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Biomedical subjects

Wim van Oeveren

Publications and source records attributed to Wim van Oeveren.

13 recordsLinked to original sources
PubMed2006

Children undergoing cardiac surgery for complex cardiac defects show imbalance between pro- and anti-thrombotic activity.

INTRODUCTION: Cardiac surgery with cardiopulmonary bypass (CPB) is associated with the activation of inflammatory mediators that possess prothrombotic activity and could cause postoperative haemostatic disorders. This study was conducted to investigate the effect of cardiac surgery on prothrombotic activity in children undergoing cardiac surgery for complex cardiac defects. METHODS: Eighteen children (ages 3 to 163 months) undergoing univentricular palliation with total cavopulmonary connection (TCPC) (n = 10) or a biventricular repair (n = 8) for complex cardiac defects were studied. Prothrombotic activity was evaluated by measuring plasma levels of prothrombin fragment 1+2 (F1+2), thromboxane B2 (TxB2), and monocyte chemoattractant protein-1 (MCP-1). Anti-thrombotic activity was evaluated by measuring levels of tissue factor pathway inhibitor (TFPI) before, during, and after cardiac surgery. RESULTS: In all patients, cardiac surgery was associated with a significant but transient increase of F1+2, TxB2, TFPI, and MCP-1. Maximal values of F1+2, TxB2, and MCP-1 were found at the end of CPB. In contrast, maximal levels of TFPI were observed at the beginning of CPB. Concentrations of F1+2 at the end of CPB correlated negatively with the minimal oesophageal temperature during CPB. Markers of prothrombotic activity returned to preoperative values from the first postoperative day on. Early postoperative TFPI levels were significantly lower and TxB2 levels significantly higher in patients with TCPC than in those with biventricular repair. Thromboembolic events were not observed. CONCLUSION: Our data suggest that children with complex cardiac defects undergoing cardiac surgery show profound but transient imbalance between pro- and anti-thrombotic activity, which could lead to thromboembolic complications. These alterations are more important after TCPC than after biventricular repair but seem to be determined mainly by low antithrombin III.

Antithrombin III↗
PubMed2005

The impact of heparin-coated circuits on hemodynamics during and after cardiopulmonary bypass.

This study was performed to investigate if heparin-coated extracorporeal circuits can reduce the systemic inflammatory reaction with the subsequent release of vasoactive substances during and after cardiopulmonary bypass. Fifty-one patients scheduled for coronary artery bypass grafting were perfused with either a heparin-coated or an uncoated circuit. During bypass the mean arterial pressure was maintained as near as possible to 60 mm Hg. Mediators for inflammation, hemodynamic, and oxygen parameters were determined during and after bypass. To reach the target mean arterial pressure in the first hour of bypass the pump flow in the uncoated group had to be increased (P<0.05), consequently the systemic vascular resistance index decreased (P<0.05). After bypass more inotropic support was necessary in this group to reach this pressure. In the coated group less bradykinin, complement activation, and elastase was generated during bypass (P<0.05). The results of this study suggest that heparin coating not only improves biocompatibility, but also ameliorates the hemodynamic instability during and after bypass.

Analysis of Variance↗
PubMed2005

Dexamethasone: benefit and prejudice for patients undergoing on-pump coronary artery bypass grafting: a study on myocardial, pulmonary, renal, intestinal, and hepatic injury.

STUDY OBJECTIVES: Cardiac surgery with cardiopulmonary bypass (CPB) results in perioperative organ damage caused by the systemic inflammatory response syndrome (SIRS) and ischemia/reperfusion injury. Administration of corticosteroids before CPB has been demonstrated to inhibit the activation of the systemic inflammatory response. However, the clinical benefits of corticosteroid therapy are controversial. This study was designed to document the effects of dexamethasone on cytokine release and perioperative myocardial, pulmonary, renal, intestinal, and hepatic damage, as assessed by specific and sensitive biomarkers. DESIGN AND PATIENTS: A prospective, double-blind, placebo-controlled, randomized trial for dexamethasone was conducted in 20 patients receiving either dexamethasone (1 mg/kg before anesthesia induction and 0.5 mg/kg after 8 h; n = 10) or placebo (n = 10). Different markers were used to assess the SIRS: interleukin (IL)-6, IL-8, IL-10, C-reactive protein (CRP), and tryptase; and organ damage: heart (plasma heart-type fatty acid binding protein, cardiac troponin I [cTnI], creatine kinase-MB), kidneys (N-acetyl-glucosaminidase [NAG], microalbuminuria), intestine (intestinal-type fatty acid binding protein [I-FABP]/liver-type fatty acid binding protein [L-FABP]), and liver (alpha-glutathione S-transferase). RESULTS: Dexamethasone modulated the SIRS with lower proinflammatory (IL-6, IL-8) and higher antiinflammatory (IL-10) IL levels. CRP and tryptase were lower in the dexamethasone group. cTnI values were lower in the dexamethasone group at 6 h in the ICU (p = 0.009). Patients in the dexamethasone group had a longer time to tracheal extubation (18.86 +/- 1.13 h vs 15.01 +/- 0.99 h, p = 0.02 [mean +/- SEM]), with a lower oxygenation index at that time: Pa(O2)/fraction of inspired oxygen ratio, 37.17 +/- 1.8 kPa vs 29.95 +/- 2.1 kPa (p = 0.009). The postoperative glucose level (10.7 +/- 0.6 mmol/L vs 7.4 +/- 0.5 mmol/L, p = 0.005) was higher in the dexamethasone group. Serum glucose was independently associated with intestinal injury (urine I-FABP peak, R2 = 42.5%, beta = 114.4 +/- 31.4, significant at p = 0.002; urine L-FABP peak, R2 = 47.3%, beta = 7,714.1 +/- 1,920.9, significant at p = 0.001) and renal injury (urine NAG, R2 = 32.1%, beta = 0.21 +/- 0.07, significant at p = 0.009). Tryptase peaks correlated negatively with peaks of intestinal and renal injury biomarkers. CONCLUSION: Even while inhibiting SIRS, dexamethasone treatment offered no protection against transient, subclinical, perioperative abdominal organ damage. Tryptase release could have a preconditioning effect, offering protection against perioperative intestinal and renal damage. Dexamethasone treatment resulted in more pronounced postoperative pulmonary dysfunction, prolonged time to tracheal extubation, and initiated postoperative hyperglycemia in patients undergoing elective on-pump coronary artery bypass graft surgery.

Anti-Inflammatory Agents↗
PubMed2004

Activation of the inflammatory reaction within minutes after birth in ventilated preterm lambs with neonatal respiratory distress syndrome.

To study the activation of the inflammatory reaction within minutes after birth, we measured parameters of inflammation before and immediately after birth. To assess whether respiratory distress syndrome (RDS) or birth itself initiates activation, we compared preterm ventilated lambs with term nonventilated lambs. Preterm lambs were delivered by cesarean section at 132 days gestational age (term 145 days) and were ventilated by conventional ventilation (n = 9). Before clamping the cord, 5, 10 and 15 min after birth, blood was sampled from umbilical catheters. Term lambs (n = 9) were born spontaneously after 140-145 days gestational age. Immediately after birth, a venous umbilical catheter was inserted. Blood was sampled before the first breath and 5, 10, 15 and 20 min after birth while the lamb was breathing spontaneously. Blood was analyzed for AP50 (complement activation), number of polymorphonuclear leukocytes (PMNs) and beta-glucuronidase (released from activated PMNs). In preterm lambs, we found a decreased number of PMNs and increased levels of beta-glucuronidase already at 5 min after birth. In the term lambs, we found only a short-term mild decrease in PMNs and short-term increase in beta-glucuronidase. We conclude that systemic activation of the inflammatory reaction can be found in ventilated preterm lambs with RDS within 5 min after birth. This very early activation is mild, transient and less pronounced in term-born spontaneously breathing lambs compared with preterm, ventilated lambs with RDS.

Animals↗
PubMed2004

In vitro degradation and biocompatibility of poly(DL-lactide-epsilon-caprolactone) nerve guides.

Bridging nerve gaps by means of autologous nerve grafts involves donor nerve graft harvesting. Recent studies have focused on the use of alternative methods, and one of these is the use of biodegradable nerve guides. After serving their function, nerve guides should degrade to avoid a chronic foreign body reaction. The in vitro degradation, in vitro cytotoxicity, hemocompatibility, and short-term in vivo foreign body reaction of poly((65)/(35) ((85)/(15) (L)/(D)) lactide-epsilon-caprolactone) nerve guides was studied. The in vitro degradation characteristics of poly(DLLA-epsilon-CL) nerve guides were monitored at 2-week time intervals during a period of 22 weeks. Weight loss, degree of swelling of the tube wall, mechanical strength, thermal properties, and the intrinsic viscosity of the nerve guides were determined. Cytotoxicity was studied by measuring the cell proliferation inhibition index (CPII) on mouse fibroblasts in vitro. Cell growth was evaluated by cell counting, while morphology was assessed by light microscopy. Hemocompatibility was evaluated using a thrombin generation assay and a complement convertase assay. The foreign body reaction against poly(DLLA-epsilon-CL) nerve guides was investigated by examining toluidine blue stained sections. The in vitro degradation data showed that poly(DLLA-epsilon-CL) nerve guides do not swell, maintain their mechanical strength and flexibility for a period of about 8-10 weeks, and start to lose mass after about 10 weeks. Poly(DLLA-epsilon-CL) nerve guides were classified as noncytotoxic, as cytotoxicity tests demonstrated that cell morphology was not affected (CPII 0%). The thrombin generation assay and complement convertase assay indicated that the material is highly hemocompatible. The foreign body reaction against the biomaterial was mild with a light priming of the immunesystem. The results presented in this study demonstrate that poly((65)/(35) ((85)/(15) (L)/(D)) lactide-epsilon-caprolactone) nerve guides are biocompatible, and show good in vitro degradation characteristics, making these biodegradable nerve guides promising candidates for bridging peripheral nerve defects up to several centimeters.

Animals↗
PubMed2003

Effect of brain death and non-heart-beating kidney donation on renal function and injury: an assessment in the isolated perfused rat kidney.

OBJECTIVES: Ischemic injury to the renal allograft prior to implantation is considered as the major cause of primary non and never-function (PNF) and delayed graft function (DGF). Evidence has been put forward that brain dead and non-heart-beating (NHB) donor organs are of marginal quality compared to living donors. The purpose of this study was to evaluate renal function and injury of brain dead and NHB donor kidneys using the isolated perfused rat kidney. MATERIAL AND METHODS: Fisher F344 rats were either maintained brain death for 4 hr or subjected to cardiac arrest for 45 min (NHB). Living rats served as controls. To omit additional effects of cold ischemia, kidneys were immediately reperfused. Renal function and injury were assessed by monitoring urine production, glomerular filtration rate (GFR), Na+ and K+ reabsorption, glucose metabolism and reabsorption, as well as release of brush border, lysosomal, and intracellular enzymes. RESULTS: Renal dysfunction and injury were most pronounced in NHB donor kidneys reflected by a highly reduced urine production, anaerobic glucose metabolism resulting in lactate formation, and significant higher luminal release of intracellular and lysosomal enzymes. Brain dead kidneys showed an increased urine production and were functionally abnormal in K+ reabsorption showing a net excretion of K+, probably as a result of ATP depletion. Loss of brush border occurred during brain death and cardiac arrest. CONCLUSIONS: Both, brain death and cardiac arrest have deleterious effects on renal function and renal injury. The ischemically injured NHB donor kidney was functionally inferior compared to the brain dead donor kidney and living donor kidneys. However, both brain dead and NHB kidneys showed considerable renal damage compared to kidneys from living donors.

Alkaline Phosphatase↗
PubMed2002

Influence of abciximab on the adhesion of platelets on a shielded plasma gradient prepared on polyethylene.

INTRODUCTION: Thrombotic effects of biomaterial implants are mediated merely through activation of the platelet glycoprotein IIb-IIIa (GpIIb-IIIa) receptor. Consequently, platelet GpIIb-IIIa receptor inhibitors are successfully used during stent implantation procedures to prevent thrombosis. However, currently a new generation of stents contains surface coating, which changes the surface to more hydrophobic or hydrophilic. This change markedly affects the interaction of platelets and may influence the efficiency of GpIIb-IIIa inhibitors. MATERIALS AND METHODS: To study the influence of the wettability of biomaterials on the effectiveness of abciximab, 5-cm polyethylene gradients with contact angles of 100 degrees to 40 degrees were made by means of glow discharge. Fresh whole blood with or without abciximab was recirculated over this gradient. RESULTS: Inhibition of platelet adhesion by abciximab was maximal, but not complete, on the hydrophobic and moderate hydrophobic part of the gradient, with contact angles of 55 degrees to 90 degrees. Percentage inhibition by abciximab was maximal around 60 degrees. CONCLUSIONS: Intermediate hydrophobicity of currently applied stent materials, such as stainless steel, seems optimal in combination with abciximab. However, on hydrophobic and particularly on hydrophilic materials, abciximab is less effective.

Abciximab↗
PubMed2002

Platelet adhesion and activation on a shielded plasma gradient prepared on polyethylene.

Contact of blood with foreign materials evokes thrombogenic effects to an extent determined partly by the wettability of the biomaterials surface. Tools to study blood response towards a variation in materials wettability with minimal variation in chemistry are "gradient surfaces". However, most gradients have been prepared by diffusion or density immersion techniques, which results in a limited gradient range. Through glow discharge with partial shielding, gradients on polymers were prepared over a length of 5 cm, which facilitated studies to platelet adhesion on separate gradient sections. On polyethylene, advancing water contact angles varied from 90 degrees to 40 degrees, with a hysteresis of 30 degrees. ESCA indicated an increasing incorporation of oxygen towards the hydrophilic end. To examine the role of materials wettability on the activation of adhering platelets, sections of shielded plasma gradients were incubated in anticoagulated whole human blood. Fewer platelets adhered to the hydrophobic end, but those platelets were more activated than those on the hydrophilic end, as judged from their morphology and exposure of GpIIb-IIIa complex. However, partly related to the increased binding of platelets, the clotting activation after platelet deposition was highest on the hydrophilic end. Concluding, this new technique results in a large gradient range, which facilitates studies of formed blood elements in relation to the wettability. Platelets are more activated on hydrophobic polyethylene, while on moderate hydrophilic polyethylene more platelet adhesion and activation of the clotting system occurs.

Biocompatible Materials↗
PubMed2002

Off-pump coronary revascularization attenuates transient renal damage compared with on-pump coronary revascularization.

STUDY OBJECTIVES: Cardiopulmonary bypass (CPB) represents a specific risk factor for renal damage during coronary revascularization. The purpose of this study was to compare the perioperative renal damage in patients undergoing on-pump and off-pump coronary surgery. DESIGN AND PATIENTS: The progress and extent of renal damage was prospectively studied in two groups of patients undergoing cardiac surgery without concomitant morbidity, undergoing elective coronary revascularization with (n = 12) and without (n = 10) CPB. Markers of glomerular function (creatinine clearance) and damage (microalbuminuria), and markers of tubular function (fractional excretion of sodium [FENa] and free water clearance) and damage (N-acetyl-beta-D glucosaminidase [NAG]) were evaluated. Measuring plasma concentrations of free hemoglobin assessed hemolysis. Plasma and urinary specimens were obtained at the following points: (1) baseline; (2) heparinization; (3) the end of CPB or completing graft for off-pump surgery; (4) skin closure; (5) the sixth hour in the ICU; and (6) the second postoperative day. Free water and creatinine clearances, FENa, and the urinary excretion of microalbumin and NAG were calculated for the corresponding time intervals. SETTING: University hospital. RESULTS: We found that off-pump coronary revascularization induced significantly less changes in microalbuminuria, FENa, free water clearance, NAG, and free hemoglobin as compared with operations with CPB. Markers returned to baseline within 2 days after the operation, and there was no clinical or laboratory evidence of overt renal dysfunction in both groups. CONCLUSION: Off-pump coronary surgery attenuates transient renal injury compared with traditional on-pump coronary artery bypass grafting.

Aged↗
PubMedDate not supplied

Acute isovolemic hemodilution triggers proinflammatory and procoagulatory endothelial activation in vital organs: role of erythrocyte aggregation.

OBJECTIVES: The essential role of erythrocytes as oxygen carriers is historically well established, but their function to aggregate and the consequences on the microcirculation is under debate. The pathogenic potential of low erythrocyte aggregation could be important for patients undergoing on-pump cardipopulmonary bypass. These patients are severely hemodiluted due to preoperative isovolemic hemodilution (IHD), circuit priming, and large fluid infusions perioperatively. Considering the vascular endothelium sensitivity to variations in blood rheology, the authors hypothesize that low erythrocyte aggregation will be responsible for activation of vascular endothelium during acute IHD. METHODS: Acute IHD (30 mL/kg exchange transfusion with colloid solutions) was induced in an "aggregating species"(pigs, n = 15). The hypoxic oxidative stress (plasma malondialdehyde, ex vivo oxygen radicals production in heart, lung, kidney, liver, and ileum tissue biopsies), erythrocyte aggregation (LORCA), and endothelial activation (real-time quantitative RT-PCR on von Willebrand factor (vWF), E- and P-selectins, endothelial nitric oxide synthase gene-expression in tissue biopsies) were investigated. RESULTS: The production of superoxide and hydroxyl radicals, measured as H2O2 generation, was similar at all times in sham-operated and hemodiluted animals, proving a maintained oxygen delivery to tissues. Acute IHD was followed by a dramatic drop in erythrocyte aggregation and immediate prothrombotic (significant vWF mRNA upregulation in heart, lungs, kidney, liver, ileum) and proinflammatory (significant E- and P-selectins mRNA upregulation in lungs and ileum) endothelial activation. Low erythrocyte aggregation was significantly correlated with increased mRNA-expression of vWF (heart, liver, ileum) and P-selectin (lungs, ileum, and heart). CONCLUSIONS: These results suggest that low erythrocyte aggregation might trigger endothelium-dependent thrombogenic and proinflammatory response during acute isovolemic hemodilution.

Animals↗
PubMedDate not supplied

The impact of heparin coated circuits upon metabolism in vital organs: effect upon cerebral and renal function during and after cardiopulmonary bypass.

During cardiopulmonary bypass (CPB), the brain and the kidneys may be damaged because of microemboli, ischemia, and inflammation. The latter has been reduced by the use of heparin coated circuits. We questioned whether heparin coated circuits could also reduce cerebral and renal damage and whether inflammatory markers correlate with damage to the brain and the kidneys. Fifty-one patients scheduled for coronary artery bypass grafting were perfused with either a heparin coated or an uncoated circuit. To compare the effect of a heparin coated circuit with an uncoated circuit upon cerebral and renal function in relation to inflammation, we assessed markers of cerebral (S100beta) and renal (N-acetyl-beta-D-glucosaminidase [NAG], creatinine, and urea) function, inflammation, and oxygen metabolism. S100beta levels and NAG levels increased during CPB in both groups as compared with baseline levels (p < 0.01), without differences between the groups. After 15 minutes on CPB, C4b/c levels were significantly higher in the coated group compared with the uncoated group (p < 0.02). C4b/c correlated with S100beta (p < 0.01). Total body oxygen delivery (DO2) and consumption (VO2) decreased significantly in both groups during CPB (p < 0.01), but recovery was better in the coated group. After protamine infusion, total body oxygen delivery and consumption correlated negatively with S100beta levels (both p < 0.05) and with NAG levels (both p < 0.01). This study suggests that, if adequate tissue perfusion is not maintained, the use of a heparin coated circuit gives no additional benefit beyond that of the uncoated circuit. The inverse relationship of both cerebral and renal markers with DO2 and VO2 suggests that increased levels of S100beta and NAG during CPB may primarily be caused by an oxygen deficit and secondary to the inflammatory response.

Acetylglucosaminidase↗