[Carotid atherosclerosis and white matter hypodensities: a controversial relationship]

INTRODUCTION: White matter hypodensities of presumed vascular origin, are recognized as an important cause of morbidity with established clinical and cognitive consequences. Nonetheless, many doubts remain on its physiopathology. Our goal is to clarify the potential role of carotid atherosclerosis and other vascular risk factors in the development of white matter hypodensities of presumed vascular origin. MATERIAL AND METHODS: We included patients that underwent CT brain scan and neurosonologic evaluation within a one-month period. Full assessment of vascular risks factors was performed. We seek to find independent associations between white matter hypodensities of presumed vascular origin, carotid intima-media thickness and vascular risk factors. RESULTS: 472 patients were included, mean age was 67.32 (SD: 14.75), 274 (58.1%) were male. The independent predictors of white matter hypodensities of presumed vascular origin were age (OR: 1.067, 95% IC: 1.049 - 1.086, p < 0.001) and hypertension (OR: 1.726, 95% IC: 1.097 - 2.715, p = 0.018). No association was found between IMT (OR: 2.613, 95% IC: 0.886 - 7.708, p = 0.082) or carotid artery stenosis (OR: 1.021, 95% IC: 0.785 - 1.328, p = 0.877) and white matter hypodensities of presumed vascular origin. DISCUSSION: Only age and hypertension proved to have an independent association with white matter hypodensities of presumed vascular origin. Carotid atherosclerosis, evaluated by IMT and the degree of carotid artery stenosis, showed no association with white matter hypodensities of presumed vascular origin. Since atherosclerosis is a systemic pathology, these results suggest that alternative mechanisms are responsible for the development of white matter hypodensities of presumed vascular origin. CONCLUSION: Age and hypertension seem to be the main factors in the development of white matter hypodensities of presumed vascular origin. No association was found between carotid atherosclerosis and white matter hypodensities of presumed vascular origin.

Impact of splenic artery ligation after major hepatectomy on liver function, regeneration and viability

It was reported that prevention of acute portal overpressure in small-for-size livers by inflow modulation results in a better postoperative outcome. The aim is to investigate the impact of portal blood flow reduction by splenic artery ligation after major hepatectomy in a murine model. Forty-eight rats were subjected to an 85% hepatectomy or 85% hepatectomy and splenic artery ligation. Both groups were evaluated at 24, 48, 72 and 120 post-operative hours: liver function, regeneration and viability. All methods and experiments were carried out in accordance with Coimbra University guidelines. Splenic artery ligation produces viability increase after 24 h, induces a relative decrease in oxidative stress during the first 48 hours, allows antioxidant capacity increment after 24 h, which is reflected in a decrease of half-time normalized liver curve at 48 h and at 72 h and in an increase of mitotic index between 48 h and 72 h. Splenic artery ligation combined with 85% hepatectomy in a murine model, allows portal inflow modulation, promoting an increase in hepatocellular viability and regeneration, without impairing the function, probably by inducing a less marked elevation of oxidative stress at first 48 hours.