RESUMO
Decreased cerebral blood flow (CBF) leads to impaired cerebral hemodynamics, which causes an increased risk of stroke. Revascularization has been shown to improve CBF in patients with moyamoya disease. The study is devoted to the retrospective study of clinical features and cerebral hemodynamic characteristics of 17 patients with moyamoya disease before, during and after surgical treatment using extracranial-intracranial (EC-IC) bypass by STA-MCA type. Patients underwent superficial temporal artery-middle cerebral artery bypass surgeries. All patients were carried out by DSA, MSCT-angiography, and MSCT-perfusion imagine (MSCTPI) before and 6 months after surgery. The hemodynamic parameters during MSCTPI, changes in cerebral vascular pattern, and clinical outcomes were evaluated. Cerebral blood flow and mean transit time (MTT) were measured using MSCT-perfusion imaging to identify areas of hypoperfusion. Intraoperative indocyanine green (ICG) analysis was performed to assess local cerebral hemodynamics before and after the creation of the STA-MCA bypass. Results showed that hemodynamics improved significantly on the surgery side after revascularization. After STA-MCA bypass CBF increased and MTT reduced by almost 2 times compared to the level before the bypass. The modified Rankin Scale scores demonstrated an improvement in the neurological status of patients following surgical revascularization. Thus, STA-MCA-type surgical revascularization significantly improved cerebral perfusion parameters and reduced the risk of stroke in patients with moyamoya disease. MSCTPI can serve as an effective and noninvasive method for monitoring cerebral hemodynamics in these patients. Intraoperative ICG angiography is a safe method that can display hemodynamic characteristics in the surgical area.
Assuntos
Revascularização Cerebral , Circulação Cerebrovascular , Hemodinâmica , Doença de Moyamoya , Acidente Vascular Cerebral , Humanos , Doença de Moyamoya/cirurgia , Doença de Moyamoya/diagnóstico por imagem , Doença de Moyamoya/fisiopatologia , Feminino , Masculino , Revascularização Cerebral/métodos , Circulação Cerebrovascular/fisiologia , Adulto , Acidente Vascular Cerebral/cirurgia , Acidente Vascular Cerebral/etiologia , Acidente Vascular Cerebral/fisiopatologia , Pessoa de Meia-Idade , Estudos Retrospectivos , Artéria Cerebral Média/cirurgia , Artéria Cerebral Média/diagnóstico por imagem , Artéria Cerebral Média/fisiopatologia , Adolescente , Adulto Jovem , Artérias Temporais/cirurgia , Artérias Temporais/diagnóstico por imagem , Angiografia Cerebral , Resultado do TratamentoRESUMO
The system insulin-like growth factors (IGF) occupies an important place in the development and growth of the central nervous system (CNS). Gene expression of insulin-like growth factor I (IGF-1) and IGF-1 receptor are represented in all parts of the brain and are heavily concentrated in the cerebral vessels. IGF-1 is involved in neuro-, angiogenesis, in the stimulation of cell proliferation, and repair responses to damage for both the central and peripheral nervous system. IGF- 1 exerts antioxidant, anti-inflammatory and protective effects on the CNS. The review discusses the importance and the role of IGF-I in vascular diseases of the brain, in particular, aneurysms, the ischemic stroke, the aneurysmal subarachnoid hemorrhage, as well as neuroprotection.
Assuntos
Aneurisma/metabolismo , Isquemia Encefálica/metabolismo , Fator de Crescimento Insulin-Like I/genética , Acidente Vascular Cerebral/metabolismo , Hemorragia Subaracnóidea/metabolismo , Aneurisma/genética , Aneurisma/patologia , Aneurisma/prevenção & controle , Animais , Encéfalo/irrigação sanguínea , Encéfalo/metabolismo , Encéfalo/patologia , Isquemia Encefálica/genética , Isquemia Encefálica/patologia , Isquemia Encefálica/prevenção & controle , Regulação da Expressão Gênica , Humanos , Fator de Crescimento Insulin-Like I/metabolismo , Fator de Crescimento Insulin-Like I/farmacologia , Neovascularização Fisiológica/fisiologia , Neurogênese/genética , Fármacos Neuroprotetores/farmacologia , Receptor IGF Tipo 1/genética , Receptor IGF Tipo 1/metabolismo , Transdução de Sinais , Acidente Vascular Cerebral/genética , Acidente Vascular Cerebral/patologia , Acidente Vascular Cerebral/prevenção & controle , Hemorragia Subaracnóidea/genética , Hemorragia Subaracnóidea/patologia , Hemorragia Subaracnóidea/prevenção & controleRESUMO
Isolated using Langendorff technique hearts of male Wistar rats were ischemized for 30 min and reperfused for 40 min. Both iNOS expression determined by immunoblotting, and its activity shown by a modified Griess method have been found to predominate in the right ventricle over the left one, as compared to cNOS activity which prevailed in the left ventricle. The latter significantly diminished after an ischemic injury in the left ventricle. On the contrary, an expression of iNOS and the total NOS activities increased progressively after ischemia and postischemic reperfusion; all the values in the right ventricle were higher than in the left one. The high level of iNOS expression in the right ventricle in a postischemic period decreased during reperfusion, although an activity of the enzyme went on elevating. These data can give an evidence for different regulation of NO synthesis in right or left ventricles of the heart, including normal conditions or ischemia.
Assuntos
Isquemia Miocárdica/enzimologia , Traumatismo por Reperfusão Miocárdica/enzimologia , Óxido Nítrico Sintase/biossíntese , Óxido Nítrico Sintase/metabolismo , Animais , Western Blotting , Ventrículos do Coração/enzimologia , Técnicas In Vitro , Masculino , Isquemia Miocárdica/complicações , Traumatismo por Reperfusão Miocárdica/etiologia , Óxido Nítrico Sintase Tipo II , Óxido Nítrico Sintase Tipo III , Ratos , Ratos WistarRESUMO
The effects of non-enzymatic disintegration of SIN-1 products (nitric oxide, superoxide anion and peroxynitrite) on Ca(2+)-transport of sarcoplasmic reticulum were studied on homogenates of rats myocardium. It was shown that SIN-1 (30 microM) exerts a significant activating effect on ryanodine-sensitive calcium channels resulted in three-fold increase of Ca2+ release rate via these channels. Such effect of SIN-1 realized mainly by nitric oxide effect and, partially, superoxide radical. SIN-1 did not effect the Ca(2+)-ATPase activity of sarcoplasmic reticulum.
