The relationship between neurocognitive decline and the heart‐lung machine

Tamargo, Christina; Botros, Mousa; Saveanu, Radu V.

doi:10.1111/jocs.14505

Cited by 2 publications

(2 citation statements)

References 59 publications

(110 reference statements)

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“…In the long term, it reduces the quality of life and even increases the long-term mortality rate. During CPB, low perfusion or mean arterial pressure, unstable hemodynamics, cerebral thrombosis, systemic inflammatory response, anemia, hyperglycemia, and CBP trauma of CPB lead to neurocognitive decline after operation [ 13 ]. In the present study, the CPB rat model was established and treated with a KOR agonist, and its impacts on cognitive function, inflammatory response, oxidative stress injury and cell apoptosis were investigated.…”

Section: Discussionmentioning

confidence: 99%

κ-Opioid Receptor Agonist Ameliorates Postoperative Neurocognitive Disorder by Activating the Ca2+/CaMKII/CREB Pathway

Ding

Sun

et al. 2021

Journal of Healthcare Engineering

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Objective. Cardiopulmonary bypass (CPB) is an important cardiac operation and also a high-risk procedure, leading to postoperative neurocognitive disorder. However, there are few effective drugs to treat the aftermath of CPB. Therefore, we observe the effect of kappa opioid receptor (KOR) agonist on cognitive disorders of rats after cardiopulmonary bypass (CPB) and investigate the mechanism of the Ca2+/calmodulin-dependent protein kinase (CaMKII)/cAMP responsive element-binding protein (CREB) pathway. Methods. A total of 40 Sprague Dawley rats were randomly divided into the sham operation group (sham group, n = 10), CPB model group (CPB group, n = 10), CPB + KOR agonist U50488H group (UH group, n = 10), and CPB + specific CaMKII antagonist + U50488H group (CKU group, n = 10). The changes in the rats’ cognitive function were evaluated using the Morris water maze, the hippocampal histopathological changes were observed via hematoxylin-eosin (H&E) staining, and the apoptosis rate of neuronal cells was detected through terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. Moreover, enzyme-linked immunosorbent assay (ELISA) was applied to examine the changes in brain injury markers, inflammatory factors, and oxidative stress factors. The hippocampal variations in Ca2+ concentration and oxidative stress index (ROS) levels were measured by immunofluorescence staining, and western blotting was performed to determine the expression changes in the Ca2+/CaMKII/CREB pathway. Results. The KOR agonist could shorten latency, increase the swimming distance and residence time in the target quadrant, and ameliorate postoperative neurocognitive disorder (PND). Meanwhile, the KOR agonist relieved CPB-induced hippocampal and oxidative stress injuries, reduced NSE and S-100β expression, decreased the apoptosis rate, and repressed the inflammatory response, which alleviated the brain injury. In addition, U50488H was able to decrease Ca2+ influx and glutamate (Glu) level, inhibit N-methyl-D-aspartate receptor (NMDAR) expression, upregulate CaMKII expression, promote CREB phosphorylation, and increase the brain-derived neurotrophic factor (BDNF) level in CPB rats. However, the protective effects of KORs against PND were suppressed following the application of the CaMKII-specific antagonist. Conclusion. The KOR agonist activates the Ca2+/CaMKII/CREB pathway, which improves the brain injury and relieves PND in CPB rats.

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Section: Discussionmentioning

confidence: 99%

κ-Opioid Receptor Agonist Ameliorates Postoperative Neurocognitive Disorder by Activating the Ca2+/CaMKII/CREB Pathway

Ding

Sun

et al. 2021

Journal of Healthcare Engineering

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“…Other adverse effects are atrial fibrillation, pulmonary damage including edema and ischemia, renal failure, and neurocognitive deficits. While some of these are not common effects, research has shown that they certainly are possible and harmful (Steidl, 2011;Tamargo et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Heart Failure with Reduced Ejection Fraction, Multiple-Valve Diseases, And Left Atrial Thrombus: A Case Report of Determining Whether to Do Intervention Strategies or Conservative Medical Therapies Only

M.R.D.¹,

Andrianto²,

Subagjo³

2021

IJRP

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Structural valvular heart disease (VHD) may be the cause of heart failure or may worsen the clinical status of patients with heart failure. Heart failure patients with VHD are at increased risk of events including sudden cardiac death. Before considering intervention (surgical or percutaneous) all patients should receive appropriate medical therapy. Numerous percutaneous and/or hybrid procedures have been introduced in the past few years and they are changing the management of VHD. In patients with heart failure and valvular heart disease, either primary or functional, the whole process of decision-making should be staged through a comprehensive evaluation of the risk-benefit ratio of different treatment strategies. In this case, a heart failure patient with multiple-valve diseases, LA thrombus, and dilated cardiomyopathy was referred to a faraway cardiac center to undergo intervention procedures. This is a case report of a 59-yo female who presented to the emergency ward, she was referred with the diagnosis of Chronic Heart Failure due to multiple-valve diseases, atrial fibrillation, hypo-potassium, and low blood pressure. From echocardiography, we found severe mitral stenosis, severe aortic stenosis, moderate aortic insufficiency, moderate tricuspid stenosis, severe tricuspid insufficiency, mild pulmonic insufficiency, with left atrial thrombus, and dilated cardiomyopathy. However, after the evaluation was made and had a discussion with the patient about the risk-benefit of intervention procedures, the patient chose to not undergoing the intervention procedures even though there was no contraindication found in the patients to the procedures that should be done to the patient.

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The relationship between neurocognitive decline and the heart‐lung machine

Cited by 2 publications

References 59 publications

κ-Opioid Receptor Agonist Ameliorates Postoperative Neurocognitive Disorder by Activating the Ca2+/CaMKII/CREB Pathway

κ-Opioid Receptor Agonist Ameliorates Postoperative Neurocognitive Disorder by Activating the Ca2+/CaMKII/CREB Pathway

Heart Failure with Reduced Ejection Fraction, Multiple-Valve Diseases, And Left Atrial Thrombus: A Case Report of Determining Whether to Do Intervention Strategies or Conservative Medical Therapies Only

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