RESUMEN
Diabetes mellitus increases the risk of cerebrovascular disease, the effects of hypercapnia on CBF (cerebral blood flow) and cerebrovascular reactivity during diabetes are still inconsistent. Here, we have established a new microangiographic technique using synchrotron radiation (SPring-8, Japan), which enabled us to visualize rat cerebral vessels with high spatial resolution in real time. The goal of the study presented here was to identify the effects of chronic hyperglycemia on hypercapnia-induced vascular responses (endothelium-dependent vasodilatation) and nitric oxide (NO) donor- induced vascular responses (endothelium-independent) of perforating arteries and of the deeply located large cerebral arteries. We found a significant vasodilatation of rat perforating arteries after hypercapnia with a maximum diameter of approximately 140% of baseline in normal Wistar rats. Chronic hyperglycemia impaired vasodilatation of perforating arteries in genetically diabetic GK rats. SNP (sodium nitroprusside) caused a similar vasodilatation of perforating vessels in normal and chronic hyperglycemia, indicating that endothelium-dependent vasodilatation of perforating arteries may be specifically impaired in chronic hyperglycemia. Possible impairment of endothelium-dependent vasodilatation in perforating vessels during chronic hyperglycemia may cause decreased vascular reserve capacity of perforating artery, resulting in the increased ischemic insults and cerebrovascular diseases in diabetes.
Asunto(s)
Arterias Cerebrales/fisiopatología , Hipercapnia/fisiopatología , Hiperglucemia/fisiopatología , Animales , Encéfalo/irrigación sanguínea , Dióxido de Carbono/administración & dosificación , Angiopatías Diabéticas/fisiopatología , Endotelio Vascular/fisiopatología , Masculino , Donantes de Óxido Nítrico/farmacología , Nitroprusiato/farmacología , Ratas , Ratas Endogámicas WKY , Vasodilatación/efectos de los fármacosRESUMEN
Diabetes mellitus and cognitive decline are major public health concerns among the elderly. In diabetic subjects without dementia, certain cognitive domains are impaired, such as memory, attention, and executive/frontal lobe function (diabetic cognitive dysfunction). Recent epidemiological studies have suggested that diabetes increases the risks for vascular dementia as well as Alzheimer's disease. There are accumulating evidences that indicate biological linkage between impaired brain glucose metabolism homeostasis and cognitive decline. Diabetes may cause serious brain damages through several mechanisms and induce a variety of cognitive decline. Most critical issue to be resolved is to identify the mechanism of dementia leading from diabetic cognitive dysfunction. Once elderly diabetics had severe cognitive decline, effective treatment of diabetes were hardly obtained. Thus, diabetic cognitive decline should be considered as an important comorbidity of the elderly diabetes and long-term management of hyperglycemia is required from a view point to sustain healthy brain function. In this short review, we are summarizing the clinical features and current biological findings of diabetic cognitive decline. Also, we introduce the comprehensive treatment of demented diabetic elderly, including therapeutic strategy, nursing and care.