scholarly journals Molecular signatures of neurotoxicity in cardiac surgery with cardiopulmonary bypass

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 341-341
Author(s):  
Jose Castillo ◽  
Vicente Ginesta ◽  
Valentin Rodriguez ◽  
Joaquin Serena ◽  
Rogelio Leira ◽  
...  

P12 Background Neurobehavioral disorders, and stroke are frequently reported after cardiac surgery. Although cerebral neuronal damage may be caused by transient or outlasting hypoxia as a consequence of embolism, the underlying mechanisms remain unsettled. Objective: To analyze changes in the biochemical markers of neurotoxicity in 26 patients who underwent CABG (n=14), valve replacement (n=10) or other cardiac surgery (n=2) with cardiopulmonary bypass (CPB). Methods: The surgical protocol recorded the total perfusion time, cross-clamp time, minimum nasopharyngeal temperature and mean arterial pressure (MAP). Canadian stroke scale was evaluated prior surgery, at 24h and 48h after CPB. Blood samples were obtained immediately before surgery, just after surgery, at 6h, and at 24h after CPB. Mean perfusion time was 105±36 min, mean cross-clamp time was 67±27 min, and mean lower temperature was 30.6±1.7°C. MAP was lower than 50 mmHg in 4 patients, and remained between 50 and 90 mmHg in 22. Results: Glutamate concentrations increased four fold, and L-arginine and GABA levels decreased 30%, just after surgery (all p<0.001). Amino acid concentrations returned to normal values at 24h. Glutamate, L-arginine and GABA levels after surgery correlated with the cross-clamp time (r=0.86, r=-0.69, and r=-0.56, respectively) (all p<0.01), but not with the lower body temperature during intervention. Glutamate levels were higher in patients with MAP<50mmHg (p=0.022). The highest glutamate concentration was observed in a patient who developed a cerebral infarct. No significant changes were found in proinflammatory parameters in blood (IL-6, TNF-α, ICAM-1 and VCAM-1). Conclusions: CPB is associated with an important increase of excitatory, and decrease of inhibitory amino acids in the blood. L-arginine consumption might reflect nitric oxide generation. These findings suggest that cerebral excitotoxicity may occur in cardiac surgery. Prophylactic neuroprotection in CPB should be investigated in clinical trials.

Perfusion ◽  
1997 ◽  
Vol 12 (3) ◽  
pp. 171-177 ◽  
Author(s):  
F Gao ◽  
D N F Harris ◽  
S Sapsed-Byrne ◽  
S Sharp

Neurone-specific enolase (NSE) and Sangtec 100 (S-100) are useful for detecting cerebral damage during cardiopulmonary bypass (CPB). However, red cells contain NSE, and the haemolysis frequently caused by CPB could produce a false rise in NSE; S-100 is not found in red cells and should not be affected. We, therefore, compared the effects of haemolysis on NSE and S-100 to see if correction was necessary and possible. From seven patients, serial dilutions of haemolysed red cells were added to plasma (1/64-1/2048), measured for absorption at 540 nm and assayed for NSE and S-100. S-100 concentrations showed no change with haemolysis. Measured NSE increased significantly with haemolysis >1/512 (an increase of 6.6 μg/ml): a correction formula is presented. In 39/48 patients after CPB, mean haemolysis was <1/256 and would not need any correction. NSE and S-100 assay can, therefore, be used throughout CPB, which allows both glial and neuronal damage to be studied.


2021 ◽  
Vol 22 (Supplement 1 3S) ◽  
pp. 183-183
Author(s):  
J.T. Salinas Alanis ◽  
N.C. Arias Pena ◽  
C.D. Hernandez Rosales ◽  
N.E. Guzman Delgado ◽  
M.E. Molina Garza

Perfusion ◽  
2016 ◽  
Vol 32 (4) ◽  
pp. 279-284 ◽  
Author(s):  
Lukas Mach ◽  
Helena Bedanova ◽  
Miroslav Soucek ◽  
Michal Karpisek ◽  
Tomas Konecny ◽  
...  

Background: Cardiac surgery and cardiopulmonary bypass (CPB) have been shown to stimulate a systemic inflammatory response which has been associated with adverse postoperative outcomes. Adipose tissue, both epicardial (EAT) and subcutaneous (SAT), is a known source of inflammatory cytokines, but its role in the pathophysiology of surgery- and CPB-induced systemic inflammatory response has not been fully elucidated. Therefore, we conducted a study to establish levels of selected cytokines in EAT and SAT prior to and after surgery with CPB. Methods: Adipose tissue samples were obtained from patients undergoing planned cardiac surgery on CPB. Samples from EAT and SAT were collected before and immediately after CPB. Levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), adipocyte fatty acid-binding protein (AFABP), leptin and adiponectin were determined by ELISA, which were adjusted for a total concentration of proteins in the individual samples. Results: Samples from 77 patients (mean age 67.68 ± 11.5 years) were obtained and analysed. Leptin, adiponectin, TNF-α and AFABP were shown to decrease their concentrations statistically significantly in the EAT after CPB while no statistically significant drop was observed in the SAT. On the contrary, IL-6 showed only a slight and statistically insignificant decrease in the EAT after CPB and it was in the SAT where a statistically significant drop was observed. Discussion: One of the most relevant findings of this study was the marked decrease in EAT levels of TNF-α, AFABP, leptin and adiponectin after the CPB termination. Our results suggest that EAT might serve as a pool of cytokines which are released into the circulation in reaction to surgery with CPB. Should these novel findings be confirmed, new strategies to assess and possibly reduce EAT contribution on adverse outcomes of cardiac surgery may be developed.


Perfusion ◽  
2001 ◽  
Vol 16 (5) ◽  
pp. 361-370 ◽  
Author(s):  
G Matheis ◽  
M Scholz ◽  
A Simon ◽  
Omer Dzemali ◽  
A Moritz

Leukocyte filtration has evolved as an important technique in cardiac surgery with cardiopulmonary bypass to prevent pathogenic effector functions mediated by activated leukocytes. The underlying mechanisms that result in an improvement of laboratory variables as well as clinical outcome are not resolved yet. Moreover, the optimum strategy for the use of current filtration technology has not been systematically evaluated. This paper, therefore, reviews how activated leukocytes may lead to tissue damage, summarizes the known effects of leukocyte filtration on clinical outcome and laboratory parameters, and deals with current experimental and clinical efforts to further limit the pathogenic effects of leukocytes in cardiac surgery.


1994 ◽  
Vol 72 (04) ◽  
pp. 511-518 ◽  
Author(s):  
Valentine C Menys ◽  
Philip R Belcher ◽  
Mark I M Noble ◽  
Rhys D Evans ◽  
George E Drossos ◽  
...  

SummaryWe determined changes in platelet aggregability following cardiopulmonary bypass, using optical aggregometry to assess macroaggregation in platelet-rich plasma (PRP), and platelet counting to assess microaggregation both in whole blood and PRP. Hirudin was used as the anticoagulant to maintain normocalcaemia.Microaggregation (%, median and interquartile range) in blood stirred with collagen (0.6 µg/ml) was only marginally impaired following bypass (91 [88, 93] at 10 min postbypass v 95 (92, 96] prebypass; n = 22), whereas macroaggregation (amplitude of response; cm) in PRP stirred with collagen (1.0µg/ml) was markedly impaired (9.5 [8.0, 10.8], n = 41 v 13.4 [12.7,14.3], n = 10; p <0.0001). However, in PRP, despite impairment of macroaggregation (9.1 [8.5, 10.1], n = 12), microaggregation was near-maximal (93 [91, 94]), as in whole blood stirred with collagen. In contrast, in aspirin-treated patients (n = 14), both collagen-induced microaggregation in whole blood (49 [47, 52]) and macroaggregation in PRP (5.1 [3.8, 6.6]) were more markedly impaired, compared with control (both p <0.001).Similarly, in PRP, macroaggregation with ristocetin (1.5 mg/ml) was also impaired following bypass (9.4 [7.2, 10.7], n = 38 v 12.4 [10.0, 13.4]; p <0.0002, n = 20), but as found with collagen, despite impairment of macroaggregation (7.2 [3.5,10.9], n = 12), microaggregation was again near-maximal (96 [93,97]). The response to ristocetin was more markedly impared after bypass in succinylated gelatin (Gelo-fusine) treated patients (5.6 [2.8, 8.6], n = 17; p <0.005 v control), whereas the response to collagen was little different (9.3 v 9.5). In contrast to findings with collagen in aspirin-treated patients, the response to ristocetin was little different to that in controls (8.0 v 8.3). Impairment of macroaggregation with collagen or ristocetin did not correlate with the duration of bypass or the platelet count, indicating that haemodilution is not a contributory factor.In conclusion: (1) Macroaggregation in PRP, as determined using optical aggregometry, is specifically impaired following bypass, and this probably reflects impairment of the build-up of small aggregates into larger aggregates. (2) Impairment of aggregate growth and consolidation could contribute to the haemostatic defect following cardiac surgery.


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