vasopressin and methylene blue administration, has been based on an understanding of the pathophysiology of vasomotor dysfunction after graft reperfusion, which includes cAMP-dependent vasoconstriction, cGMP/ nitric oxide–dependent vasoconstriction, vasopressin deficiency, and hyperpolarization-dependent vasoconstriction.5,6 Methylene blue can be used as a last-resort pharmacologic agent to treat vasopressor-refractory vasoplegic syndrome.5 Compared with vasoplegic syndrome, PRS is defined as a decrease in mean arterial blood pressure of >30% below the baseline value for at least 1 minute, occurring during the first 5 minutes after reperfusion.7,8 The sudden influx of cold, acidic, hyperkalemic blood from the grafted liver into the systemic circulation, hypothermia, hypocalcemia, minor air and thrombus embolization, and release of vasoactive substances or inflammatory mediators from the grafted liver and ischemia–reperfusion gut may lead to the development of PRS by decreasing SVR or due to myocardial dysfunction.7,8 Based on previous studies, treatment of PRS includes volume expansion, correction of abnormal acid-base status, vasopressor and inotropic agents, prophylactic ischemia reperfusion injury agents, and maintaining normal body temperature.7,8 Patients with vasoplegic syndrome seen after cardiac surgery, septic shock, and liver transplantation have different proinflammatory cytokine responses and pathophysiology processes, which may lead to the variety of cases reported by different authors, but share the hemodynamic characteristics of low SVR and high cardiac output, the mechanisms of nitric oxide, and cGMP overproduction.4–6 Zhongping Cao Guocai Tao Department of Anesthesia Southwest Hospital The Third Military Medical University Chongqing, China [email protected]

Is It Possible to Distinguish Between Vasoplegic Syndrome and Postreperfusion Syndrome During Liver Graft Reperfusion?

Is It Possible to Distinguish Between Vasoplegic Syndrome and Postreperfusion Syndrome During Liver Graft Reperfusion?

Effects of ischemic postconditioning on the expression of heme oxygenase-1 in the liver graft with ischemia and reperfusion injury in rats

To investigate the effects of ischemic postconditioning on the expression of HO-1 in the liver graft ischemia and reperfusion injury in rats. Fifty-six male SD rats were randomly divided into four groups: sham-operation group (sham) (n = 8), ischemia and reperfusion group (I/R)(n = 16), ischemic postconditioning group (IPo) (n = 16) and inhibitor of HO-1 group (ZnPP) (n = 16). Donor livers were preserved in 0 - 4 degrees C normal saline, and the period of cold preservation and anhepatic phase were 90 min and 15 min. At 6 h after portal vein reperfusion, blood samples were obtained from the abdominal aorta to determine the level of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), simultaneously liver tissues were taken to determine the level of malondialdehyde (MDA), superoxide dismutase (SOD) and heme oxygenase-1 (HO-1) mRNA. The changes of liver tissues were observed by HE staining and electron microscope. SOD activity was significantly lower whereas MDA content was significantly higher in I/R group than that in Sham group (P < 0.05). The expression of HO-1 in I/R group was higher than that in Sham group (P < 0.05). MDA content was significantly lower whereas SOD activity was significantly higher in IPO group than that in I/R group (P < 0.05), and the expression of HO-1 in IPO group was significantly stronger than that in I/R group (P < 0.05). SOD activity and the expression of HO-1 were significantly lower whereas MDA content was significantly higher in ZnPP group than that in I/R group (P < 0.05). The changes of liver tissues also proved the previous results. Ischemic postconditioning attenuates liver graft injury induced by I/R in rats. The mechanism might be related with the induction of HO-1 and enhancement of liver graft antioxidation.