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Biomedical subjects

C R Wildevuur

Publications and source records attributed to C R Wildevuur.

At least 55 records · Page 3Linked to original sources
PubMed1993

Dermal substitutes for full-thickness wounds in a one-stage grafting model.

We tested different biodegradable matrix materials as dermal substitutes in a porcine wound model. Matrixes were covered with a split-skin mesh graft and protected with a microporous, semipermeable membrane, which prevents blister formation, wound infection and provides ultimate healing conditions. Evaluation parameters were as follows: epithelization, dermal reconstitution, wound contraction, and cosmetic and functional aspect. A microfibrillar matrix of nondenatured collagen gave the best result, with immediate fibroblast ingrowth and epidermal outgrowth. Slight inflammatory reaction and minimal wound contraction were observed. Application of a split-skin mesh graft, in combination with this collagen matrix, generated a thicker dermal layer than did a split-skin mesh graft directly applied on a wound bed. However, the histologic dermal architecture was less optimal than one obtained with a full-thickness punch graft method. Other matrixes caused inflammatory reactions, interfering with epithelization and dermal reconstitution. We conclude that a nondenatured collagen matrix, in combination with a split-skin mesh graft, can provide a substitute dermis in a full-thickness wound. This combination is preferable to a split-skin mesh graft directly applied on the wound bed. With our microporous semipermeable membrane, the combined use of a dermal substitute and a split-skin mesh graft can be applied in a single-stage operation.

Journal Article↗
PubMed1993

Reduced antibody responses after immunization in rat lung transplants.

Pulmonary infections occur so frequently in recipients of lung transplants as well as of combined heart and lung transplants that it has been suggested that the function of the defense system in lung transplants is impaired. Therefore, we investigated in rats whether antibody responses against intrapulmonary antigens were impaired at various time points after transplantation. Antibody responses were induced in lungs of four experimental groups. Group 1: normal lungs (LEW); Group 2: hilar-stripped (sham-operated) lungs (LEW); Group 3: syngeneic lung transplants (LEW-to-LEW); Group 4: allogeneic lung transplants (BN-to-LEW). The operations were performed on the left lungs. All rats (including those with normal lungs) were treated with cyclosporine on Days 2 and 3 after operation, which treatment is adequate to induce permanent graft acceptance of the allografts. Rats were immunized 7, 10, 14, 21, and 28 days and at 6 months after operation with sheep red blood cells, injected selectively into the bronchus of the left lung. The resulting serum antibody titers were detected with a hemolysis assay. After immunization on Day 7, no antibody responses could be detected in all hilar-stripped and transplanted rats, whereas responses were normal in two allografted rats immunized in the nontransplanted right lung. After immunization on Day 14, responses had returned to normal in hilar-stripped rats, whereas they were still impaired in the transplanted rats. After immunization on Day 28, responses were almost normal in all rats and remained so until 6 months after transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Blood activation during neonatal extracorporeal life support.

Cardiopulmonary bypass for heart operations is associated with a whole body inflammatory reaction. The main factors involved in this reaction are the contact system and the complement system. The activation of the contact system is considered mainly responsible for impaired hemostasis because it affects platelet function. The activation of the complement system is considered the main cause for organ dysfunction, particularly of the lung, due to activation of leukocytes. This study in 10 neonates was undertaken to evaluate if there are effects of activation of the contact and the complement systems in neonatal extracorporeal life support comparable to those during cardiopulmonary bypass for cardiac operations. Two periods of blood activation during extracorporeal life support could be distinguished. The initial blood-material interaction at the onset of extracorporeal life support resulted in activation of both the contact and the complement systems. The contact activation was apparent by elevated factor XIIa-C1 esterase inhibitor complexes, decreased kallikrein inhibitory capacity, thrombin-antithrombin III formation, and moderate generation of fibrin(ogen) degradation products. The complement activation was characterized by elevated C3a, decreased leukocyte count, elastase release, and tumor necrosis factor-alpha production. This initial activation pattern subsided by 24 hours. A second activation period was observed 72 hours after the onset of extracorporeal life support, which was characterized only by increased clotting and fibrinolytic activity while no activation of the complement system was observed. We conclude that the initial activation pattern in extracorporeal life support is similar to that observed during cardiopulmonary bypass for cardiac operations. The contact activation that affects platelets might explain the continuous platelet consumption observed during extracorporeal life support. In this period, as in cardiopulmonary bypass, aprotinin given in the pump prime might be effective to prevent platelet consumption and impairment of hemostasis also in extracorporeal life support. The complement activation and leukocyte inflammatory reaction during the initial period are able to cause a capillary leak syndrome and might therefore explain the frequently observed temporary compromised lung function in extracorporeal life support. This reaction, as in cardiopulmonary bypass, might be reduced by the use of specific drugs or heparin coating also in extracorporeal life support. The cause of the second period of activation during extracorporeal life support requires further studies before adequate measures can be recommended.

Acute-Phase Proteins↗
PubMed1993

Preoperative therapy of low-dose aspirin in internal mammary artery bypass operations with and without low-dose aprotinin.

The effect of preoperative low-dose aspirin (1 mg/kg of body weight) and intraoperative low-dose aprotinin (2 million kallikrein inactivator units) treatment on perioperative blood loss and blood requirements in patients who undergo internal mammary artery bypass operations is unknown. Therefore, we retrospectively studied 75 matching patients who underwent internal mammary artery operations, and they were allocated to one of three groups: low-dose aspirin and aprotinin treatment (group 1, n = 25), low-dose aspirin treatment without aprotinin (group 2, n = 25), and neither aspirin nor aprotinin treatment (group 3, n = 25). Although the perioperative blood loss was similar, the blood requirements tended to be higher (p = 0.09) in the patients who were treated with aspirin (group 2) than in the control patients (group 3). When aprotinin was added to the priming solution in patients who were treated with aspirin (group 1), blood loss was significantly lower (p < 0.05) than that of group 2 patients but not of control patients. Blood requirements were significantly lower (p < 0.01) than those of patients in groups 2 and 3. Blood products were needed in 29%, 62%, and 75% of patients in groups 1, 2, and 3, respectively.

Aprotinin↗
PubMed1992

Fabrication and characterization of an asymmetric polyurethane membrane for use as a wound dressing.

To prevent wound dehydration and bacterial penetration, a wound dressing should be occlusive, but on the other hand it should also be permeable for wound exudate to prevent bullae formation. To meet these requirements a new type of polyurethane wound dressing which consists of a microporous top layer (pore size less than 0.7 mum) supported by a sublayer with a highly porous sponge-like structure containing micropores (pore size less than 10 mum) as well as macropores (pore size: 50-100 mum) was designed. The pores of both layers are interconnected and form a continuous structure in the membrane. Membranes according to this design were prepared either by means of a two-step or by means of a one-step casting process. Both fabrication methods are based on phase inversion techniques. Asymmetric polyurethane Biomer membranes prepared by the two-step casting process were tested in vivo as full thickness skin substitutes using guinea pigs. Neither wound dehydration nor infections were observed while the drainage capacity of the wound dressing was effective in preventing bullae formation. Furthermore the wound dressing remained firmly adhered to the wound surface during the whole process of wound healing. In contrast to all other commercial wound dressings currently available the polyurethane wound dressing applied on excised clean wounds did not need to be replaced during healing but could be left on the wound until full regeneration of the skin had taken place after which it was spontaneously repelled.

Animals↗
PubMed1992

Low-dose aprotinin in internal mammary artery bypass operations contributes to important blood saving.

The effect on postoperative blood loss and blood use of blood-saving treatment with or without 280 mg of low-dose aprotinin (2 million kallikrein inactivator units) was studied in 200 consecutive patients undergoing either unilateral or bilateral internal mammary artery bypass grafting. Postoperative blood loss and total units of homologous blood products were similar in patients having either bypass procedure without aprotinin treatment. In patients given aprotinin, postoperative blood loss and use of homologous blood products were significantly lower (p < 0.05). The use of any donor blood product was prevented in 78% of the patients given aprotinin versus only 45% of patients treated without aprotinin. None of the aprotinin-treated patients underwent repeat thoracotomy for excessive bleeding; repeat thoracotomy was indicated in 8% of the patients having bilateral internal mammary artery grafting without aprotinin treatment. These results demonstrate that low-dose aprotinin reduces blood loss and blood use significantly and prevents excessive bleeding.

Aprotinin↗
PubMed1992

Endotoxin release and tumor necrosis factor formation during cardiopulmonary bypass.

Endotoxin, when released into the systemic circulation during cardiopulmonary bypass (CPB), might induce activation of plasmatic systems and blood cells during CPB, in addition to a material-dependent blood activation during CPB. However, the role of endotoxin in the development of this so-called whole-body inflammatory reaction in CPB is still unclear. We investigated the release of endotoxin into the systemic circulation in relation with the activation of the complement system and in particular the formation of tumor necrosis factor in 10 patients undergoing CPB. Immediately after the start of CPB the endotoxin concentrations increased significantly (p less than 0.01), accompanied by increases in C3a concentration (p less than 0.05). After release of the aortic cross-clamp, there was a second increase in endotoxin followed by a continuous increase in tumor necrosis factor, reaching a peak concentration 1 hour after the end of CPB (p less than 0.01). These observations demonstrate a release of endotoxin into the systemic circulation associated with tumor necrosis factor formation, which contributes to the whole-body inflammatory reaction associated with CPB.

Aged↗
PubMed1992

Leukocyte activation with increased expression of CR3 receptors during cardiopulmonary bypass.

The effects of cardiopulmonary bypass (CPB) on the expression of leukocyte adhesive receptors, ie, complement receptor type 3 (CR3), were studied in 16 patients. The CR3 expression on leukocytes was determined by time-resolved fluoroimmunoassay on a standardized number of cells isolated from blood samples taken during various times during CPB. The results demonstrated that CR3 expression on leukocytes increased immediately after the start of CPB (p less than 0.05), concomitant with an early sharp increase of plasma concentrations of C3a (p less than 0.01). After release of the aortic cross-clamp, a second peak of leukocyte CR3 expression was induced (p less than 0.05), paralleled by a significant increase of leukotriene B4 (p less than 0.05) and elastase (p less than 0.05) levels in the late period of CPB. In vitro studies with leukocytes isolated from healthy donors (n = 5) showed a dose-dependent increase of CR3 expression stimulated by zymosan-activated plasma, indicating that the rapid CR3 expression on leukocytes is likely mediated by complement activation. However, the mechanisms for the second peak of leukocyte CR3 expression during CPB remain to be further elucidated. In conclusion, CR3 expression on leukocytes increased immediately after the start of CPB and was followed by a second peak of expression in the late phase of CPB. Pharmacological blockage of these adhesive receptors might reduce the leukocyte-mediated deleterious effects of CPB.

Cardiopulmonary Bypass↗
PubMed1992

In vivo fragmentation of microporous polyurethane- and copolyesterether elastomer-based vascular prostheses.

A previous study showed that microporous, compliant and (bio)degradable vascular prostheses prepared from a polyurethane/poly(L-lactic acid) mixture can function as a temporary scaffold for the regeneration of small-calibre arteries. In this study the mechanism of fragmentation of vascular prostheses made of polyurethane, copolyesterether and blends of either polyurethane or copolyesterether with polymers differing in biodegradability, crystallinity and glass transition temperature is investigated. Animal studies revealed that after 6 wk of implantation only the prostheses made of blends containing a second polymer which was non-elastic at 37 degrees C were fragmented extensively, whether the second polymer was (bio)degradable or not. It is concluded that fragmentation of the prostheses is mainly caused by alternating stresses induced by the arterial pulsations and that (bio)degradation plays a minor role.

Animals↗
PubMed1992

Late airway changes caused by chronic rejection in rat lung allografts.

Airway disease after lung or heart-lung transplantation is one of late major complications, affecting the prognosis of the transplants. Little is known about the causes of airway changes. We performed rat lung transplantation and investigated the late airway changes of the long-term surviving lung grafts: allografts, BN to Lewis; isografts, BN to BN rat. All recipients were treated with CsA. We found airway changes, i.e., mucosal ulceration, granulation, submucosal fibrosis, which was located in the large airways, in four of five allografted lungs. The lung isografts showed no pathological abnormalities. Immunopathological studies disclosed the localized expression of MHC class II antigens on the bronchial epithelium of the large airways where recipient type dendritic cells accumulated in the submucosa and CD4 positive predominant lymphocytes infiltrated. These findings support the idea that the late airway changes in lung transplants are caused by immunologically mediated chronic rejection.

Animals↗
PubMed1992

A heparin-coated circuit reduces complement activation and the release of leukocyte inflammatory mediators during extracorporeal circulation in a rabbit.

Heparin coating modifies complement activation during extracorporeal circulation much more effectively than systemically administered heparin. This rabbit study was undertaken to address possible mechanisms responsible for this difference. We evaluated the effect of heparin coating on complement activation and subsequently the release of leukocyte inflammatory mediators during extracorporeal circulation through a simplified circuit. We found in the heparin-coated group a significantly reduced complement hemolytic activity (CH50), remaining higher leukocyte numbers, significantly decreased release of beta-glucuronidase, and most strikingly a complete prevention of tumor necrosis factor (TNF) formation. The significantly reduced CH50 activity in the heparin-coated groups indicates the reduction of one or more native classical complement products. This could be explained by the absorption of complement components by the circuit, which results in reduced activity of the complement cascade. We conclude therefore that heparin coating reduces complement activation and consequently reduces the release of leukocyte inflammatory mediators.

Animals↗
PubMed1992

The effect of postoperative normovolaemic anaemia and autotransfusion on blood saving after internal mammary artery bypass surgery.

The efficacy of two blood conservation techniques in decreasing and in preventing the use of homologous blood products was retrospectively studied in 150 patients undergoing internal mammary artery bypass surgery. Patients were matched according to prebypass blood haemoglobin (Hb) content and body surface area and were allocated to one of three groups: in the patients of group 1 (n = 50), normovolaemic anaemia (NA) was accepted postoperatively (haematocrit [Hct] was accepted to a minimum level of 25%); the patients of group 2 (n = 50) were treated with postoperative autotransfusion (AT) of mediastinal shed blood and acceptance of NA. Group 3 (n = 50) contained control patients, not treated with NA or with AT (Hct was accepted to a minimum level of 30%). Patients of group 1 required 3.0 +/- 0.3 units of homologous blood products, but the patients of groups 2 and 3 received significantly more (p less than 0.01) units: 3.9 +/- 0.2 and 4.5 +/- 0.3 units. No donor blood products were needed in 36%, 9% and 5% of the patients in groups 1, 2 and 3 respectively. The net postoperative blood loss was similar in the groups: 1229 +/- 92 ml in group 1, 1098 +/- 74 ml in group 2 and 1243 +/- 72 ml in group 3. However, total blood loss (1982 +/- 135 ml), including the retransfused part (954 +/- 89 ml), was significantly larger (p less than 0.01) in group 2, than in groups 1 and 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Anemia↗
PubMed1992

Blood loss and use of blood in internal mammary artery and saphenous vein bypass grafting with and without adding a single, low-dose of aprotinin (2 million units) to the pump prime.

In comparison with saphenous vein bypass grafting (SVG) without a pleurotomy, internal mammary artery (IMA) bypass surgery might enhance more blood loss by the intrathoracic wound and a wide opened pleura. Low-dose aprotinin (Trasylol) reduces blood loss and consequently, the use of homologous blood. We studied the blood loss and blood requirements peri-operatively in 70 patients, who underwent either SVG-(n = 35) or IMA-surgery (n = 35) without aprotinin and another 70 patients who underwent SVG- (n = 35) or IMA-surgery (n = 35) with a single dose of aprotinin, added to the pump prime. We also determined the hemoglobin and total protein content of the shed blood. Without aprotinin administration, the mean intra-operative and post-operative blood loss was significantly less (p < 0.01) in SVG-patients, than in IMA-patients. We observed no statistical differences in the mean blood requirements between SVG- and IMA-surgery (1.2 units and 1.6 units). The use of any homologous blood product was similarly averted in 39% of the SVG-patients, and in 48% of the IMA-patients. Treatment with aprotinin significantly lessened (p < 0.01) the mean intra-operative blood loss only in IMA-patients. Post-operative blood loss was diminished with 45% in IMA-patients and 33% in SVG-patients, being significantly less (p < 0.01) after SVG, than after IMA-surgery. Blood requirements were significantly lowered (p < 0.01): a total mean of 0.2 units in SVG- and 0.6 units in IMA-patients (NS). Any homologous blood product was prevented in 78% of the IMA-patients and in 87% of the SVG-patients (NS). The mean loss of hemoglobin and total protein per 100 ml of shed blood was similar in IMA-, and SVG-patients with or without aprotinin, although aprotinin diminished the total amounts in both groups with 50% (p < 0.01).

Adult↗
PubMed1992

Rapid endothelialization of vascular prostheses by seeding autologous venous tissue fragments.

A method was developed to obtain rapid endothelialization of a fabric vascular prosthesis by seeding autologous venous tissue fragments into its wall. In an animal study, complete endothelialization was observed in the entire inner surface of the prosthesis within 2 weeks after implantation. A piece of peripheral vein was minced with scissors and then stirred into saline to create a tissue suspension. This suspension was enmeshed into the wall of a highly porous fabric vascular prosthesis by repeated pressurized injections with a syringe. The prostheses (7 mm inside diameter and 5.7 cm in length), seeded with tissue fragments, were implanted into the descending thoracic aorta of 25 dogs, and they were removed from 1 hour to 2 months after implantation. Twenty-five prostheses, preclotted with fresh blood, were used as control prostheses. In the seeded graft, a thin fibrin layer covered the inner surface just after implantation, but countless numbers of endothelial cells migrated from the fragments and came up to the luminal surface like multiple "mushrooms" under the fibrin layer. Smooth muscle cells made multiple layers underneath the endothelial cell layer. The healing proceeded equally at every part. By this active migration and proliferation, the inner surface was completely healed within 2 weeks.

Animals↗
PubMed1992

[Development of a method to prevent degenerative changes of the vein graft for arterial reconstruction].

Autologous vein graft is frequently used for arterial reconstruction in vascular surgery. Its' long-term patency rate, however, is low because of the degenerative changes of the vein wall. Of the basis of our hypothesis that the degenerative changes are mainly caused by an over-distension of vein wall in arterial system, in this study, autologous vein grafts of rabbit (N = 56) were implanted in the carotid arteries. To prevent overdistension, some of the grafts were covered with prosthesis which was made of microporous, compliant biodegradable polyurethane and were compared with those without prosthesis. The integrity of the architecture of the vein wall covered with prosthesis was well preserved at 6 weeks after implantation, where the biodegradation of prosthesis induced an optimal arterialization of the vein grafts. The results indicate that this method may prevent the degenerative changes of vein wall such as fibrosis and intimal hyperplasia, which would cause poor long-term patency of vein graft used for arterial reconstruction.

Animals↗
PubMed1992

Improved healing of small-caliber polytetrafluoroethylene vascular prostheses by increased hydrophilicity and by enlarged fibril length. An experimental study in rats.

This study was undertaken to test whether increasing the hydrophilicity of small-caliber polytetrafluoroethylene vascular prostheses by alcohol pretreatment or increasing their fibril length might improve their healing without affecting their patency. Polytetrafluoroethylene vascular prostheses (length 1 cm, inside diameter 1.2 mm) (1) with a fibril length of 30 microns (control group; n = 18), (2) pretreated with alcohol (n = 18), or (3) with a fibril length of 60 microns (n = 18) were implanted into the abdominal aorta of rats. The prostheses were evaluated by means of routine light and scanning electron microscopy during a 6-week period after implantation. All prostheses were patent at harvesting. On implantation, the control polytetrafluoroethylene vascular prostheses were only scarcely covered with platelets. At 6 weeks they had healed in a small area adjacent to the anastomoses only. In contrast, both the alcohol-pretreated polytetrafluoroethylene prostheses and the polytetrafluoroethylene prostheses with a fibril length of 60 microns were completely covered by a thin clot layer on implantation. At 6 weeks after implantation these prostheses had almost completely healed as a result of organization of the thin clot layer by ingrowth of both endothelial and smooth muscle cells. These results demonstrate that increasing hydrophilicity of polytetrafluoroethylene vascular prostheses by alcohol pretreatment or enlarging their fibril length improves their healing by induction of a thin luminal clot layer. This clot layer provides a suitable matrix for ingrowth of both endothelial and smooth muscle cells and does not lead to thromboembolic complications.

Animals↗
PubMed1991

Activation of plasma systems and blood cells by endotoxin in rabbits.

Endotoxin plays an important role in the pathogenesis of septicaemia by activation of cellular and plasmatic systems. This study was performed to investigate the effects of infusion of endotoxin in rabbits by measuring the activation of cellular and plasma systems. Endotoxin was infused at a rate of 1 mg/kg body wt for 10 min, which caused death of all rabbits within 72 h. Endotoxin induced early leukopenia and thrombopenia, increased plasma levels of beta-glucuronidase and leukotriene B4 (LTB4), and decreased complement total hemolytic activity (CH50) and tissue plasminogen activator (t-PA) activity. These observations correlate with the cellular and plasma changes that have been documented in severely ill endotoxemic patients. Therefore, we conclude that this endotoxin model in rabbits is a valuable tool for investigation of pathophysiology and treatment of endotoxic shock.

Animals↗