Cerebral tumor necrosis factor alpha expression and long-term neurocognitive performance after cardiopulmonary bypass in rats.
OBJECTIVE
Cerebral inflammatory reaction is discussed as a contributor to adverse cerebral outcome after cardiac surgery with cardiopulmonary bypass. This study was designed to determine the effect of cardiopulmonary bypass on both cerebral expression of tumor necrosis factor alpha and neurocognitive outcome in rats.


METHODS
With institutional review board approval, 50 rats were randomly assigned to one of 3 groups: rats of the cardiopulmonary bypass group were subjected to 75 minutes of normothermic cardiopulmonary bypass. Sham-operated animals underwent identical preparation but were not connected to cardiopulmonary bypass, whereas rats of the control group were neither anesthetized nor cannulated. Ten rats per group survived 4 hours after cardiopulmonary bypass or the sham operation for immediate postoperative determination of tumor necrosis factor alpha-expressing cells (immunohistochemistry) and cerebral tumor necrosis factor alpha mRNA levels (polymerase chain reaction). The remaining animals survived 10 days for neurocognitive assessment by using the modified hole-board test and for analysis of cerebral tumor necrosis factor alpha activation in the late postoperative period.


RESULTS
Expression of tumor necrosis factor alpha mRNA was increased 4 hours after cardiopulmonary bypass and the sham operation, with higher expression in the cardiopulmonary bypass group (chi(2) [2] = 25.08, P < .001). Both experimental groups demonstrated larger numbers of tumor necrosis factor alpha-positive cells in the early and late postoperative periods (F [1] = 13.08, P < or = .001) and an impaired neurocognitive performance on the first postoperative days compared with that seen in the control group (F [2, 24] = 4.26, P = .02).


CONCLUSIONS
Cerebral tumor necrosis factor alpha activation in both experimental groups during the early postoperative period was accompanied by transient neurocognitive impairment. Therefore cardiopulmonary bypass alone demonstrated no effect on cerebral inflammation and neurocognitive outcome.
Jungwirth
Bettina
B
Klinik für Anaesthesiologie, Technische Universität München, Klinikum rechts der Isar, München, Germany. b.jungwirth@lrz.tum.de
Kellermann
Kristine
K
Qing
Ma
M
Mackensen
G Burkhard
GB
Blobner
Manfred
M
Kochs
Eberhard F
EF
D000818:Animals; D001522:Behavior, Animal; D001921:Brain / Q000378:metabolism*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D007150:Immunohistochemistry; D008297:Male; D008568:Memory; D011597:Psychomotor Performance; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D014409:Tumor Necrosis Factor-alpha