RESUMO
We compared the intensity of apoptosis in the peri-infarction area of the brain after isolated and combined exposure to hypoxia and hypercapnia prior to focal ischemic stroke modeling. Hypoxia and hypercapnia reduced the number of TUNEL-positive cells in the peri-infarction area, and their combination was most effective in comparison with effects of isolated exposures. The maximum neuroprotective effect of combined exposure to hypoxia and hypercapnia in comparison with isolated exposures was determined by inhibition of apoptosis in the peri-infarction zone.
Assuntos
Apoptose , Isquemia Encefálica/patologia , Hipercapnia/patologia , Hipóxia Encefálica/patologia , Animais , Córtex Cerebral/patologia , Precondicionamento Isquêmico , Masculino , Fatores de Proteção , Ratos WistarRESUMO
We studied the expression of chaperone GRP-78 and transcription factor NF-kB during the development of ischemic tolerance of the brain after combined and isolated exposure to hypoxia and hypercapnia. Combined exposure to hypoxia and hypercapnia maximally increased the expression of chaperone GRP-78 and transcription factor NF-kB, while the formation of ischemia-induced tolerance under conditions of hypercapnic hypoxia can be associated with activation of adaptive stress mechanisms in the endoplasmic reticulum. Under these conditions, hypercapnia in combination with hypoxia is a priority factor for activation of GRP-78 and transcription factor NF-kB.
Assuntos
Hipóxia Celular/fisiologia , Retículo Endoplasmático/metabolismo , Hipercapnia/metabolismo , Acidente Vascular Cerebral/metabolismo , Animais , Hipercapnia/fisiopatologia , Masculino , Neurônios/metabolismo , Neurônios/fisiologia , Ratos , Ratos Wistar , Acidente Vascular Cerebral/fisiopatologiaRESUMO
We studied the role of the role of mitoK+ATp channels and Al-adenosine receptor in the mechanism of increasing the resistance to acute hypoxia after hypoxic, hypercapnic and hypercapnic-hypoxic preconditioning. It is shown that mitochondrial ATP-sensitive potassium channels and Al-adenosine receptors, an important mechanism of preconditioning have a high value to increase the resistance to acute hypoxia/ischemia in the combined effect of hypoxia and hypercapnia. However, with regard to the adenosine receptor, this mechanism is realized without the participation hypercapnic component, which apparently starts neuroprotection without activation of the adenosine Al receptors.
