Red blood cell damage during experimental prolonged perfusion with membrane oxygenation using fresh human blood
Identifieur interne : 002E40 ( Main/Merge ); précédent : 002E39; suivant : 002E41Red blood cell damage during experimental prolonged perfusion with membrane oxygenation using fresh human blood
Auteurs : P. Bergman ; G. Friberg ; B. Liu ; N. Al-Khaja ; A. Belboul ; G. Mellgren ; D. RobertsSource :
- Perfusion [ 0267-6591 ] ; 1993-05.
English descriptors
- Teeft :
- Artif intern organs, Bladder reservoir, Blood cell, Blood cell damage, Blood cells, Blood gases, Blood rheology, Blood trauma, Cardiopulmonary, Cardiovasc, Cardiovascular surgery, Cell deformability, Cell filtration rate, Cell morphology, Cell rheology, Cell suspension, Cell suspension fluid, Continuous loss, Corpuscular volume, Deformability, Distress syndrome, Ecmo, Extracorporeal, Extracorporeal circulation, Extracorporeal membrane oxygenation, Filtration, Important factor, Mechanical trauma, Membrane oxygenation, Membrane oxygenator, Normal levels, Organ dysfunction, Oxygenation, Perfusion, Plusmn, Pore, Postoperative thrombosis, Ppmo, Reference value, Rheological, Rheological parameters, Rheology, Sahlgrenska sjukhuset, Surg, Thorac, Thorac cardiovasc surg, Tissue oxygenation, Total haemoglobin, Trauma, Travenol reservoir, White cells, Whole blood.
Abstract
The effects of prolonged perfusion of oxygenated blood have previously been studied with respect to haemolysis and cell morphology. The aim of this study was to examine the effect of mechanical trauma on the microrheology of red blood cells during experimental prolonged perfusion with membrane oxygenation (PPMO). Red blood cell damage was assessed by blood rheological parameters using a St George's filtrometer. Red blood cell filtration rate (RFR, μl/s), clogging rate (RBC-CR, 102%/ml), clogging particle (RBC-CP, 106/ml), mean corpuscular volume (MCV) and haematocrit (Hct) were analysed at the start of PPMO and after 24, 48 and 72 hours. RFR values were 81.3 ± 3.7 at the start, 79.2 ± 7.6 (24 h, p < 0.01), 42.3 ± 8.4 (48 h, p < 0.001) and 25.1 ± 7.0 (72 h, p < 0.001). The mean RBC-CR was 2.45 ± 0.53 at the start; this increased to 3.58 ± 0.9, 6.62 ± 0.92 and then reduced to 4.77 ± 1.39 at 24 (p < 0.0001), 48 (p < 0.0001) and 72 (p < 0.02) hours respectively. Mean RBC-CP at the start was 3.29 ± 0.55; this increased to 3.42 ± 0.72, 5.29 ± 0.68 and 6.09 ± 1.07 at 24, 48 and 72 hours respectively (NS at 24 h and 48 h, p < 0.04 at 72 h). The mean MCV (fl) at the start was 86 ± 4; this increased to 101 ± 2, 111 ± 4 and 119 ± 4 at 24, 48 and 72 hours respectively (p < 0.001). Mean Hct (%) at the start was 33 ± 2; this increased to 38 ± 2, 38 ± 2 and 48 ± 2 at 24, 48 and 72 hours respectively (p < 0.05 at 24 and 48 hours, p < 0.001 at 72 hours). The mean pH and CO 2 (kPa.s) levels were 7.38 ± 0.04 and 4.1 ± 0.7 respectively. This study suggested that there was a continuous loss of red cell rheology during PPMO, which could lead to disturbed microcirculation, thereby increasing the risk of organ ischaemia, hypoxia, dysfunction and failure.
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DOI: 10.1177/026765919300800305
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Belboul</name></author><author wicri:is="90%"><name sortKey="Mellgren, G" sort="Mellgren, G" uniqKey="Mellgren G" first="G." last="Mellgren">G. Mellgren</name></author><author wicri:is="90%"><name sortKey="Roberts, D" sort="Roberts, D" uniqKey="Roberts D" first="D." last="Roberts">D. 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Bergman</name><affiliation><wicri:noCountry code="subField">Gothenburg</wicri:noCountry></affiliation></author><author wicri:is="90%"><name sortKey="Friberg, G" sort="Friberg, G" uniqKey="Friberg G" first="G." last="Friberg">G. Friberg</name><affiliation><wicri:noCountry code="subField">Gothenburg</wicri:noCountry></affiliation></author><author wicri:is="90%"><name sortKey="Liu, B" sort="Liu, B" uniqKey="Liu B" first="B." last="Liu">B. Liu</name><affiliation><wicri:noCountry code="subField">Gothenburg</wicri:noCountry></affiliation></author><author wicri:is="90%"><name sortKey="Al Khaja, N" sort="Al Khaja, N" uniqKey="Al Khaja N" first="N." last="Al-Khaja">N. Al-Khaja</name><affiliation><wicri:noCountry code="subField">Gothenburg</wicri:noCountry></affiliation></author><author wicri:is="90%"><name sortKey="Belboul, A" sort="Belboul, A" uniqKey="Belboul A" first="A." last="Belboul">A. Belboul</name><affiliation><wicri:noCountry code="subField">Gothenburg</wicri:noCountry></affiliation></author><author wicri:is="90%"><name sortKey="Mellgren, G" sort="Mellgren, G" uniqKey="Mellgren G" first="G." last="Mellgren">G. Mellgren</name><affiliation><wicri:noCountry code="subField">Gothenburg</wicri:noCountry></affiliation></author><author wicri:is="90%"><name sortKey="Roberts, D" sort="Roberts, D" uniqKey="Roberts D" first="D." last="Roberts">D. Roberts</name><affiliation><wicri:noCountry code="subField">Gothenburg</wicri:noCountry></affiliation></author></analytic><monogr></monogr><series><title level="j">Perfusion</title><idno type="ISSN">0267-6591</idno><idno type="eISSN">1477-111X</idno><imprint><publisher>Sage Publications</publisher><pubPlace>Sage CA: Thousand Oaks, CA</pubPlace><date type="published" when="1993-05">1993-05</date><biblScope unit="volume">8</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="225">225</biblScope><biblScope unit="page" to="232">232</biblScope></imprint><idno type="ISSN">0267-6591</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0267-6591</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Artif intern organs</term><term>Bladder reservoir</term><term>Blood cell</term><term>Blood cell damage</term><term>Blood cells</term><term>Blood gases</term><term>Blood rheology</term><term>Blood trauma</term><term>Cardiopulmonary</term><term>Cardiovasc</term><term>Cardiovascular surgery</term><term>Cell deformability</term><term>Cell filtration rate</term><term>Cell morphology</term><term>Cell rheology</term><term>Cell suspension</term><term>Cell suspension fluid</term><term>Continuous loss</term><term>Corpuscular volume</term><term>Deformability</term><term>Distress syndrome</term><term>Ecmo</term><term>Extracorporeal</term><term>Extracorporeal circulation</term><term>Extracorporeal membrane oxygenation</term><term>Filtration</term><term>Important factor</term><term>Mechanical trauma</term><term>Membrane oxygenation</term><term>Membrane oxygenator</term><term>Normal levels</term><term>Organ dysfunction</term><term>Oxygenation</term><term>Perfusion</term><term>Plusmn</term><term>Pore</term><term>Postoperative thrombosis</term><term>Ppmo</term><term>Reference value</term><term>Rheological</term><term>Rheological parameters</term><term>Rheology</term><term>Sahlgrenska sjukhuset</term><term>Surg</term><term>Thorac</term><term>Thorac cardiovasc surg</term><term>Tissue oxygenation</term><term>Total haemoglobin</term><term>Trauma</term><term>Travenol reservoir</term><term>White cells</term><term>Whole blood</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The effects of prolonged perfusion of oxygenated blood have previously been studied with respect to haemolysis and cell morphology. The aim of this study was to examine the effect of mechanical trauma on the microrheology of red blood cells during experimental prolonged perfusion with membrane oxygenation (PPMO). Red blood cell damage was assessed by blood rheological parameters using a St George's filtrometer. Red blood cell filtration rate (RFR, μl/s), clogging rate (RBC-CR, 102%/ml), clogging particle (RBC-CP, 106/ml), mean corpuscular volume (MCV) and haematocrit (Hct) were analysed at the start of PPMO and after 24, 48 and 72 hours. RFR values were 81.3 ± 3.7 at the start, 79.2 ± 7.6 (24 h, p < 0.01), 42.3 ± 8.4 (48 h, p < 0.001) and 25.1 ± 7.0 (72 h, p < 0.001). The mean RBC-CR was 2.45 ± 0.53 at the start; this increased to 3.58 ± 0.9, 6.62 ± 0.92 and then reduced to 4.77 ± 1.39 at 24 (p < 0.0001), 48 (p < 0.0001) and 72 (p < 0.02) hours respectively. Mean RBC-CP at the start was 3.29 ± 0.55; this increased to 3.42 ± 0.72, 5.29 ± 0.68 and 6.09 ± 1.07 at 24, 48 and 72 hours respectively (NS at 24 h and 48 h, p < 0.04 at 72 h). The mean MCV (fl) at the start was 86 ± 4; this increased to 101 ± 2, 111 ± 4 and 119 ± 4 at 24, 48 and 72 hours respectively (p < 0.001). Mean Hct (%) at the start was 33 ± 2; this increased to 38 ± 2, 38 ± 2 and 48 ± 2 at 24, 48 and 72 hours respectively (p < 0.05 at 24 and 48 hours, p < 0.001 at 72 hours). The mean pH and CO 2 (kPa.s) levels were 7.38 ± 0.04 and 4.1 ± 0.7 respectively. This study suggested that there was a continuous loss of red cell rheology during PPMO, which could lead to disturbed microcirculation, thereby increasing the risk of organ ischaemia, hypoxia, dysfunction and failure.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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