Loss of anticoagulant effect of heparin during circulation of human blood in vitro.
Device-induced thrombogenesis was studied in an in vitro model using human blood circulated through an artificial ventricle. A new constant pressure filtration technique was used to detect circulating microemboli, the activated partial thromboplastin time (APTT) test was used to monitor the blood for the presence of anticoagulant activity of heparin, and hemolysis was quantified by measuring the plasma free hemoglobin level. Circulation of blood through a 20-ml stroke volume pneumatically driven ventricle for 6-9 h resulted in a significant reduction of APTT, indicating the loss of the anticoagulant effect of heparin. Microemboli concentration was minimal until the APTT decreased below 125 s, at which time the microemboli concentration increased rapidly. This was presumed to be due to the formation of thrombi following a decrease in heparin activity. A significant increase in hemolysis was also noted when blood was pumped. None of these changes was noted in the nonpumped control blood. Spontaneous loss of heparin activity in blood circulated by a pneumatically driven pump may have clinical implications and may help understanding of the problems associated with device-induced thrombogenesis.
Pijl
A J
AJ
Artificial Heart Research Laboratory, University of Utah, Salt Lake City 84103.
Solen
K A
KA
Mohammad
S F
SF
Monson
R
R
Yu
L S
LS
van Griensven
J M
JM
Olsen
D B
DB
Kolff
W J
WJ
D000328:Adult; D001775:Blood Circulation / Q000502:physiology*; D001777:Blood Coagulation; D001792:Blood Platelets; D004617:Embolism / Q000097:blood; D006353:Heart-Assist Devices; D006493:Heparin / Q000097:blood*; D006801:Humans; D008297:Male; D010314:Partial Thromboplastin Time
D006493:Heparin