Impact of Model for End-stage Liver Disease Score in Post-Liver Transplantation Prognosis.

Although the Model for End-Stage Liver Disease (MELD) score has been used to evaluate mortality of patients on the waiting list for liver transplantation, it has not established if it correlates with post-liver transplantation prognosis. The aim of this study is to assess if there is a relationship between pretransplantation MELD and post-transplantation results, especially regarding 30-day post-LT survival rates. We analyzed data from 172 patients who underwent deceased-donor liver transplantation between February 2013 and May 2015 in a single center. The sample was divided in two groups according to their MELD scores: group 1, with MELD <25 (n = 134), and group 2, with MELD ≥25 (n = 38). The groups were compared with regard to 1-, 3-, and 12-month postoperative survival; total length of stay and in intensive care unit; and perioperative blood transfusion. The global 30-day post-liver transplantation survival rate was 87.2% (89.55% for group 1 and 78.99% for group 2 (P = .090). The evaluation of 3- and 12-month survival showed that in group 2 the mortality was higher (P = .01). Our data suggests a positive relationship between the higher MELD group and longer length of stay in intensive care unit (P = .0345), but not for total time of hospital admission (P = .524). Perioperative blood product transfusion was needed in 35.82% of patients in group 1 and 71.05% in group 2; this correlated with a higher 30- day postoperative mortality (P < .001).

Inhibition of autonomic storm by epidural anesthesia does not influence cardiac inflammatory response after brain death in rats.

BACKGROUND: After brain death (BD) donors usually experience cardiac dysfunction, which is responsible for a considerable number of unused organs. Causes of this cardiac dysfunction are not fully understood. Some authors argue that autonomic storm with severe hemodynamic instability leads to inflammatory activation and myocardial dysfunction. OBJECTIVES: To investigate the hypothesis that thoracic epidural anesthesia blocks autonomic storm and improves graft condition by reducing the inflammatory response. METHODS: Twenty-eight male Wistar rats (250-350 g) allocated to four groups received saline or bupivacaine via an epidural catheter at various times in relation to brain-death induction. Brain death was induced by a sudden increase in intracranial pressure by rapid inflation of a ballon catheter in the extradural space. Blood gases, electrolytes, and lactate analyses were performed at time zero, and 3 and 6 hours. Blood leukocytes were counted at 0 and 6 hours. After 6 hours of BD, we performed euthanasia to measure vascular adhesion molecule (VCAM)-1, intracellular adhesion molecule (ICAM)-1, interleukin (IL)-1ß, tumor necrosis factor (TNF)-α, Bcl-2 and caspase-3 on cardiac tissue. RESULTS: Thoracic epidural anesthesia was effective to block the autonomic storm with a significant difference in mean arterial pressure between the untreated (saline) and the bupivacaine group before BD (P < .05). However, no significant difference was observed for the expressions of VCAM-1, ICAM-1, TNF-α, IL-1ß, Bcl-2, and caspase-3 (P > .05). CONCLUSION: Autonomic storm did not seem to be responsible for the inflammatory changes associated with BD; thoracic epidural anesthesia did not modify the expression of inflammatory mediators although it effectively blocked the autonomic storm.

Effect of methylprednisolone on perivascular pulmonary edema, inflammatory infiltrate, VEGF and TGF-beta immunoexpression in the remaining lungs of rats after left pneumonectomy

Pneumonectomy is associated with high rates of morbimortality, with postpneumonectomy pulmonary edema being one of the leading causes. An intrinsic inflammatory process following the operation has been considered in its physiopathology. The use of corticosteroids is related to prevention of this edema, but no experimental data are available to support this hypothesis. We evaluated the effect of methylprednisolone on the remaining lungs of rats submitted to left pneumonectomy concerning edema and inflammatory markers. Forty male Wistar rats weighing 300 g underwent left pneumonectomy and were randomized to receive corticosteroids or not. Methylprednisolone at a dose of 10 mg/kg was given before the surgery. After recovery, the animals were sacrificed at 48 and 72 h, when the pO2/FiO2 ratio was determined. Right lung perivascular edema was measured by the index between perivascular and vascular area and neutrophil density by manual count. Tissue expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-β) were evaluated by immunohistochemistry light microscopy. There was perivascular edema formation after 72 h in both groups (P = 0.0031). No difference was observed between operated animals that received corticosteroids and those that did not concerning the pO2/FiO2 ratio, neutrophil density or TGF-β expression. The tissue expression of VEGF was elevated in the animals that received methylprednisolone both 48 and 72 h after surgery (P = 0.0243). Methylprednisolone was unable to enhance gas exchange and avoid an inflammatory infiltrate and TGF-β expression also showed that the inflammatory process was not correlated with pulmonary edema formation. However, the overexpression of VEGF in this group showed that methylprednisolone is related to this elevation.

Effect of methylprednisolone on perivascular pulmonary edema, inflammatory infiltrate, VEGF and TGF-beta immunoexpression in the remaining lungs of rats after left pneumonectomy.

Pneumonectomy is associated with high rates of morbimortality, with postpneumonectomy pulmonary edema being one of the leading causes. An intrinsic inflammatory process following the operation has been considered in its physiopathology. The use of corticosteroids is related to prevention of this edema, but no experimental data are available to support this hypothesis. We evaluated the effect of methylprednisolone on the remaining lungs of rats submitted to left pneumonectomy concerning edema and inflammatory markers. Forty male Wistar rats weighing 300 g underwent left pneumonectomy and were randomized to receive corticosteroids or not. Methylprednisolone at a dose of 10 mg/kg was given before the surgery. After recovery, the animals were sacrificed at 48 and 72 h, when the pO(2)/FiO(2) ratio was determined. Right lung perivascular edema was measured by the index between perivascular and vascular area and neutrophil density by manual count. Tissue expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-ß) were evaluated by immunohistochemistry light microscopy. There was perivascular edema formation after 72 h in both groups (P = 0.0031). No difference was observed between operated animals that received corticosteroids and those that did not concerning the pO(2)/FiO(2) ratio, neutrophil density or TGF-ß expression. The tissue expression of VEGF was elevated in the animals that received methylprednisolone both 48 and 72 h after surgery (P = 0.0243). Methylprednisolone was unable to enhance gas exchange and avoid an inflammatory infiltrate and TGF-ß expression also showed that the inflammatory process was not correlated with pulmonary edema formation. However, the overexpression of VEGF in this group showed that methylprednisolone is related to this elevation.

Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats

Pneumonectomy is associated with high mortality and high rates of complications. Postpneumonectomy pulmonary edema is one of the leading causes of mortality. Little is known about its etiologic factors and its association with the inflammatory process. The purpose of the present study was to evaluate the role of pneumonectomy as a cause of pulmonary edema and its association with gas exchange, inflammation, nitric oxide synthase (NOS) expression and vasoconstriction. Forty-two non-specific pathogen-free Wistar rats were included in the study. Eleven animals died during or after the procedure, 21 were submitted to left pneumonectomy and 10 to sham operation. These animals were sacrificed after 48 or 72 h. Perivascular pulmonary edema was more intense in pneumonectomized rats at 72 h (P = 0.0131). Neutrophil density was lower after pneumonectomy in both groups (P = 0.0168). There was higher immunohistochemical expression of eNOS in the pneumonectomy group (P = 0.0208), but no statistically significant difference in the expression of iNOS. The lumen-wall ratio and pO2/FiO2 ratio did not differ between the operated and sham groups after pneumonectomy. Left pneumonectomy caused perivascular pulmonary edema with no elevation of immunohistochemical expression of iNOS or neutrophil density, suggesting the absence of correlation with the inflammatory process or oxidative stress. The increased expression of eNOS may suggest an intrinsic production of NO without signs of vascular reactivity.

Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats.

Pneumonectomy is associated with high mortality and high rates of complications. Postpneumonectomy pulmonary edema is one of the leading causes of mortality. Little is known about its etiologic factors and its association with the inflammatory process. The purpose of the present study was to evaluate the role of pneumonectomy as a cause of pulmonary edema and its association with gas exchange, inflammation, nitric oxide synthase (NOS) expression and vasoconstriction. Forty-two non-specific pathogen-free Wistar rats were included in the study. Eleven animals died during or after the procedure, 21 were submitted to left pneumonectomy and 10 to sham operation. These animals were sacrificed after 48 or 72 h. Perivascular pulmonary edema was more intense in pneumonectomized rats at 72 h (P = 0.0131). Neutrophil density was lower after pneumonectomy in both groups (P = 0.0168). There was higher immunohistochemical expression of eNOS in the pneumonectomy group (P = 0.0208), but no statistically significant difference in the expression of iNOS. The lumen-wall ratio and pO(2)/FiO(2) ratio did not differ between the operated and sham groups after pneumonectomy. Left pneumonectomy caused perivascular pulmonary edema with no elevation of immunohistochemical expression of iNOS or neutrophil density, suggesting the absence of correlation with the inflammatory process or oxidative stress. The increased expression of eNOS may suggest an intrinsic production of NO without signs of vascular reactivity.

Inclusion of lidocaine in cardioplegic solutions provides additional myocardial protection.

AIM: Lidocaine inhibits depolarization by blocking sodium and calcium influx and potassium release, abolishing the action potentials of cells in the Hiss-Purkinje system and myocit cells. As it can directly influence cardiac electric and mechanical activities, this study evaluated the efficacy of lidocaine in providing myocardial protection during normothermic blood cardioplegia. METHODS: Twenty-six dogs were randomly assigned to groups based on the cardioplegic induction solution they were to receive. Group I dogs (n=10) received a solution consisting of lidocaine (5 mg/kg), KCL (41.6 mEq/L) and 180 ml of normothermic blood. Group II dogs (n=10) received the same solution, except for the lidocaine and group III dogs (n=6) received only normothermic blood. In addition, 120 ml of normothermic blood was reinfused every 20 min. All dogs underwent cardiopulmonary bypass, 2 hours of global myocardial ischemia and 3 hours of reperfusion. Statistical differences were determined with the chi squared test, the two-way analysis of variance and Bonferroni's test. RESULTS: There were no deaths in group I. The survival rate in group II was 60%, and no dogs in group III survived (p=0.025). No difference in lactate liberation or left ventricular function (i.e., cardiac outflow and ejection fraction) was observed between groups. However, animals in group I demonstrated less enzymatic releases (troponin I, p=0.049 and CK, p=0.026) and less mitochondrial ultrastructural changes (p=0.022). CONCLUSIONS: Lidocaine offers myocardium additional protection against ischemia during cardiopulmonary bypass.

Randomized comparative study of radial artery and right gastroepiploic artery in composite arterial graft for CABG.

OBJECTIVES: Arterial grafts have been used to achieve better long-term results and improve graft patency in coronary artery bypass grafting. Composite graft was proposed to overcome inconveniences of proximal anastomoses to the aorta and increase the use and surgical options of arterial grafts. However, lack of prospective randomized studies with this kind of grafts is evident. We compare the results of composite Y-grafts of the radial artery (RA) and the right gastroepiploic artery (RGEA) proximally anastomosed to the left internal thoracic artery (LITA) for CABG, evaluated through angiography, in a prospective randomized study. METHODS: Between August 1998 and November 1999, 60 patients were randomly divided into two groups: group I (GI) received RGEA graft and group II (GII), RA graft. LITA was used to graft the left anterior descending artery and RGEA or RA was placed to obtuse marginal or first diagonal branch. The right coronary artery branches was grafted with saphenous vein graft (SVG) when necessary. All coronary arteries receiving arterial grafts had > or =75% proximal stenosis and diameter > or =1.5 mm. RESULTS: GI and GII preoperative data were similar, 63 distal anastomoses were performed with the LITA, 32 with the RA and 32 with the RGEA. There were two perioperative deaths (3.3%), one in each group, none related to cardiac causes. Four (6.6%) q-wave myocardial infarctions were found and two (3.3%) patients showed low cardiac output syndrome. Angiography was performed in all surviving patients from the 8th to 15th postoperative day and showed a patency rate of 96.5% (56/58) for LITA, 89.6% (26/29) for RA and 68.9% (20/29) for RGEA, with a statistically significant difference between RGEA and RA (P=0.025). CONCLUSIONS: Radial artery had better early results than right gastroepiploic artery. Use of the LITA as inflow graft seems not to affect its good patency. Use of the RGEA as composite graft should not be encouraged. Long-term follow-up with objective investigation and randomized trials is required to confirm better results of composite conduits.

Assistência circulatória mecânica como ponte para o transplante cardíaco / Mechanical circulatory support as a bridge to heart transplantation

A utilizaçäo de dispositivos de assistência circulatória mecânica como ponte para a posterior realizaçäo de transplante cardíaco representa a única opçäo de tratamento para portadores de insuficiência cardíaca severa que evoluem em choque cardiogênico refratário à terapêutica medicamentosa. Os dispositivos utilizados com esse objetivo têm sido o baläo intra-aórtico, as bombas centrífugas, os ventrículos artificiais pneumáticos ou eletromecânicos e o coraçäo artificial total, podendo ser instituída sistência ventricular direita, esquerda ou biventricular. Resultados multicêntricos internacionais demonstram que cerca de 70 por cento dos pacientes submetidos a assistência circulatória mecânica conseguem ser submetidos a transplante, sendo observada mortalidade hospitalar após o transplante em torno de 31 por cento. Por causa das limitaçöes observadas com os outros tipos de aparelhos, os ventrículos artificiais pneumáticos e eletromecânicos apresentam os melhores resultados, sendo os dispositivos de tlizaçäo preferencial.