title: Reconsideration of total erythrocyte destruction phenomenon.
abstract: During a particular long-term in vitro hemolysis test, the plasma free hemoglobin suddenly increased even though the hemolysis level had risen linearly for the previous several hours. This phenomenon was dubbed the total destruction of erythrocytes (TDE) phenomenon, and it was hypothesized that this was the result of the accumulation of sublethal damage to erythrocytes. It was suggested that the TDE might demonstrate the hemolytic characteristics of a pump more sensitively than a conventional hemolysis test. However, the previous report did not consider the effects of temperature or contamination. To study these effects, 3 long-term hemolysis tests were concluded under the following conditions. For Study 1 blood temperature was maintained at 27 degrees C (n = 2); for Study 2, at 37 degrees C (n = 4); and for Study 3, at 37 degrees C with gentamicin (n = 4). The BioMedicus and Nikkiso pumps were used as they were in our previous report. Gas sterilization of all circuits and pumps preceded experimentation. In Studies 1 and 3, hemolysis increased linearly for 29 h. However, in Study 2 a sudden increase of hemolysis occurred for both pumps. Possible causes of this were the dramatic changes in environmental factors such as severe acidosis, high O2 and glucose consumption, and CO2 accumulation. In contrast, neither Study 1 nor Study 3 showed a sudden increase in hemolysis. The plasma free hemoglobin increased linearly in both groups until 29 h of pumping. The environmental changes resulting from contamination were considered to be the cause of the sudden increase in hemolysis. In conclusion, the TDE did not reflect mechanical blood cell damage, but rather different environment situations. Hemolysis increased linearly up to 29 h in either 27 degrees C or germ-free conditions.
authors.affiliation: Department of Surgery, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: E
authors.initials: E
authors.lastname: Tayama
authors.forename: T
authors.initials: T
authors.lastname: Shimono
authors.forename: K
authors.initials: K
authors.lastname: Makinouchi
authors.forename: S
authors.initials: S
authors.lastname: Ohtsubo
authors.forename: T
authors.initials: T
authors.lastname: Nakazawa
authors.forename: Y
authors.initials: Y
authors.lastname: Takami
authors.forename: Y
authors.initials: Y
authors.lastname: Niimi
authors.forename: J
authors.initials: J
authors.lastname: Glueck
authors.forename: Y
authors.initials: Y
authors.lastname: Nosé
mesh_terms: D000818:Animals; D001806:Blood Urea Nitrogen; D002245:Carbon Dioxide / Q000009:adverse effects; D002417:Cattle; D004866:Equipment Contamination; D004912:Erythrocytes / Q000166:cytology / Q000473:pathology*; D005027:Ethylene Oxide / Q000737:chemistry; D005839:Gentamicins / Q000009:adverse effects; D005947:Glucose / Q000009:adverse effects; D006353:Heart-Assist Devices / Q000009:adverse effects* / Q000592:standards; D006454:Hemoglobins / Q000378:metabolism; D006461:Hemolysis; D006863:Hydrogen-Ion Concentration; D009994:Osmolar Concentration; D010101:Oxygen Consumption / Q000502:physiology; D010313:Partial Pressure; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood; D013242:Sterilization / Q000592:standards; D013696:Temperature
chemical_list: D005839:Gentamicins; D006454:Hemoglobins; D002245:Carbon Dioxide; D012964:Sodium; D005947:Glucose; D005027:Ethylene Oxide; D011188:Potassium