The transition from the bubble oxygenator to the microporous membrane oxygenator

Perfusion ◽  
2003 ◽  
Vol 18 (3) ◽  
pp. 179-183 ◽  
Author(s):  
Ronald J Leonard
Blood ◽  
1987 ◽  
Vol 69 (1) ◽  
pp. 324-330 ◽  
Author(s):  
YT Wachtfogel ◽  
U Kucich ◽  
J Greenplate ◽  
P Gluszko ◽  
W Abrams ◽  
...  

Abstract Cardiopulmonary bypass, especially when prolonged, may result in hemostatic failure and pulmonary dysfunction, which has been attributed to changes in platelets and leukocytes, respectively. It has been well documented that contact of blood with synthetic surfaces causes platelet activation. In this report, we explore mechanisms of the activation of neutrophils during simulated in vitro extracorporeal circulation and document the release of neutrophil lactoferrin and elastase during clinical cardiopulmonary bypass (CCB). Inhibition in the simulated circuit by prostaglandin E1 (PGE1) and lidocaine suggests different mechanisms for release of neutrophil-specific proteins. During CCB with a bubble oxygenator it was observed that platelet counts fell to 42% +/- 2% of baseline. In addition, beta- thromboglobulin antigen (beta TG), a platelet-specific, alpha-granule protein marker reflecting the release reaction, increased from 0.15 +/- 0.05 to 0.84 +/- 0.11 microgram/mL. Neutrophil counts decreased to 67% +/- 7% of prebypass levels but then gradually rose as bypass continued. Both lactoferrin, a neutrophil-specific granule marker, and neutrophil elastase, an azurophilic granule marker, increased in plasma threefold to 1.66 +/- 0.33 micrograms/mL and 1.65 +/- 0.68 microgram/mL, respectively, just before bypass was stopped. When fresh heparinized human blood was recirculated within an extracorporeal membrane oxygenator bypass circuit for 120 minutes, plasma beta-TG rose to 5.13 micrograms/mL, lactoferrin increased from 0.13 +/- 0.04 to 1.62 +/- 0.22 micrograms/mL, and neutrophil elastase rose from 0.05 +/- 0.02 to 1.86 +/- 0.41 micrograms/mL. At 120 minutes, lidocaine (100 mumol/L), which inhibits neutrophil activation, delayed release of lactoferrin (1.33 +/- 0.26 micrograms/mL) and markedly inhibited release of elastase (0.24 +/- 0.05 microgram/mL) but did not inhibit release of beta-TG antigen (5.66 micrograms/mL at 120 minutes). PGE1 (0.3 mumol/L) inhibited significantly the release of beta-TG (0.31 microgram/mL) and elastase (0.52 +/- 0.11 microgram/mL) and attenuated the release of lactoferrin (1.57 +/- 0.45 micrograms/mL).


1977 ◽  
Vol 185 (4) ◽  
pp. 397-401 ◽  
Author(s):  
K. E. KARLSON ◽  
R. J. MASSIMINO ◽  
G. N. COOPER ◽  
A. K. SINGH ◽  
L. L. VARGAS

1986 ◽  
Vol 41 (3) ◽  
pp. 297-300 ◽  
Author(s):  
P.W. Boonstra ◽  
F.E.E. Vermeulen ◽  
J.A. Leusink ◽  
E.H. de Nooy ◽  
A. van Zalk ◽  
...  

Perfusion ◽  
1987 ◽  
Vol 2 (4) ◽  
pp. 289-295 ◽  
Author(s):  
Ludwig von Segesser

Ten mongrel dogs were connected to cardiopulmonary bypass by cavoaortic cannulation, classic roller pump and either Bentley BOS-CM 40 hollow fibre membrane oxygenator or Polystan VT5000 Venotherm bubble oxygenator for eight hours, with mean flow rate of 100 ml/kg min. Platelet counts (all values corrected by prebypass haematocrit) were significantly lower in the bubble oxygenator group after two hours of cardiopulmonary bypass (p < 0·01). Plasma haemoglobin production was significantly higher after two hours of cardiopulmonary bypass in the bubble oxygenator group (p < 0·01). Venous oxygen saturation (SvO2) was above 65% during the eight hours perfusion in the membrane oxygenator group. In the bubble oxygenator group, however, SvO2 was below 60% after six hours of cardiopulmonary bypass. After eight hours perfusion the difference in SvO2 between the two groups was significant (p < 0·05). Thus membrane oxygenators such as the Bentley BOS-CM 40 appear to be indicated in cardiopulmonary bypass of more than two hours duration.


Perfusion ◽  
1987 ◽  
Vol 2 (1) ◽  
pp. 27-33 ◽  
Author(s):  
PW Boonstra ◽  
Fee Vermeulen ◽  
JA Leusink ◽  
EH de Nooy ◽  
A. van Zalk ◽  
...  

We determined to what extent a 27 micron depth filter (Bentley Polyfilter bypass blood filter PF427, Bentley Lab., Irvine, California, USA) in the arterial line of a bubble oxygenator (BO) system is responsible for the difference in haemocompatibility between this BO system and a membrane oxygenator (MO) system in which no arterial line filter is used. We studied three groups of patients subjected to long perfusions of approximately three hours: BO perfusion with ( n = 8) and without ( n = 8) the arterial line filter and MO perfusion ( n = 10) without filter. Platelet and erythrocyte damage were evaluated at seven sampling points during perfusion. Also pre- and postoperative bleeding times and postoperative blood loss and blood transfusions up to 18 hours after perfusion were determined. We found that the 27 micron depth filter in the arterial line impairs the haemocompatibility of the BO only to a small extent; the MO remains haematologically superior over the BO even when the arterial line filter is absent from the BO circuit.


2008 ◽  
Vol 15 (1) ◽  
pp. 15-22 ◽  
Author(s):  
Yehuda Tamari ◽  
Anthony J. Tortolani ◽  
Melanie Maquine ◽  
Kerri Lee-Sensiba ◽  
John Guarino

Perfusion ◽  
1989 ◽  
Vol 4 (1) ◽  
pp. 9-24 ◽  
Author(s):  
D.T. Pearson ◽  
B. McArdle

During clinical hypothermic cardiopulmonary bypass (CPB), the haemocompatibility of six groups of membrane oxygenators (Cobe CML2, Shiley M2000, Maxima, Bard HF4000, Bard HF5000, Capiox E has been studied in 60 patients having open-heart surgery. A standardized anaesthetic and perfusion protocol was used, during which the abilityof the perfusionist to achieve target blood gas values (PaO2 20kPa and PaCO2 5.3kPa: alpha-stat) using inline electrodes was assessed. Haemocompatibility was evaluated by measurement of platelet numbers and function, betathromboglobulin (BTG), plasma haemoglobin, complement (C3a des Arg) and white blood cell (WBC) count pre- and post-CPB. Platelet and WBC numbers were also measured every five minutes throughout CPB. All oxygenators allowed the perfusionist to control blood gases adequately to prescribed levels. There were only minor differences in the degree and pattern of platelet depletion, reduction in platelet aggregation, elevation of BTG and C3a des Arg observed between oxygenator groups, which did not appear to be influenced by membrane type (flat plate versus hollow fibre). The membrane oxygenator haematological data was amalgamated with that obtained in previous clinical studies using membrane and bubble oxygenators (Cobe CML, Polystan Venotherm, Harvey H 1700, Bentley BIO-10, Bentley 1 0B, Bentley 1 OPlus, Gambro 10 and Shiley S100A HED) in which a similar evaluation protocol was employed. Comparison of the percentage change in platelet count when the pre- and post-CPB values were compared, demonstrated statistically significantly less platelet depletion (p <0.001 ) in the membrane oxygenator groups (-0.2 ± 8.3%) when compared to the bubble oxygenator groups (-21.7 ± 8.7%). A significantly lower percentage rise in BTG was also observed in the membrane oxygenator group when compared to the bubble oxygenator groups (p <0.001 ). All oxygenator groups showed elevation of both WBC count and plasma haemoglobin with a nonspecific fall in platelet aggregation over the period of bypass but no significant differences could be found between the two types of oxygenator. Membrane oxygenators, when compared to bubble oxygenators, exhibit lower GME production and improved haemocompatibility and allow superior blood gas control. Membrane oxygenators manifestly must be the oxygenator type of choice for clinical CPB.


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