Biomedical subjects

C R Wildevuur

Publications and source records attributed to C R Wildevuur.

At least 37 records · Page 2Linked to original sources

PubMed1996

Clinical outcome after coronary surgery with heparin-coated extracorporeal circuits for cardiopulmonary bypass.

In this prospective randomized trial, we studied whether heparin-coated extracorporeal circuits (ECC), known to reduce complement activation, could improve the clinical outcome of 200 patients undergoing coronary artery surgery. Patients have been divided into two groups (heparin-coated ECC and uncoated ECC groups) which were similar in terms of age, gender, left ventricle function, preoperative aspirin use and consequent intraoperative aprotinin use, number of grafts, duration of aortic cross-clamping and cardiopulmonary bypass. Univariate analysis showed that heparin coating did not reduce significantly postoperative bleeding (640 +/- 311 versus 682 +/- 342 ml with uncoated ECC) nor the need for transfusion (19% of patients versus 25% with uncoated ECC). Adverse events, including all mortality and morbidity noticed during the five first postoperative days, occurred in 20 patients of the uncoated ECC group and in eight patients of the heparin-coated ECC group (p = 0.013). The most frequent complications were supraventricular arrhythmias that occurred in 13 patients of the uncoated ECC group and in four patients of the heparin-coated ECC group (p = 0.02). Multivariate analysis by stepwise logistic regression showed that only heparin coating of the ECC was shown as a significant predictive factor of adverse events reduction (p = 0.01; odds ratio = 0.34). These data suggest that heparin coating reduced postoperative complications in patients undergoing coronary artery surgery.

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PubMed1995

Inadequate antibody response against respiratory viral infection in long-surviving rat lung allografts.

Lung transplant recipients suffer from a high number of viral infections. It has been suggested that the defense against viral infections is impaired in lung transplants. Therefore, we investigated in rat lung transplants whether antibody responses against an intrapulmonary viral infection were impaired in 3 groups of rats with: (1) BN-to-LEW allogeneic lung transplants, (2) LEW-to-LEW syngeneic lung transplants, and (3) nontransplanted LEW lungs. All rats (including those with nontransplanted, normal lungs) were treated with cyclosporine on days 2 and 3 after operation; this treatment is adequate to induce permanent graft acceptance of the allografts. Six months after transplantation, viral infections with Sendai virus (parainfluenza type I) were induced intratracheally. At day 0, immediately before infection, and at days 4, 7, 21, and 56 after infection, 4 rats in each group were killed for histological evaluation of the lungs. The number of antibody-positive cells in the bronchus-associated lymphoid tissue (BALT) in the lungs and in the spleen, and presence of the virus in the lungs were determined by immunohistology. Serum antibody titers were followed for 56 days after infection. The allogeneically transplanted lungs failed to respond adequately against the virus: the number of antibody-positive cells in the BALT did not increase after infection, serum antibody titers were hardly detectable, and virus was present in the airways of the lungs up to day 21 after infection. In contrast, in the syngeneically and nontransplanted lungs, the number of antibody-forming cells in the BALT increased steeply until day 7, serum antibody titers rose until day 14, and virus could be detected only on day 4 after infection. This study shows that in rat lung allografts, both the local antibody production in the BALT and the systemic antibody response against a respiratory viral infection are inadequate. As a consequence, the virus is present longer in these allografted lungs and can exert its damaging effect over a longer period of time. These results may explain why lung transplants are so susceptible to viral infections.

Animals↗

PubMed1995

Hemostatic efficacy of dipyridamole, tranexamic acid, and aprotinin in coronary bypass grafting.

Sixty patients (four groups of 15 patients) were entered in a randomized, controlled study to compare the efficacy of prophylactic treatment with dipyridamole, tranexamic acid, and aprotinin to reduce bleeding after elective coronary artery bypass grafting. Only patients with a preoperative platelet count of less than 246 x 10(9)/L were selected because a previous study showed that these individuals are at risk for increased postoperative bleeding. Compared to control subjects, postoperative blood loss 6 hours after operation was significantly reduced by tranexamic acid (674 +/- 411 versus 352 +/- 150 mL; p < 0.05) and by aprotinin (270 +/- 174 mL; p < 0.01). Dipyridamole did not reduce postoperative blood loss and was associated with complications in 3 patients. We conclude that hemostasis after cardiac operations can be improved with tranexamic acid and aprotinin. Dipyridamole appeared to be ineffective.

Aprotinin↗

PubMed1995

Reduction in prime volume attenuates the hyperdynamic response after cardiopulmonary bypass.

BACKGROUND: A hyperdynamic response to cardiopulmonary bypass is characteristically observed in the post-operative course. To determine the effect of prime volume on the hemodynamic response, a database study was performed on patients who underwent elective coronary artery bypass grafting with an extracorporeal circuit with either a large prime volume (2,350-mL prime, n = 20) or a small prime volume (1,400-mL prime, n = 20). METHODS: Measurements were carried out at fixed time points before and after cardiopulmonary bypass (until 18 hours postoperatively) and include hematocrit, colloid oncotic pressure, fluid balance, and hemodynamic profile (mean of three measurements). RESULTS: The lower colloid oncotic pressure in the large prime group (16.2 +/- 0.6 mm Hg versus 19.1 +/- 1.1 mm Hg, p = 0.0002) was associated with a highly positive fluid balance (5.5 +/- 0.9 L versus 2.8 +/- 0.7 L, p = 0.0001). With the on-bypass hematocrit aimed at 22% to 23%, autologous blood was predonated by 16 patients in the small prime group but by none in the large prime group. Reinfusion of autologous blood resulted in a reduction in blood bank requirements (p = 0.03). Mean arterial pressure was 83 +/- 4 mm Hg for small prime versus 76 +/- 4 mm Hg for large prime (p = 0.01). Cardiac index was 2.9 +/- 0.2 L.min-1.m-2 for small prime versus 3.8 +/- 0.3 L.min-1.m-2 for large prime (p = 0.0001). Pulmonary vascular resistance index was 281 +/- 40 dyne.s.cm5.m-2 for small prime versus 188 +/- 22 dyne.s.cm5.m-2 for large prime (p = 0.0009). Oxygen delivery was 42 +/- 5 mL.min-1.m-2 for small prime versus 51 +/- 3 mL.min-1.m-2 for large prime (p = 0.004). Vasoactive medication was not different among groups. CONCLUSIONS: Reduction in prime volume attenuates the hyperdynamic response after cardiopulmonary bypass. Furthermore, an important reduction in blood bank products can be obtained with small prime volumes.

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PubMed1995

Myocardial performance in elderly patients after cardiopulmonary bypass is suppressed by tumor necrosis factor.

The aim of this study was to determine whether elderly patients (aged > or = 65 years, n = 20) in comparison with younger patients (aged < or = 55 years, n = 23) demonstrate a different biochemical and hemodynamic response to coronary artery bypass operations. In the elderly group, we calculated a smaller body surface area (p < 0.01) than that in the younger group, and more female patients were included in this group (p < 0.05). During cardiopulmonary bypass, the elderly had higher endotoxin plasma concentrations (p < 0.01) than the younger patients, and significantly more circulating tumor necrosis factor-alpha was found after operation (p < 0.04). In the intensive care unit, the elderly patients had a significantly higher pulmonary capillary wedge pressure (p < 0.001), a higher mean pulmonary artery pressure (p < 0.01), and a lower calculated left ventricular stroke work index (p < 0.05). Multivariate analysis for the postoperative outcome showed that the intergroup differences in tumor necrosis factor-alpha, mean pulmonary artery pressure, and pulmonary capillary wedge pressure could be explained mainly by the difference in age between the groups and that the calculated left ventricular stroke work index difference could be explained by the difference in circulating tumor necrosis factor-alpha levels. Thus in elderly patients higher circulating endotoxin and tumor necrosis factor-alpha concentrations were detected than in younger patients, which clinically resulted in a suppressed myocardial performance.

Age Factors↗

PubMed1995

Hemostatic function of aspirin-treated platelets vulnerable to cardiopulmonary bypass. Altered shear-induced pathway.

The impaired hemostasis of aspirin-treated patients is an annoying problem during and after cardiopulmonary bypass. The hemostatic function of platelets comprises two mechanisms: the shear-induced and the cyclooxygenase pathways. Because the latter is inhibited in aspirin-treated patients, the hemostatic function depends mainly on the former pathway. To investigate the effect of cardiopulmonary bypass on the shear-induced pathway, a double-blind study of preoperative aspirin treatment (325 mg) and placebo was conducted in 40 patients undergoing coronary artery bypass grafting. Postoperative blood loss was higher in the aspirin-treated patients than in the placebo-treated patients (p < 0.05). The shear-induced hemostasis was monitored by the in vitro bleeding test (Thrombostat), which mimics bleeding through an injured arteriole. The shear-induced pathway of aspirin-treated platelets was not affected before cardiopulmonary bypass, but it was impaired more during the operation (p < 0.01) and remained worse afterward (p < 0.05), compared with that of placebo-treated platelets. The inhibitory effects of aspirin on thromboxane production and on collagen-induced platelet aggregation remained throughout the operation. In aspirin-treated platelets, the aggregation capacity induced by adenosine diphosphate was inhibited before the operation (p < 0.05) and showed substantial recovery during the operation (p < 0.05). These results suggest that the shear-induced pathway of aspirin-treated platelets is more vulnerable to cardiopulmonary bypass than the pathway in normal platelets and causes severe impairment of hemostasis afterward.

Adenosine Diphosphate↗

PubMed1995

Reduced complement activation and improved postoperative performance after cardiopulmonary bypass with heparin-coated circuits.

A randomized controlled trial that involved 30 patients undergoing elective coronary artery bypass grafting was done to determine the effect of heparin-coated circuits and full heparinization on complement activation, neutrophil-mediated inflammatory response, and postoperative clinical recovery. Peak concentrations of terminal complement complex were 38% lower (p = 0.004) in 15 patients treated with heparin-coated circuits (median 775 micrograms/L, interquartile range 600 to 996) compared with those in 15 patients treated with uncoated circuits (median 1249 micrograms/L, interquartile range 988 to 1443). Although no significant intergroup differences in concentrations of polymorphonuclear neutrophil elastase were found, a positive correlation (rs = 0.74, p < 0.0007) was calculated between peak concentrations of terminal complement complex and polymorphonuclear neutrophil elastase. Differences in patient recovery were analyzed with use of a score composed of fluid balance, postoperative intubation time, and the difference between rectal temperature and skin temperature. The score was significantly lower in patients treated with heparin-coated circuits (p = 0.03), whereas its components showed no intergroup significance. We conclude that the use of heparin-coated circuits with full systemic heparinization results in improved biocompatibility, as assessed by complement activation, and leads to an improved postoperative recovery of the patient.

Body Temperature↗

PubMed1995

Defective bronchus-associated lymphoid tissue in long-term surviving rat lung allografts.

In a previous study we found that a local immune response did not develop in the bronchus-associated lymphoid tissue (BALT) of infected rat allografts. We hypothesized that the BALT in rat lung allografts was damaged after allotransplantation. Therefore, we investigated three prerequisites for a normal function of the BALT, i.e., its structure, the uptake of antigens, and the lymphocyte migration to the BALT in three groups of rats (n = 10 each): (1) Brown Norway(BN)-to-Lewis (LEW) allografts; (2) LEW-to-LEW isografts; and (3) normal LEW rats. All rats were immunosuppressed with CsA (injected on days 2 and 3). Six mo after transplantation the structure of the BALT and the uptake of intrabronchially injected carbon particles in the BALT were determined histologically; the migration of intravenously injected, fluoroscein-isothiocyanate labeled lymphocytes to the BALT was determined immunohistochemically. In the allografts the BALT was defective in all three investigated aspects. It was reduced in size and lymphocyte density and was largely replaced by fibrous tissue. Twenty-four h after administration no carbon particles and only a few labeled lymphocytes were found in the BALT. In contrast, in the syngeneically transplanted and nontransplanted lungs the BALT consisted of a large and dense collection of lymphocytes. In these BALTs large numbers of carbon particles and labeled lymphocytes were found. In conclusion, after allogeneic transplantation the BALT in the lung becomes defective in structure and function. The BALT is most likely damaged by rejection, since the BALT is syngeneic lung transplants was perfectly normal.

Animals↗

PubMed1994

Aprotinin preserves hemostasis in aspirin-treated patients undergoing cardiopulmonary bypass.

Various clinical trials have shown that hemostasis is improved by the administration of aprotinin during cardiopulmonary bypass. However, this effect has not been proved for those patients treated preoperatively with aspirin. Therefore, a double-blind, placebo-controlled study was conducted to test the efficacy of low-dose aprotinin (2 x 10(6) KIU in the pump prime solution) in preserving hemostasis in 40 aspirin-treated (325 mg) patients undergoing coronary artery bypass grafting. Aprotinin brought about a decrease in the postoperative blood loss (p < 0.05). The in vitro bleeding test (Thrombostat) demonstrated that aprotinin preserved the platelet hemostatic function in aspirin-treated patients during cardiopulmonary bypass (p < 0.05). The inhibitory effects of aspirin on collagen-induced platelet aggregation and thromboxane production were not influenced by aprotinin treatment. The findings from the present study indicate that aprotinin preserves hemostasis in aspirin-treated patients during cardiopulmonary bypass, but aspirin's effect on platelets is maintained. Therefore, aprotinin seems to be a useful adjunct treatment in aspirin-treated patients undergoing coronary artery bypass grafting.

Aprotinin↗

PubMed1994

Systemic blood activation during and after autotransfusion.

To evaluate the extent of shed blood activation in two autotransfusion systems and the effect of circulating blood activation upon autotransfusion, we performed a prospective study in 18 patients undergoing internal mammary artery bypass operation and a control group of 10 patients. The autotransfusion systems were from Sorin (n = 9) consisting of a hard shell reservoir with a filter having a small contact area (0.32 m2), and from Dideco (n = 9) consisting of a hard shell reservoir with a filter having a larger contact area (4.64 m2). We found high concentrations of thromboxane, fibrinogen degradation products, complement split product C3a, and elastase in the shed blood and, with the exception of C3a, in the circulating blood of autotransfused patients. There was no such activation in control patients. The degree of the systemic inflammatory reaction was determined by the type of autotransfusion system and by the amount of infused shed blood. The Dideco system provoked more inflammatory response than did the Sorin. This was reflected by the larger shed blood loss during autotransfusion in the Dideco patients than in Sorin patients, resulting in infusion of more shed blood (means, 737 mL versus 566 mL; not significant). After autotransfusion, Dideco patients shed significantly more blood than did Sorin or control patients (p < 0.05). Dideco patients also needed more colloid/crystalloid solution per 24 hours than Sorin patients (p < 0.05). This became clinically relevant only after infusion of more than 800 mL of shed blood (p < 0.001): hemodilution indicated the need for packed cells in 4 Dideco patients and in 1 Sorin patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Loss, Surgical↗

PubMed1994

Supporting, microporous, elastomeric, degradable prostheses to improve the arterialization of autologous vein grafts.

Arterial reconstructions with vein grafts fail more frequently than with arterial grafts. One of the causes of graft failure is damage due to overstretching of the graft wall. Overstretching is caused because the vein graft, which has a poorly developed medium, cannot withstand the arterial blood pressures. The aim of this study is to evaluate whether damage due to overstretching can be prevented and a gradual adaptation of the vein graft to the arterial blood pressures can be induced by applying a microporous, elastomeric, degradable prosthesis around the vein graft. Therefore, autologous vein grafts (length 1.0 cm) with and without supporting prostheses (composite vein grafts and control vein grafts, respectively) were interposed into both carotid arteries of rabbits. Microporous, elastomeric, biofragmentable polyurethane-based prostheses and microporous, elastomeric, biodegradable prostheses made of poly-epsilon-caprolactone or a copolymer of epsilon-caprolactone and 3.6-dimethyl-1,4-morpholine-2,5-dione with a monomer ratio of 95.5:4.5 were prepared. The grafts were evaluated up to 6 wk after implantation. The control vein grafts showed severe destructive changes such as de-endothelialization, disruption of the media with oedema, degradation of the elastic laminae and infiltration of polymorphonuclear leucocytes into the vein graft wall, leading eventually to a fibrotic wall. In contrast, the composite vein grafts showed a preservation of the smooth muscle cell layers and the elastic laminae with only few polymorphonuclear leucocytes infiltrated into the vein graft wall.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Perfusion-related factors of endotoxin release during cardiopulmonary bypass.

To investigate whether the release of endotoxin during cardiopulmonary bypass (CPB) is determined by perfusion-related factors, endotoxin concentrations were determined before, during, and after CPB in 21 male patients (age range 45-75 years) undergoing elective coronary artery bypass grafting. Hemodynamic parameters and oncotic pressure were also measured. Significant increases in endotoxin concentrations were observed after the start of CPB (P < 0.005), before aortic cross-clamp release (P < 0.05), and after aortic cross-clamp release (P < 0.05). The median endotoxin concentration after cessation of CPB was 0.264 EU/ml (range < 0.036-0.480 EU/ml). Endotoxin concentrations derived from the prime solutions were not contributory. Positive correlations were found between arterial pressure after the start of CPB and the endotoxin concentration 10 min after (r = 0.58, P < 0.01) and between the duration of aortic cross-clamping and the endotoxin concentration after the cessation of CPB (r = 0.64, P < 0.005). Arterial pressure after the start of CPB, the duration of aortic cross-clamping, and decrease in oncotic pressure appeared to be independent variables in a forward variable selection model that predicted endotoxin concentrations after CPB. We conclude that in patients undergoing elective coronary artery bypass grafting, an early phase of endotoxin release during CPB could be demonstrated, and that this is due to vasoconstriction. The endotoxin concentrations after the cessation of CPB were determined by early vasoconstriction, duration of aortic cross-clamping, and hypo-oncotic hemodilution.

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PubMed1993

Oxygen consumption after cardiopulmonary bypass--implications of different measuring methods.

OBJECTIVE: To determine whether intra-pulmonary oxygen consumption or whole body oxygen consumption is the main determinant of the hypermetabolic response after cardiopulmonary bypass. Secondly, which method of measuring oxygen consumption best quantifies this hyperdynamic response. DESIGN: We measured oxygen consumption by analysing respiratory gas (VO2-gas), carbon dioxide excretion (VCO2), and respiratory exchange ratio (RER = VCO2/VO2), and calculated oxygen consumption using the Fick-method (VO2-Fick) and intra-pulmonary oxygen consumption (VO2-gas - VO2-Fick) in patients at fixed times before and after elective cardiac surgery. Next, comparisons were made between methods and also between measurements at different times before and after bypass. SETTING: University hospital. PATIENTS: 10 elective cardiac surgical patients. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: VO2-gas, VCO2 and RER were measured with an open circuit indirect calorimeter. VO2-Fick was calculated: VO2-Fick = cardiac index x (arterial - mixed venous oxygen content). Intrapulmonary oxygen consumption was calculated as the difference between VO2-gas and VO2-Fick. Both VO2-gas and VO2-Fick were about 20% higher after bypass than after induction of anaesthesia. Absolute values of VO2-gas were about 30% higher than VO2-Fick. Intra-pulmonary oxygen consumption accounted for 32% of whole body oxygen consumption after induction of anaesthesia and did not increase after bypass. CONCLUSION: Whole body oxygen consumption and not intra-pulmonary oxygen consumption is the main determinant of the hypermetabolic response after bypass. Increased intra-pulmonary oxygen consumption is not related to bypass. VO2-gas best quantifies this hypermetabolic response directly after bypass, and not VO2-Fick, VCO2 or intra-pulmonary oxygen consumption, since VO2-Fick excludes intra-pulmonary oxygen consumption and VCO2 does not reflect metabolism directly after bypass.

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PubMed1993

Heparin-coated circuits reduce the inflammatory response to cardiopulmonary bypass.

Cardiopulmonary bypass generates a systemic inflammatory response including the activation of the complement cascade and leukocytes contributing to postoperative morbidity. To evaluate whether the use of heparin-coated extracorporeal circuits could reduce these activation processes, we performed a study on 30 patients undergoing coronary artery bypass grafting who were randomly perfused with a heparin-coated circuit (Duraflo II, n = 15) or with a similar noncoated circuit (control, n = 15). Standardized systemic heparinization was applied for every patient before cardiopulmonary bypass. The use of heparin-coated circuits resulted in a reduction of systemic leukocyte activation during cardiopulmonary bypass reflected by reduced elastase release (p < 0.05) and tumor necrosis factor generation (p < 0.05) manifest after release of the aortic cross-clamp. In addition, blood samples taken from both the right and left atria after reperfusion revealed that the elastase release from the pulmonary microcirculation was absent in the Duraflo II group in contrast to the control group (p < 0.05). The pattern of complement activation, likely initiating this inflammatory reaction, was modified by heparin coating in two different aspects. There was a significant reduction of C3a generation after protamine administration in patients perfused with heparin-coated circuits, and there was a decrease of complement hemolytic capacity in pooled human serum incubated with heparin-coated tubing. These observations suggest that heparin coating might bind some of the complement components from the classic pathway, thereby reducing the inflammatory response to cardiopulmonary bypass.

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PubMed1993

Intraoperative predonation contributes to blood saving.

The merits of reinfusing prebypass-removed autologous blood (intraoperative predonation) to salvage blood and improve postoperative hemostasis are still debated, specifically for patients at a higher risk for bleeding. To evaluate the effect of intraoperative predonation on the platelet count, blood hemoglobin content, and blood saving postoperatively, we retrospectively studied 100 matching patients. All patients underwent internal mammary artery bypass surgery resulting in a considerable blood loss postoperatively. Intraoperative predonation (800 ml), reinfusion of the residual volume of the extracorporeal circuit, autotransfusion of shed blood, and acceptance of normovolemic anemia postoperatively was the approach adopted in 50 patients (group 1). A similar blood salvage program, excluding intraoperative predonation, was carried out in the other 50 patients (group 2), and these served as the control group. The platelet counts and blood hemoglobin content were significantly higher postoperatively (p < 0.01) in the predonated patients than in the control patients. However, the net blood loss, the amount of retransfused shed blood, and the blood requirements postoperatively were significantly less (p < 0.01) in the predonated patients than in the control patients, whereas 65% of the predonated patients versus 10% of the control patients did not need any donor blood products. In conclusion, predonation reduces the postoperative blood loss and thereby importantly ameliorates the blood-saving effect of a blood salvage program after IMA procedures.

Blood Loss, Surgical↗

PubMed1993

Autologous vein supported with a biodegradable prosthesis for arterial grafting.

To evaluate the potential of a supporting, compliant, biodegradable prosthesis to function as a temporary protective scaffold for autologous vein grafts in the arterial circulation, we implanted vein grafts into the carotid arteries of rabbits, either with (composite grafts) or without (control grafts) such a supporting prosthesis, and evaluated them up to 6 weeks. The control vein grafts showed edema and severe medial disruption with infiltration of polymorphonuclear cells on day 1. Over the study, irregular fibrocyte formation resulted in the formation of a fibrotic vein wall. In contrast, the composite vein grafts showed preservation of smooth muscle cell layers and elastic laminae with a minor inflammatory response. Regular proliferation of fibroblasts, which in some areas were circularly oriented, was observed. We conclude that a supporting, compliant, biodegradable prosthesis can function as a protective scaffold for vein grafts in the arterial circulation, thus reducing damage to the vein graft wall and allowing gradual arterialization.

Animals↗

PubMed1993

Degradation of a supporting prosthesis can optimize arterialization of autologous veins.

In a previous study, we implanted autologous vein grafts in the carotid artery of rabbits supported by a compliant, biodegradable prosthesis to prevent vein wall damage due to the higher arterial pressure. We showed that such a supporting prosthesis indeed reduces damage to these vein grafts and allows for more regular and gradual arterialization than that afforded by unsupported vein grafts. To evaluate the influence of the rate of biodegradation of such a supporting prosthesis on the process of arterialization of autologous vein grafts, we implanted vein grafts supported with prostheses, which degrade within 3 weeks (group I), 6 weeks (group II), or 3 months (group III), into the carotid artery of rabbits, and then evaluated them up to 6 weeks after implantation. At 6 weeks, the group I vein grafts showed a thinner vein wall than did the adjacent artery during dilatation. In group II, the vein wall thickness and luminal diameter had completely adjusted to that of the adjacent carotid artery. The group III vein grafts showed a significantly thinner vein wall in the absence of dilatation. All supported vein grafts showed regular longitudinally oriented and, in some areas, circularly oriented cell layers, together with thin elastic laminae, which were most pronounced in group II. We conclude that a supporting, compliant prosthesis can stimulate, regulate, and optimize the arterialization of autologous vein grafts in rabbits. If the rate of degradation is carefully chosen, the radius and wall thickness of the vein graft can completely adjust to that of the adjacent artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Autotransfusion of shed blood contributes additionally to blood saving in patients receiving aprotinin (2 million KIU).

Aprotinin decreases the hemoglobin content of shed blood significantly and thereby could potentially reduce the contribution of autotransfusion of shed blood to the blood-saving program. In part 1, by means of a prospective randomized study, we evaluated the effect of autotransfusion (AT) of shed blood on the reduction and avoidance of donor blood requirements in 40 matched patients undergoing internal mammary artery bypass (IMA) surgery and treatment with low-dose aprotinin (2 million KIU). Twenty patients (Group 1) received AT with a hard shell cardiotomy reservoir; twenty patients (Group 2, control) did not receive AT. In part 2, we studied at random the hemoglobin and total-protein content of shed blood in 10 patients of group 2 and in 10 IMA patients not receiving aprotinin. Retransfused patients required 0.1 +/- 0.3 units of donor blood versus 0.8 +/- 0.2 units in non-retransfused patients (not significant). The use of any blood product was avoided in 95% and 80% of the patients, respectively (not significant). Patients receiving aprotinin lost 50% less (P < 0.05) hemoglobin (62 g) and total-protein (28 g) in their drainage system than patients not receiving aprotinin. It was calculated that autotransfusion of about 530 ml of shed blood in aprotinin-treated patients, is equivalent to 0.4 units of homologous packed cells. In conclusion, autotransfusion of shed blood may contribute to blood saving in IMA patients treated with aprotinin, which reduces the shed blood hemoglobin and total protein content by 50%.

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