Hypothesis related to the regulation of inducible nitric oxide synthase during carotid endarterectomy
| Autor: | Nikola Bogdanovic, Dragana Unic-Stojanovic, Julijana Stanimirovic, Miljana Obradović, Djordje Radak, Esma R. Isenovic |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Free Radicals Cell Survival medicine.medical_treatment Ischemia Hemodynamics Nitric Oxide Synthase Type II Pilot Projects Carotid endarterectomy Nitric Oxide Antioxidants Nitric oxide Brain Ischemia Brain ischemia 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Internal medicine medicine Homeostasis Humans Lymphocytes cardiovascular diseases Thrombus Inducible nitric oxide synthase Inflammation Neurons Endarterectomy Carotid biology business.industry General Medicine Models Theoretical medicine.disease 3. Good health Nitric oxide synthase Stroke 030104 developmental biology chemistry Reperfusion Cardiology biology.protein Stress Mechanical business 030217 neurology & neurosurgery Signal Transduction |
| Zdroj: | Medical Hypotheses |
| Popis: | Sudden occlusion of an artery caused by a thrombus or emboli is the most frequent cause of acute brain ischemia (ABI). Carotid endarterectomy (CEA) represents the gold standard for preventing strokes of carotid origin. However, neuronal damage caused by ischemia and/or reperfusion may contribute to a poor clinical outcome after CEA. In response to shear stress caused by hypoxic-ischemic conditions in patients undergoing CEA, stimulation of the hypothalamic-pituitaryadrenal axis leads to biological responses known as hypermetabolic stress, characterized by hemodynamic, metabolic, inflammatory and immunological changes. These changes maintain homeostasis and assist recovery, but an unregulated inflammatory response could lead to further tissue damage and death of neurons. Nitric oxide (NO) is an important signaling molecule involved in several physiological and pathological processes, including ABI. However, an excess of NO could have detrimental effects. We hypothesized that the hypoxic-ischemic state induced by carotid clamping leads to overexpression of inducible NO synthase and that uncontrolled production of NO could adversely affect outcome after CEA. © 2018 Elsevier Ltd |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|