Biomedical subjects

E Fosse

Publications and source records attributed to E Fosse.

At least 55 records · Page 3Linked to original sources

PubMed1997

Endothelin-1 and neutrophil activation during heparin-coated cardiopulmonary bypass.

BACKGROUND: Heparin-coated circuits attenuate the systemic inflammatory response to cardiopulmonary bypass. The present study compares two different heparin coatings in terms of the release of endothelin-1 and neutrophil glycoproteins. METHODS: Forty low-risk patients undergoing coronary artery bypass grafting were investigated, having cardiopulmonary bypass with a Duraflo II heparin-coated circuit (n = 10), an identical but uncoated circuit (n = 10), a Carmeda BioActive Surface heparin-coated circuit (n = 10), or an identical but uncoated circuit (n = 10). A standard systemic heparin dosage was used in all patients. Endothelin-1 and the neutrophil glycoproteins lactoferrin and myeloperoxidase were quantified throughout the operation and 3 hours postoperatively. RESULTS: Enhanced plasma levels of endothelin-1, lactoferrin, and myeloperoxidase were observed during and after uncoated cardiopulmonary bypass, but this was not associated with clinical side effects. Compared with the respective uncoated controls, Duraflo II attenuated only the lactoferrin levels, whereas Carmeda BioActive Surface was associated with lower levels of both endothelin-1, lactoferrin, and myeloperoxidase. Of the two heparin coatings, Carmeda BioActive Surface proved more effective than Duraflo II in attenuating the levels of these substances. CONCLUSIONS: The plasma levels of endothelin-1, lactoferrin, and myeloperoxidase increase during cardiopulmonary bypass in coronary artery bypass grafting, but this has no clinical side effects in low-risk patients. The increase is attenuated using heparin-coated extracorporeal circuits, and then more effectively by Carmeda BioActive Surface than by Duraflo II.

Cardiopulmonary Bypass↗

PubMed1997

Intraoperative angiography in minimally invasive direct coronary artery bypass grafting.

Intraoperative angiography in minimally invasive direct coronary artery bypass grafting without cardiopulmonary bypass and in hybrid procedures is reported. Twelve procedures were performed in a specially designed surgical-radiologic suite with a cross-disciplinary organization. In 2 patients the anastomosis was successfully revised on the basis of angiographic findings. In 4 of the 12 patients anastomosis of the left internal mammary artery to the left anterior descending coronary artery performed as a minimally invasive direct coronary artery bypass grafting procedure was combined with percutaneous transluminal coronary angioplasty of lesions in other coronary vessels in the same session. Intraoperative angiography allows a reliable diagnosis of an anastomosis or graft failure and prompt and reliable correction, and it allows the combination of minimally invasive direct coronary artery bypass grafting and angioplasty in one session.

Aged↗

PubMed1997

Duraflo II coating of cardiopulmonary bypass circuits reduces complement activation, but does not affect the release of granulocyte enzymes : a European multicentre study.

OBJECTIVE: This study was carried out to: (a) compare complement and granulocyte activation during cardiac operations in patients operated with cardiopulmonary bypass coated with heparin by the Duraflo II method, with activation in patients operated with uncoated circuits; and (b) relate complement, and granulocyte activation to selected adverse effects. METHODS: In a multicentre study among Rikshospitalet, Ullevaal Hospital in Norway and Uppsala University Hospital in Sweden, plasma concentrations of the complement activation products C4b/iC4b/C4c (C4bc), C3b/iC3b/C3c (C3bc), the terminal SC5b-9 complement complex (TCC), and the granulocyte proteins myeloperoxidase and lactoferrin were assessed in two groups of patients undergoing aortocoronary bypass. Seventy-six patients underwent surgery operated with circuits coated by the Duraflo II heparin coating and 75 uncoated circuits. The same amount of systemic heparin was administered to all patients. RESULTS: In both groups a significant increase in C4bc was first seen by the end of operation, from 86.7 +/- 12.5 to 273.0 +/- 277.4 nM in controls and from 86.9 +/- 18.5 to 320.2 +/- 190.5 nM in the control group, confirming previous documentation that the classical pathway is not activated during CPB, but as a consequence of protamin administration. The formation of C4bc did not differ significantly between the two groups. In the uncoated group the C3bc concentration increased from 124.0 +/- 15.3 to a maximum of 1176.1 +/- 64.7 nM (P < 0.01) and in the coated group it increased from 129.8 +/- 16.1 to a maximum of 1019.4 +/- 54.9 nM (P < 0.01) during CPB. Summary values but not peak values differed significantly between the groups. In the uncoated group the TCC concentration increased from 0.52 +/- 0.03 to a maximum value of 8.09 +/- 0.57 AU/ml (P < 0.01) while in the coated group the TCC concentration increased from a baseline of 0.53 +/- 0.03 to a peak value of 5.2 +/- 0.24 AU/ml (P <0.01). The difference between the peak values was statistically significant (P = 0.00002). In both groups a significant increase in myeloperoxidase and lactoferrin release was observed by the end of operation. There was no difference in myeloperoxidase or lactoferrin release between the two groups. TCC levels were compared to the occurrence of perioperative infarction, development of lung or renal failure, postoperative bleeding, time on ventilator and days in hospital. Three patients developed perioperative infarction; the peak levels of TCC were significantly higher in these patients than in the 148 patients that did not develop infarction. The reduction in TCC formation in the heparin-coated group was not associated with differences in any of the other clinical parameters. Few adverse effects occurred in the study. The peak values of C3bc were higher in the patients needing inotropic support that in those who did not, the relevance of this finding remains uncertain. CONCLUSION: It is concluded that the Duraflo II heparin coating reduces complement activation, particularly TCC formation, during CPB, but not the release of specific neutrophil granule enzymes. No certain correlation was established between complement and granulocyte activation and clinical outcome.

Aged↗

PubMed1997

Effects of heparin coating on the expression of CD11b, CD11c and CD62L by leucocytes in extracorporeal circulation in vitro.

Leucocyte adhesion molecules are involved in the leucocyte-endothelial interaction and in the activation of coagulation and binding of complement and endotoxin. Thus, they are important in inflammation, systemic acute phase reaction, ischaemia reperfusion injury and resistance against infections. The expression of the adhesion molecules CD11b, CD11c and CD62L on leucocytes and changes in plasma products of neutrophil activation (myeloperoxidase, lactoferrin) and complement activation (C3bc, SC5b-9 (TCC)) were examined in an extracorporeal circulation (ECC) model and the effects of Carmeda bioactive surface (CBAS) heparin coating (n = 7) of the circuits were compared to uncoated control circuits (n = 5). In this model, new 'unactivated' cells mobilized from the bone marrow could not interfere with descriptive measures of cell activation as seen in in vivo studies. In the control group, CD11b and CD11c were upregulated on monocytes and granulocytes during ECC, whereas CD62L was downregulated. Heparin coating reduced the increase in CD11b and CD11c on granulocytes (p < 0.02 at 2 h), but the delayed increase in CD11c on monocytes and the delayed downregulation of CD62L on granulocytes and monocytes did not reach statistical significance. Further, heparin coating also reduced the initial decrease in the absolute cell counts of monocytes and granulocytes (p = 0.01 at 2 h), reflecting reduced adhesion to the oxygenator/tubing. The increases in plasma myeloperoxidase, lactoferrin, C3bc and TCC were lower in the heparin-coated group compared to the control group. The increases in plasma myeloperoxidase and lactoferrin correlated significantly to the increase in CD11b (r = 0.71, p = 0.02 and r = 0.64, p = 0.05, respectively) and CD11c (r = 0.72, p = 0.008 and r = 0.72, p = 0.008, respectively) on granulocytes, suggesting interacting regulatory pathways in the process of neutrophil adhesion, activation and degranulation. Thus, in this in vitro ECC model, heparin coating of oxygenator/tubing sets reduced leucocyte activation and leucocyte adhesion-related phenomena.

Blood Cell Count↗

PubMed1996

[Changing the use of albumin at the Oslo hospital].

An increasing demand for albumin in Oslo hospitals in the early 1990s instigated measures to reduce its use. During the autumn of 1993 a letter was sent to all doctors at Ullevål hospital informing them about the lack of documentation that albumin supplementation has a positive effect on outcome in critically ill with an albumin concentration of more than 20 g/l. In May 1994 the blood bank at Ullevål hospital stopped supplying 4% albumin solutions. A 20% reduction in use of albumin was observed after the letter of information, followed by a 50% reduction after the 4% solution was withdrawn. It is concluded that greater awareness of lack of information about the effects of albumin in critically ill patients has led to a more restrictive use of albumin. During the same period the use of polygeline increased, leading to the assumption that colloids other than albumin are being used for volume substitution.

Albumins↗

PubMed1996

Centrifugal pump and heparin coating improves cardiopulmonary bypass biocompatibility.

BACKGROUND: Centrifugal pumps are being used increasingly for short-term extracorporeal circulation purposes such as during heart operations. Whether the centrifugal pump improves the cardiopulmonary bypass biocompatibility has not been fully documented. METHODS: A roller pump (n = 20) was compared in vivo with a centrifugal pump (n = 20) in groups of patients in which cardiopulmonary bypass circuits that were either totally heparin coated (Carmeda BioActive Surface; n = 20) or uncoated (n = 20) were used. We expected the heparin coating to attenuate blood activation, thus possibly making the comparison of the two pumps easier with respect to their different blood activation potentials. Samples of blood plasma, obtained during cardiopulmonary bypass from low-risk coronary artery bypass grafting patients, were analyzed for hemolysis (plasma haemoglobin), complement activation (C3bc and the terminal complement complex), a complement lytic inhibitor (vitronectin), coagulation activation (fibrinopeptide A), granulocyte activation (lactoferrin), and platelet activation (beta-thromboglobulin). RESULTS: The concentrations of terminal complement complex, lactoferrin, and beta-thromboglobulin were significantly lower in association with heparin-coated surfaces. The concentration of plasma hemoglobin was significantly lower in association with the centrifugal pump. In uncoated circuits, the beta-thromboglobulin level was significantly higher in association with the roller pump than with the centrifugal pump, but this significant reduction in the beta-thromboglobulin level did not hold true for the heparin-coated circuit group. CONCLUSIONS: A heparin-coated cardiopulmonary bypass surface reduces the blood activation potential during cardiopulmonary bypass, and the centrifugal pump causes less hemolysis than the roller pump.

Adult↗

PubMed1996

Complete heparin-coated cardiopulmonary bypass and low heparin dose reduce complement and granulocyte activation.

Complete heparin-coated extracorporeal circuits, including cardiotomy reservoir, have recently become available for routine cardiac surgery. The effects on complement and granulocyte activation using a heparin-coated circuit in combination with reduced systemic heparinization (activated clotting time (ACT) > 250 s) were studied in 33 patients undergoing elective first time myocardial revascularization. The patients were prospectively randomized either to a heparin-coated group (Group H, n = 17), or to a control group (Group C, n = 16) treated with an identical uncoated circuit and full heparin dose (ACT > 480 s). During cardiopulmonary bypass (CPB) the C3 activation products C3b, iC3b, and C3c (C3bc) and the terminal SC5b-9 complement complex (TCC) increased markedly in both groups compared to baseline, but to a much lesser extent in the heparin-coated group. The maximal increase of C3bc during the operation was a median of 28 arbitrary units (AU)/ml in the heparin-coated group, compared to 45 AU/ml in the control group (P = 0.01). Similarly, in Group H the maximal increase of TCC was significantly lower (median 0.8 AU/ml) than the levels recognized in Group C (median 1.9 AU/ml) (P < 0.0001). The release of the granulocyte activation enzymes lactoferrin and myeloperoxidase also increased during CPB in both groups compared to baseline level. The maximal increase of lactoferrin concentration was a median of 229 micrograms/l in Group H and significantly lower than 647 micrograms/l in the control group (P = 0.0002). As for myeloperoxidase, there were no significant intergroup differences. In conclusion, a complete heparin-coated circuit and low systemic heparinization for CPB in coronary artery surgery were associated with reduced activation of the complement system and less release of lactoferrin. The results indicate improved biocompatibility of this option for extracorporeal circulation.

Adult↗

PubMed1996

Left ventricular rupture following external chest compression.

A case of a 62-year-old woman suffering an acute cardiac arrest during a court dispute is presented. Cardiopulmonary resuscitation was immediately started by bystanders. In hospital there were signs of intrathoracic bleeding. A left thoracotomy revealed a cardiac rupture of the left ventricle and a large pericardial tear. Intraoperative evaluation of the heart as well as postoperative enzyme levels and ECG did not indicate acute myocardial infarction. The rupture may therefore be traumatic. The cardiac rupture was sutured five hours after the initial resuscitation, and the patient discharged from the intensive care unit two days after the rupture without clinical signs of neurological injury. A precordial thump is advised before start of external chest compression. One beneficial effect may be that the ventricles empty and the risk of traumatic rupture during compression is reduced.

Cardiopulmonary Resuscitation↗

PubMed1996

Differences in blood activation related to roller/centrifugal pumps and heparin-coated/uncoated surfaces in a cardiopulmonary bypass model circuit.

An in vitro model cardiopulmonary bypass (CPB) circuit consisting ot tubing, oxygenator and venous reservoirs with either a roller or a centrifugal pump, and with either heparin-coated (Carmeda Bioactive Surface, CBAS) or uncoated surfaces, was studied with respect to 'blood activation', using small-scale-based blood volume (450 + 500 ml). Sixteen circuits were tested in each pump group, eight with and eight without heparin-coated surfaces, by circulating heparinized fresh human blood for 72 hours at 30 degrees C. Blood plasma, sampled at defined intervals, was analysed for haemolysis (lactate dehydrogenase and potassium), complement activation (C3bc and C5b-9 (TCC)), complement lytic inhibitors (vitronectin and clusterin), coagulation activation (fibrinopeptide A), granulocyte (lactoferrin and myeloperoxidase) and platelet (beta-thromboglobulin) activation and contaminating endotoxin. The heparin coating significantly reduced the concentrations of C3bc, TCC, fibrinopeptide A, lactoferrin, myeloperoxidase and beta-thromboglobulin. The two pump types did not differ with respect to these parameters, but the roller pump caused significantly higher increases in plasma LDH and potassium and significantly greater reductions in clusterin and vitronectin than the centrifugal pump. Endotoxin concentration was low at the start and after 24 hours in all groups. These results confirm that heparin-coated CPB surfaces reduce blood activation, and suggest that centrifugal pumps cause less haemolysis and less reduction in lytic complement inhibitors than roller pumps.

Blood Coagulation↗

PubMed1995

[Thoracoscopic surgery].

Thoracoscopic operations were performed on 91 patients. In 52 patients operated on by thoracoscopic pleurodesis for pneumothorax, the results were compared with the results in 41 patients previously operated on by transaxillary thoracotomy. The groups did not differ with respect to duration of stay in hospital or minor complications, but the duration of postoperative sick leave was significantly reduced after thoracoscopic operation. In nine cases lung metastasis or primary lung tumours were removed thoracoscopically. Thoracoscopic evacuation were performed in seven cases of empyema or pleural haematoma. Two of these patients were later operated on by open decortication. The main advantages of thoracoscopic surgery are less postoperative pain and a shorter time away from work after operation than with open procedures.

Adolescent↗

PubMed1995

[Horner syndrome following insertion of a chest tube].

We describe a case of Horner syndrome following insertion of a chest tube in a 27 year old male. The syndrome was discovered the day after insertion of the tube and persisted for at least three months. By the time of a control examination six months after insertion the symptoms had disappeared. Caution must be taken when inserting a chest tube. Pressure of the tip of the tube against the thoracic aperture should be avoided.

Adult↗

PubMed1995

High and low heparin dose with heparin-coated cardiopulmonary bypass: activation of complement and granulocytes.

BACKGROUND: Cardiopulmonary bypass with heparin-coated circuits allows reduced amounts of systemic heparin. Heparin inhibits activation of the complement cascade experimentally, but the effects of different levels of systemic heparin on activation of complement and granulocytes in patients have remained unknown. METHODS: Fifty-two patients undergoing coronary artery bypass procedures were studied. Cardiopulmonary bypass circuits completely coated with surface-bound heparin were used for one group given low-dose heparin (n = 17) (activated clotting time > 250 seconds), and was compared with a second group having normal high-dose heparin (activated clotting time > 480 seconds) (n = 18). A third control group was perfused with ordinary uncoated circuits and a full heparin dose (n = 17). RESULTS: During cardiopulmonary bypass, the C3 activation products C3b, iC3b, and C3c increased markedly in all three groups compared with baseline, but significantly less in the two heparin-coated groups (high dose, median maximal increase 58 arbitrary units (AU)/mL; low dose, 48 AU/mL) compared with the uncoated control group (74 AU/mL) (p < 0.01). The difference between the two coated groups was not significant. Similarly, the maximal increase in terminal SC5b-9 complement complex was considerably lower in the heparin-coated groups (high dose, 2.5 AU/mL; low dose, 2.6 AU/mL) compared with the level observed in the uncoated control group (5.3 AU/mL) (p < 0.01). The release of the granulocyte activation enzymes myeloperoxidase and lactoferrin increased from the beginning of the operation, with peak levels at the end of cardiopulmonary bypass (p < 0.01). The concentration of lactoferrin was significantly (p < 0.01) reduced in the low heparin dose group compared with the two other groups receiving normal high heparin doses, indicating that circulating heparin is an important granulocyte agonist, acting independently of the presence or absence of heparin-coated surfaces. Also for myeloperoxidase a higher level was observed in the high heparin dose group. CONCLUSIONS: Complement activation was significantly reduced in both heparin-coated groups and was independent of the level of systemic heparinization, whereas granulocyte activation was reduced only in patients who received low doses of systemically administered heparin. The results indicate that a moderate reduction of the systemic heparin dose may be an advantage with regard to improved biocompatibility when using heparin-coated cardiopulmonary bypass circuits.

Adult↗

PubMed1995

Disparity in blood activation by two different heparin-coated cardiopulmonary bypass systems.

BACKGROUND: Several studies have indicated reduced "blood activation" in heparin-coated cardiopulmonary bypass systems. The present study compares the effect of two different heparin coatings on different blood activation indices. METHODS: Low-risk patients (n = 40) were randomized to coronary artery bypass grafting using cardiopulmonary bypass with surfaces coated entirely by either the Duraflo II heparin coat or the Carmeda Biological Active Surface, or with identical uncoated equipment. In all cases, a standard systemic heparin dosage was used. Complement activation (C3 activation products C3bc and C3a and formation of fluid phase terminal SC5b-9 complement complex), neutrophil activation (lactoferrin and myeloperoxidase), and lytic inhibitors (vitronectin and clusterin) were quantified during cardiopulmonary bypass and 6 hours postoperatively. RESULTS: Heparin coating by either method reduced the formation of terminal SC5b-9 complement complex and the release of lactoferrin and myeloperoxidase compared with uncoated systems. Lactoferrin and myeloperoxidase levels increased significantly during cardiopulmonary bypass in the Duraflo II group, whereas no significant increase was observed in the Carmeda Biological Active Surface group. The least formation of terminal SC5b-9 complement complex and neutrophil activation was observed with the Maxima Carmeda Biological Active Surface-coated equipment. The vitronectin and clusterin concentrations were significantly less reduced in the Duraflo II compared with the control group. This study underlines the importance of terminal SC5b-9 complement complex as a suitable marker in the evaluation of complement activation during cardiopulmonary bypass. CONCLUSIONS: Both heparin coatings reduce blood activation, probably more so with Carmeda Biological Active Surface than with Duraflo II.

Anticoagulants↗

PubMed1995

Complement and granulocyte activation in two different types of heparinized extracorporeal circuits.

Complement and granulocyte activation were studied in cardiopulmonary bypass circuits completely coated with either end-attached covalent-bonded heparin, the Carmeda BioActive Surface, or with the Duraflo II bonded heparin, in combination with reduced systemic heparinization (activated clotting time > 250 seconds). The control groups were perfused with uncoated circuits and full heparin dose (activated clotting time > 480 seconds). Altogether 67 patients undergoing elective first-time myocardial revascularization were investigated, having extracorporeal perfusion with a Duraflo II coated circuit (n = 17), an identical but uncoated circuit (n = 17), a Carmeda coated circuit (n = 17), or an equivalent uncoated circuit (n = 16). During cardiopulmonary bypass, the C3 activation products C3b, iC3b, and C3c (C3bc) and the terminal SC5b-9 complemented complex increased markedly in all four groups compared with baseline, but significantly less in the two coated groups than in their control groups. Additionally, a significantly lower concentration of C3bc was observed in the Carmeda coated group, with maximal increase of median 28 AU/ml compared with 50 AU/ml in the Duraflo II coated group (p = 0.003). Similarly, in the Carmeda coated group, the maximal increase of terminal complement complex was considerably lower (0.8 AU/ml) than the levels recognized in the Duraflo II coated group (2.4 AU/ml) (p < 0.001). The release of the granulocyte activation myeloperoxidase and lactoferrin increased from the beginning of the operation, with peak levels at the end of bypass. A significant reduction of lactoferrin release was recognized when comparing the coated groups with the control groups. The difference between the two coated groups (Carmeda 228 micrograms/L; Duraflo II 332 micrograms/L; p = 0.05) was marginally significant. For myeloperoxidase, no significant differences were observed between the coated and uncoated groups. In conclusion, both types of heparin-coated circuits reduced complement activation and release of lactoferrin, but the Carmeda circuit proved to be more effective than the Duraflo II equipment.

Aged↗

PubMed1995

A new model for evaluation of biocompatibility: combined determination of neoepitopes in blood and on artificial surfaces demonstrates reduced complement activation by immobilization of heparin.

An in vitro technique was developed for assessment of the biocompatibility of materials for use in clinical applications. Artificial materials were exposed to blood, and the resulting complement activation was quantified both in the plasma and on the material surface by enzyme immunoassays based on monoclonal antibodies specific for neoepitopes exposed in complement activation products. Several materials were evaluated, and the effect of surface modifications, including end-point immobilized heparin, was studied. The results revealed widely varying complement activation properties of the different materials and confirmed that heparin markedly improves biocompatibility. The present method is superior to analysis limited to either the fluid phase or solid phase since certain materials adsorb activation products (exemplified by Tecoflex) whereas others do not although activation was evident from fluid-phase assay (silicone). Furthermore, direct determination of activation-specific neoepitopes on the surface represents an improvement compared with previously described methods for detection of adsorbed components.

Biocompatible Materials↗

PubMed1994

Reduced complement and granulocyte activation with heparin-coated cardiopulmonary bypass.

Plasma concentrations of the complement activation products C3b, iC3b, and C3c; the terminal C5b-9 complement complex; and the granulocyte proteins calprotectin, myeloperoxidase, and lactoferrin were assessed in two groups of patients undergoing aortocoronary bypass procedures. In 10 patients operated on, the bypass circuits were coated by the Carmeda Bio-Active Surface and systemic heparinization was reduced to 1.5 mg/kg; in another 10, the systems were uncoated and the dosage of systemic heparinization was 4 mg/kg. In both groups, significant complement activation was observed after the onset of cardiopulmonary bypass, but the maximum levels of C3b, iC3b, and C3c and the terminal C5b-9 complement complex were significantly lower in the heparin-coated group. In both groups, a significant increase in calprotectin, myeloperoxidase, and lactoferrin release was observed by the end of operation. The maximum myeloperoxidase levels were significantly lower in the heparin-coated group than those in the uncoated group (p = 0.03). There was a correlation of borderline significance between the formation of terminal C5b-9 complement complex and lactoferrin release, as well as between the formation of terminal C5b-9 complement complex and myeloperoxidase release (p = 0.05). The postoperative blood loss did not differ significantly between the two groups. We conclude that coating by end point-attached and functionally active heparin allows a significant reduction in the amount of systemic heparinization, and significantly reduces complement and granulocyte activation.

Aged↗

PubMed1994

The complement system in trauma-related and ischemic tissue damage: a brief review.

There is increasing evidence that the complement system plays an important role in tissue damage associated with trauma and ischemia. In the present review we focus on some principles of importance for a basic understanding of the complement system, particularly aimed at those not working in this field. Complement is activated by its ability to discriminate between self and non-self, primarily as a defense against microorganisms. The activation induces an inflammatory reaction which may lead to harmful effects on the host, either as local tissue damage or, in case of an extensive systemic activation, as breakdown of homeostatic mechanisms. Complement-mediated inflammation is important not only in specific immunological defense reactions, but also in the induction of tissue injury by ischemia, hypothermia or other general tissue-damaging factors. Major trauma leads to systemic complement activation and complications to trauma may enhance the activation and increase the risk of development of the whole body inflammatory reaction and even of a fatal outcome. To protect the host against self-damage, complement activation is controlled by a series of regulatory proteins inhibiting at the various levels of the cascade. Intervening with complement activation using regulatory proteins like soluble complement receptor 1 has provided direct evidence for the importance of complement in tissue damage in various experimental models. Therapeutic complement intervention using a similar approach may be a useful tool in selected patients to attenuate the degree of complement activation and thereby reduce the total inflammatory load.

Animals↗

PubMed1994

Roller and centrifugal pumps compared in vitro with regard to haemolysis, granulocyte and complement activation.

A Biomedicus centrifugal pump and a Polystan roller pump were compared in vitro with regard to differences in haemolysis, granulocyte and complement activation. Six circuits of tubing and oxygenators were connected to each pump. Heparinized fresh human blood was circulated for 72 hours in the systems. Blood samples were drawn at defined intervals. Haemolysis was assessed by determination of lactate dehydrogenase (LD) and potassium, and granulocyte activation by quantification of the granulocyte proteins calprotectin, lactoferrin and myeloperoxidase. Complement activation was assessed by measuring C3 activation products (C3b, iC3b and C3c), and the terminal C5b-9 complement complex (TCC). The results indicate more haemolysis and complement activation in the roller pump group, revealed by significantly higher concentrations of LD, potassium, C3 activation products and TCC. Calprotectin, lactoferrin and myeloperoxidase were all significantly increased in both groups, but the rise appeared earlier in the roller pump group. The concentrations of LD and potassium both correlated significantly with C3 activation products, indicating that complement activation may at least partly be responsible for the haemolysis.

Cell Adhesion Molecules, Neuronal↗