scholarly journals The report of the clinic use of Ben-10PLUS bubble oxygenator.

1990 ◽  
Vol 16 (2) ◽  
pp. 18-20
Author(s):  
YOSHIFUMI YAMASHITA
Keyword(s):  
1958 ◽  
Vol 36 (1) ◽  
pp. 23-32
Author(s):  
Eduard W. Ferbers ◽  
John W. Kirklin

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).


1978 ◽  
Vol 8 (4) ◽  
pp. 270-281 ◽  
Author(s):  
Tatsuo Tamiya ◽  
Tadashi Nishizawa ◽  
Haruo Horibe ◽  
Kageharu Koja ◽  
Ichiro Suzuki ◽  
...  

1994 ◽  
Vol 26 (4) ◽  
pp. 210-220 ◽  
Author(s):  
Rita Huber ◽  
C. Mennicke ◽  
K.U. Heitmann ◽  
H.J. Helling ◽  
P.M. Huber

1975 ◽  
Vol 181 (5) ◽  
pp. 747-753 ◽  
Author(s):  
JOHN E. LIDDICOAT ◽  
SZABOLCS M. BEKASSY ◽  
ARTHUR C. BEALL ◽  
DONALD H. GLAESER ◽  
MICHAEL E. DEBAKEY
Keyword(s):  

1960 ◽  
Vol 199 (3) ◽  
pp. 485-490 ◽  
Author(s):  
Melvin Landew ◽  
L. Thompson Bowles ◽  
Sol Gelman ◽  
Albert B. Lowenfels ◽  
Ronald Tepper ◽  
...  

By means of a partial extracorporeal bypass, incorporating a bubble counting chamber, measured quantities of oxygen and of air microbubbles, having average diameters of 100 and 76 µ, respectively, were introduced into the carotid arteries of dogs. The desired number of bubbles was produced by varying the blood level and gas flow in the bubble oxygenator. Eighty per cent of dogs receiving oxygen in volumes up to 0.43 cc/kg (approximately 12.5 million microbubbles) survived without evidence of neurologic abnormalities. Seventy per cent of the control group, which received no microbubbles, survived. Of those perfused with air, all animals receiving up to 0.19 cc/kg (9.1 million bubbles) survived with no neurologic sequelae. Those perfused with air volumes greater than 0.19 cc/kg died within 24 hours, many exhibiting evidence of neurologic damage. The emphasis upon the introduction of oxygen microbubbles as the major fault of bubble oxygenators may be unwarranted. Air microbubbles are more deleterious than are oxygen microbubbles.


1979 ◽  
Author(s):  
G.C. Davies ◽  
M. Sobel ◽  
E.W. Salzman

To study thrombin activity and platelet stimulation during interaction of blood with artificial surfaces, we measured circulating FpA (normal up to 2.3 ng/ml) and TxB2 (normal 0.08-0.32 ng/ml) by radioimmunoassay. 31 of 32 patients referred for phlebography for suspected DVT had elevated FpA (mean 49 ng/ml) but normal TxB2. 23 patients had DVT and the others had ruptured Baker’s cyst, muscle tears, hematomas, and inflammatory conditions. FpA rose further after phlebography (mean rise 34.6 ng/ml); similar changes followed arteriography and cardiac catheterization. Heparinization failed to return elevated FpA to normal. None of the procedures affected TxB2 levels.General surgical operations raised FpA but not TxB2. However intra-aortic balloon pumping elevated TxB2 (max. rise 0.44 ng/ml). In 24 of 29 patients undergoing cardiopulmonary bypass using a bubble oxygenator, TxB2 rose over 0.05 ng/ml within the first 120 min. of bypass (mean rise 0.49 ng/ml, max. rise 2.0 ng/ml). The levels detected imply sufficient in-vivo thromboxane A2 production to cause platelet aggregation and myocardial ischemia from coronary artery constriction. FpA levels were elevated even before bypass, probably because of intravascular cannulae, and did not return to normal despite “adequate” heparinization (judged by Activated Clotting Time), implying continued thrombin activity during bypass.


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