RESUMEN
The relationship between hypertension and diabetic peripheral neuropathy (DPN) has recently been reported in clinical research, but it remains unclear whether hypertension is a risk factor for DPN. To investigate the effects of hypertension on DPN, we analyzed morphological features of peripheral nerves in diabetic rats with hypertension. Male WBN/Kob rats were divided into 2 groups: alloxan-induced diabetic rats with deoxycorticosterone acetate-salt (DOCA-salt) treatment (ADN group) and nondiabetic rats with DOCA-salt treatment (DN group). Sciatic, tibial (motor) and sural (sensory) nerves were subjected to qualitative and quantitative histomorphological analysis. Systolic blood pressure in the two groups exhibited a higher value (>140 mmHg), but there was no significant difference between the two groups. Endoneurial blood vessels in both groups presented endothelial hypertrophy and narrowing of the vascular lumen. Electron microscopically, duplication of basal lamina surrounding the endothelium and pericyte of the endoneurial vessels was observed, and this lesion appeared to be more frequent and severe in the ADN group than the DN group. Many nerve fibers of the ADN and DN groups showed an almost normal appearance, whereas morphometrical analysis of the tibial nerve showed a significant shift to smaller fiber and myelin sizes in the ADN group compared with DN group. In sural nerve, the fiber and axon-size significantly shifted to a smaller size in ADN group compared with the DN group. These results suggest that combined diabetes and hypertension could induce mild peripheral nerve lesions with vascular changes.
RESUMEN
Robot-assisted minimally invasive surgery has become common in recent years. We used the da Vinci surgical system and managed anesthesia in 6 cases of bilateral internal mammary artery dissection and construction of a composite graft using the radial artery. To ensure vision inside the thoracic cavity, endoscopic robotic surgery employs the inflation of the thoracic cavity with carbon dioxide, producing a pneumothorax and turning the thoracic cavity into a positive pressure chamber. Thus, marked acidosis and circulatory changes manifest during anesthetic management. Although robotic surgery is considered "minimally invasive, such surgery involves a number of problems in terms of anesthetic management, and these problems must be examined.
Asunto(s)
Anestesia Epidural , Puente de Arteria Coronaria Off-Pump/instrumentación , Arterias Mamarias/cirugía , Sistemas Hombre-Máquina , Procedimientos Quirúrgicos Mínimamente Invasivos/instrumentación , Procedimientos Quirúrgicos Mínimamente Invasivos/métodos , Arteria Radial/trasplante , Robótica/instrumentación , Cirugía Asistida por Computador/instrumentación , Recolección de Tejidos y Órganos/instrumentación , Recolección de Tejidos y Órganos/métodos , Adulto , Anciano , Puente de Arteria Coronaria Off-Pump/métodos , Humanos , Cuidados Intraoperatorios , Masculino , Persona de Mediana Edad , Robótica/métodos , Cirugía Asistida por Computador/métodosRESUMEN
Bacterial endotoxin lipopolysaccharide (LPS) treatment of neuron-rich cells and glia-rich cells exhibited significant cell damage 12 hr after incubation, although no severe or significant cell damage induced by LPS appeared in neuron-glia co-cultured cells. Moreover, severe and significant time-dependent cell damage was induced by a larger dose treatment (10 mM) of glutamate (Glu), and this damage was seen in neuron-rich cells, neuron-glia co-cultured cells, and glia-rich cells. Examining extracellular tumor necrosis factor alpha (TNFalpha) induced by either LPS or Glu treatment, the levels of extracellular TNFalpha induced by LPS were significantly higher than those induced by Glu. These significant increases of TNFalpha were measured within 2 hr after LPS treatment in neuron-glia co-cultured cells and glia-rich cells, although no significant changes were detected in the neuron-rich cells. With Glu treatment, a significant increase in TNFalpha levels was detected after 6 hr of Glu treatment only in glia-rich cells. Our results indicate that cerebral TNFalpha is mainly produced in glia cells and that its production is dependently regulated by each stimulant. In addition, the production of TNFalpha is not directly related to the trigger of cell injury.