S100B protein and neuron-specific enolase as predictors of cognitive dysfunction after coronary artery bypass graft surgery

Silva, Fernando P.; Schmidt, André; Valentin, Lívia Stocco Sanches; Pinto, Kátia Osternack; Zeferino, S; Oses, Jean Pierre; Wiener, Carolina David; Otsuki, Denise Aya; Tort, Adriano Bretanha Lopes; Portela, Luis Valmor; Souza, Diogo O.; Auler, José Otávio Costa; Carmona, Maria José Carvalho

doi:10.1097/eja.0000000000000450

Cited by 55 publications

(40 citation statements)

References 39 publications

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“…In particular, the timescale for the increase in neuroprotein concentrations caused by neuronal damage is much shorter than damage detection by clinical routine imaging technologies. Furthermore, they can be used as predictors of cognitive dysfunction in various clinical contexts [33,34]. In summary, the observed decline in the neuroprotein levels implies a neuroprotective effect of serelaxin [35].…”

Section: Discussionmentioning

confidence: 98%

Altered Cerebral Blood Flow and Potential Neuroprotective Effect of Human Relaxin-2 (Serelaxin) During Hypoxia or Severe Hypovolemia in a Sheep Model

Schiffner

Bischoff

Irintchev

et al. 2020

IJMS

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Specific neuroprotective strategies to minimize cerebral damage caused by severe hypoxia or hypovolemia are lacking. Based on previous studies showing that relaxin-2/serelaxin increases cortical cerebral blood flow, we postulated that serelaxin might provide a neuroprotective effect. Therefore, we tested serelaxin in two emergency models: hypoxia was induced via inhalation of 5% oxygen and 95% nitrogen for 12 min; thereafter, the animals were reoxygenated. Hypovolemia was induced and maintained for 20 min by removal of 50% of the total blood volume; thereafter, the animals were retransfused. In each damage model, the serelaxin group received an intravenous injection of 30 µg/kg of serelaxin in saline, while control animals received saline only. Blood gases, shock index values, heart frequency, blood pressure, and renal blood flow showed almost no significant differences between control and treatment groups in both settings. However, serelaxin significantly blunted the increase of lactate during hypovolemia. Serelaxin treatment resulted in significantly elevated cortical cerebral blood flow (CBF) in both damage models, compared with the respective control groups. Measurements of the neuroproteins S100B and neuron-specific enolase in cerebrospinal fluid revealed a neuroprotective effect of serelaxin treatment in both hypoxic and hypovolemic animals, whereas in control animals, neuroproteins increased during the experiment. Western blotting showed the expression of relaxin receptors and indicated region-specific differences in relaxin receptor-mediated signaling in cortical and subcortical brain arterioles, respectively. Our findings support the hypothesis that serelaxin is a potential neuroprotectant during hypoxia and hypovolemia. Due to its preferential improvement of cortical CBF, serelaxin might reduce cognitive impairments associated with these emergencies.

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Section: Discussionmentioning

confidence: 98%

Altered Cerebral Blood Flow and Potential Neuroprotective Effect of Human Relaxin-2 (Serelaxin) During Hypoxia or Severe Hypovolemia in a Sheep Model

Schiffner

Bischoff

Irintchev

et al. 2020

IJMS

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“…However, these samples are limited [65]. Furthermore, they cannot be continuously assessed [28,37,67], and generally require a substantial amount of money to assess [64]. Thus, no optimal markers have emerged with regards to specificity or predictive value [68].…”

Section: Discussionmentioning

confidence: 99%

Near-Infrared Spectroscopy Monitoring in Cardiac and Noncardiac Surgery: Pairwise and Network Meta-Analyses

Ortega-Loubón

Herrera‐Gómez

Bernuy-Guevara

et al. 2019

JCM

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Goal-directed therapy based on brain-oxygen saturation (bSo2) is controversial and hotly debated. While meta-analyses of aggregated data have shown no clinical benefit for brain near-infrared spectroscopy (NIRS)-based interventions after cardiac surgery, no network meta-analyses involving both major cardiac and noncardiac procedures have yet been undertaken. Randomized controlled trials involving NIRS monitoring in both major cardiac and noncardiac surgery were included. Aggregate-level data summary estimates of critical outcomes (postoperative cognitive decline (POCD)/postoperative delirium (POD), acute kidney injury, cardiovascular events, bleeding/need for transfusion, and postoperative mortality) were obtained. NIRS was only associated with protection against POCD/POD in cardiac surgery patients (pooled odds ratio (OR)/95% confidence interval (CI)/I2/number of studies (n): 0.34/0.14–0.85/75%/7), although a favorable effect was observed in the analysis, including both cardiac and noncardiac procedures. However, the benefit of the use of NIRS monitoring was undetectable in Bayesian network meta-analysis, although maintaining bSo2 > 80% of the baseline appeared to have the most pronounced impact. Evidence was imprecise regarding acute kidney injury, cardiovascular events, bleeding/need for transfusion, and postoperative mortality. There is evidence that brain NIRS-based algorithms are effective in preventing POCD/POD in cardiac surgery, but not in major noncardiac surgery. However, the specific target bSo2 threshold has yet to be determined.

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“…Four of the included studies reported reduced levels of serum NSE in the acupuncture groups [65,67,68,73]. Both S100β and NSE have been proposed to act as predictors of cognitive dysfunction after surgery [74].…”

Section: Reduction Of Neuronal Injurymentioning

confidence: 99%

Application of Acupuncture to Attenuate Immune Responses and Oxidative Stress in Postoperative Cognitive Dysfunction: What Do We Know So Far?

Zhao

Yeung

et al. 2020

Oxidative Medicine and Cellular Longevity

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Postoperative cognitive dysfunction (POCD) is a common sequela following surgery and hospitalization. The prevention and management of POCD are important during clinical practice. POCD more commonly affects elderly patients who have undergone major surgery and can result in major decline in quality of life for both patients and their families. Acupuncture has been suggested as an effective intervention for many neurological disorders. In recent years, there are increasing interest in the use of acupuncture to prevent and treat POCD. In this review, we summarized the clinical and preclinical evidence of acupuncture on POCD using a narrative approach and discussed the potential mechanisms involved. The experimental details and findings of studies were summarized in tables and analyzed. Most of the clinical studies suggested that acupuncture before surgery could reduce the incidence of POCD and reduce the levels of systematic inflammatory markers. However, their reliability is limited by methodological flaws. Animal studies showed that acupuncture reduced cognitive impairment and the associated pathology after various types of surgery. It is possible that acupuncture modulates inflammation, oxidative stress, synaptic changes, and other cellular events to mitigate POCD. In conclusion, acupuncture is a potential intervention for POCD. More clinical studies with good research design are required to confirm its effectiveness. At the same time, findings from animal studies will help reveal the protective mechanisms, in which systematic inflammation is likely to play a major role.

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S100B protein and neuron-specific enolase as predictors of cognitive dysfunction after coronary artery bypass graft surgery

Abstract: NCT01550159.

Cited by 55 publications

References 39 publications

Altered Cerebral Blood Flow and Potential Neuroprotective Effect of Human Relaxin-2 (Serelaxin) During Hypoxia or Severe Hypovolemia in a Sheep Model

Altered Cerebral Blood Flow and Potential Neuroprotective Effect of Human Relaxin-2 (Serelaxin) During Hypoxia or Severe Hypovolemia in a Sheep Model

Near-Infrared Spectroscopy Monitoring in Cardiac and Noncardiac Surgery: Pairwise and Network Meta-Analyses

Application of Acupuncture to Attenuate Immune Responses and Oxidative Stress in Postoperative Cognitive Dysfunction: What Do We Know So Far?

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