Ilknur Ari

Perimicrovascular edema in the frontal cortex in a rat model of intraperitoneal sepsis

Septic encephalopathy is a complication of sepsis, and it is closely associated with the increased mortality of the sufferers. Pathophysiology of septic encephalopathy is not still completely understood. In an attempt to provide insight into the pathogenesis of septic encephalopathy, a light and electron microscopic investigation has been carried out in a rat model of intraperitoneal sepsis. Experimental fecal peritonitis was induced in Wistar rats which have been monitored for 6 h and sacrificed to harvest the samples of frontal cortex. Vital parameters and morphometric data obtained from investigation of the microvessels were then compared with the sham-operated and unoperated controls. In addition to the discernible drop in the blood pressure and in rectal temperature following initial increases, unstable but usually increased heart rate and marked respiratory failure were recorded. Estimation of the percentage of the microvessel area occupied by edema revealed the presence of significantly more perimicrovascular edema in the experimental fecal peritonitis group compared to both sham-operated and unoperated controls, while no significant difference was present between the latter two groups. Electron microscopic investigation confirmed the presence of distinctive perimicrovascular edema in the fecal peritonitis group although the endothelial cells were linked by tight junctions which appeared morphologically intact. Although it might be premature to draw any strict parallels between the septic encephalopathy in humans and the findings observed in the present model, the results may suggest that the edema observed around the microvessels would bare a role in the pathogenesis of the septic encephalopathy probably by affecting the exchange of oxygen and nutrients with carbon dioxide and waste products between the blood and brain parenchyma.

The peri-microvascular edema in hippocampal CA1 area in a rat model of sepsis

Encephalopathy is a common complication of sepsis. However, little is known about the morphological changes that occur in the brain during sepsis. In this study, fecal peritonitis was induced in Wistar rats, which had been monitored for 4 h before their brains were removed and samples from the CA1 area taken. In addition to higher blood pressure with a decreasing pattern and a significant drop in rectal temperature, an increased heart rate and marked respiratory failure were observed. The tissue was investigated and compared with corresponding hippocampal samples taken from sham‐operated and not operated control groups. Significantly more peri‐microvascular edema was found in the hippocampal CA1 area in the septic group. The percentages of the peri‐microvascular edema were 158.57 ± 3.6%, 122.84 ± 1.5% and 120.24 ± 1.9% in the fecal peritonitis group, sham‐operated and not operated control groups, respectively. The results may suggest that the edema observed around the microvessels may participate in the pathogenesis of the septic encephalopathy probably by causing in the microvascular permeability characteristics.

A case with coincidence of aberrant right subclavian artery and common origin of the carotid arteries.

An aortic arch variant was found in a 63 year-old male cadaver during routine dissection. An aberrant right subclavian artery (ARSA) arose from the distal aortic arch after the left subclavian artery and coursed to the right and upward behind the trachea and esophagus. A common origin for the carotid arteries (COCA) accompanied this variant of the right subclavian artery.

Morphometric Investigation of Neurons in the Hippocampal CA1, CA3 Areas and Dentate Gyrus in a Rat Model of Sepsis

Aproximadamente, la mitad de los pacientes con sepsis progresiva desarrollan encefalopatia, pero hay escaso conocimiento en cuestion de como la sepsis asociada con encefalopatia contribuye a la disfuncion cerebral. El hipocampo es una de las regiones mas vulnerables durante la sepsis experimental. En el presente estudio, fueron analizados los efectos de la sepsis sobre la densidad neuronal y la morfologia en las areas CA1, CA3 y giro dentado en un modelo de sepsis intraperitoneal en rata. Veinticuatro ratas Wistar se dividieron en tres grupos diferentes: grupo de peritonitis fecal, operacion simulada y control no operado. La densidad del volumen piramidal fue significativamente mayor en el area CA1 del grupo con peritonitis fecal en comparacion con los grupos no operados (p<0,05) y la operacion simulada (p<0,05). La densidad de volumen de las neuronas piramidales fue significativamente mayor en el area CA3 del grupo peritonitis fecal en comparacion con los no operado (p<0,05) y la operacion simulada (p<0,05). El diametro promedio nuclear de las neuronas piramidales en la zona CA1 del grupo de peritonitis fecal fue significativamente menor (p<0,05) en comparacion con el grupo de control no operado. Las neuronas fueron observadas con frecuencia reducidas y las celulas neurogliales parecen ser frecuentes en el grupo de peritonitis fecal en comparacion con grupos de control. Estos resultados en conjunto sugieren que la sepsis intraperitoneal no inicia la muerte celular en las primeras etapas de la sepsis, aunque los signos morfologicos de la neurodegeneracion empiezan a aparecer.