Inferior vena cava ultrasonography before general anesthesia cannot predict arterial hypotension in patients undergoing vascular surgery.

INTRODUCTION: Intraoperative hypotension (IH) is an independent predictor of mortality. Some experts have suggested that ultrasound measurement of the inferior vena cava (IVC) in spontaneous ventilation can predict IH. OBJECTIVE: To evaluate the capacity of ultrasound measures of IVC in spontaneous ventilation to predict episodes of IH after anaesthesia induction. PATIENTS AND METHODS: We studied 55 high-risk cardiac patients undergoing vascular surgery. The maximum (dIVCmax) and minimum (dIVCmin) diameter of the IVC were measured and the collapsibility index CI = (dIVCmax-dIVCmin)/dIVCmax was calculated prior to anaesthesia induction. Three definitions of IH were used: systolic blood pressure (SBP) less than 100 mmHg, mean arterial pressure (MAP) less than 60 mmHg, and a decrease in MAP greater than or equal to 30% compared to baseline. RESULTS: There were no significant differences in dIVCmax or in CI between patients presenting IH after anaesthesia induction and those who did not. ROC curves for dIVCmax showed an area under the curve of 0.55 (0.39-0.70), 0.69 (0.48-0.90), and 0.57 (0.42-0.73) and ROC curves for the CI were 0.62 (0.47-0.78), 0.60 (0.41-0.78) and 0.62 (0.47-0.78) for the 3 definitions of IH (<100 mmHg, MAP < 60 mmHg, and MAP ≥30% baseline), respectively. CONCLUSIONS: Ultrasound measurements of IVC in spontaneous ventilation are not good predictors of IH after anaesthesia induction in these patients. The optimal cut-off points show low specificity and moderate sensitivity for predicting IH.

Las medidas ecográficas de la vena cava inferior no predicen hipotensión arterial postinducción anestésica en pacientes tratados mediante cirugía vascular / Inferior vena cava ultrasonography before general anesthesia cannot predict arterial hypotension in patients undergoing vascular surgery

Introducción: La hipotensión arterial intraoperatoria (HIO) es un predictor independiente de mortalidad. Las medidas ecográficas de la vena cava inferior (VCI) en ventilación espontánea han sido propuestas como predictores de este evento.ObjetivoEvaluar la capacidad de las medidas ecográficas de la VCI en ventilación espontánea para predecir episodios de HIO postinducción anestésica. Pacientes y métodos: Estudiamos a 55 pacientes de alto riesgo cardíaco tratados mediante cirugía vascular. Previamente a la inducción anestésica se midió el diámetro máximo de la VCI (dVCImáx.), el diámetro mínimo (dVCImín.) y el índice de colapsabilidad (ICVCI=dVCImáx. – dVCImin.)/dVCImáx.). Se utilizaron 3definiciones de HIO: presión arterial sistólica menor de 100mmHg, presión arterial media (PAM) menor de 60mmHg o un descenso de la PAM mayor o igual al 30% respecto a la PAM basal. Resultados: No hubo diferencias significativas en el dVCImáx. ni en el ICVCI entre quienes presentaron HIO postinducción anestésica y quienes no. Las curvas ROC para el dVCImáx. mostraron un área bajo la curva de 0,55 (0,39-0,70); 0,69 (0,48-0,90) y 0,57 (0,42-0,73), mientras que para el ICVCI fueron de 0,62 (0,47-0,78); 0,60 (0,41-0,78) y 0,62 (0,47-0,78), para las definiciones de HIO de<100mmHg, PAM<60mmHg y descenso de la PAM ≥ 30%, respectivamente. Conclusiones: Las medidas ecográficas de la VCI en ventilación espontánea no son buenos predictores de HIO postinducción anestésica en estos pacientes. Los puntos de corte óptimos permiten predecir hipotensión con baja especificidad y moderada sensibilidad.(AU)

Introduction: Intraoperative hypotension (IH) is an independent predictor of mortality. Some experts have suggested that ultrasound measurement of the inferior vena cava (IVC) in spontaneous ventilation can predict IH.ObjectiveTo evaluate the capacity of ultrasound measures of IVC in spontaneous ventilation to predict episodes of IH after anaesthesia induction. Patients and methods: We studied 55 high-risk cardiac patients undergoing vascular surgery. The maximum (dIVCmax) and minimum (dIVCmin) diameter of the IVC were measured and the collapsibility index CI=(dIVCmax-dIVCmin)/dIVCmax was calculated prior to anaesthesia induction. Three definitions of IH were used: systolic blood pressure (SBP) less than 100mmHg, mean arterial pressure (MAP) less than 60mmHg, and a decrease in MAP greater than or equal to 30% compared to baseline. Results: There were no significant differences in dIVCmax or in CI between patients presenting IH after anaesthesia induction and those who did not. ROC curves for dIVCmax showed an area under the curve of 0.55 (0.39-0.70), 0.69 (0.48-0.90), and 0.57 (0.42-0.73) and ROC curves for the CI were 0.62 (0.47-0.78), 0.60 (0.41-0.78) and 0.62 (0.47-0.78) for the 3 definitions of IH (<100mmHg, MAP<60mmHg, and MAP ≥30% baseline), respectively. Conclusions: Ultrasound measurements of IVC in spontaneous ventilation are not good predictors of IH after anaesthesia induction in these patients. The optimal cut-off points show low specificity and moderate sensitivity for predicting IH.(AU)

Caloric restriction-induced weight loss with a high-fat diet does not fully recover visceral adipose tissue inflammation in previously obese C57BL/6 mice.

Caloric restriction (CR) reduces body weight and systemic inflammation, but the effects on adipose tissue under dietary lipid overload are controversial. We evaluated the effects of CR-induced weight loss with a high-fat diet on adipose tissue inflammation of obese mice. Male mice were assigned into low-fat diet (LF) and high-fat diet (HF) groups. After 8 weeks, the mice in the HF group were reassigned for another 7 weeks into the following 3 conditions: (i) kept in the HF condition; (ii) changed to low-fat diet ad libitum (LFAL); and (iii) changed to high-fat calorie-restricted (RHF) diet to reach LFAL body weight. Serum markers, adipocytokines, morphology, and inflammatory infiltrates in retroperitoneal adipose tissue (RAT) were accessed. The body weights of the LFAL and RHF groups were reduced, equaling the body weights of the LF group. The LFAL mice had restored almost all inflammatory markers as the LF mice, except tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), and adiponectin. Compared with the HF group, the RHF group had lowered visceral adiposity, retroperitoneal adipocyte sizes, and RAT inflammatory cell infiltration, as well as TNF-α, interleukin-6, and hepatic and serum C-reactive protein, which were higher than that of the LFAL group; adiponectin and MCP-1 did not change. CR with high-fat diet reduced body weight and attenuated visceral adiposity but did not fully recover visceral tissue inflammation. Novelty Caloric restriction in a high-fat diet ameliorated visceral adiposity. Caloric restriction in a high-fat diet did not recover visceral adipose tissue inflammation.

Effects of lead intoxication on intercellular junctions and biochemical alterations of the renal proximal tubule cells.

Lead intoxication is a worldwide health problem which frequently affects the kidney. In this work, we studied the effects of chronic lead intoxication (500 ppm of Pb in drinking water during seven months) on the structure, function and biochemical properties of rat proximal tubule cells. Lead-exposed animals showed increased lead concentration in kidney, reduction of calcium and amino acids uptake, oxidative damage and glucosuria, proteinuria, hematuria and reduced urinary pH. These biochemical and physiological alterations were related to striking morphological modifications in the structure of tubule epithelial cells and in the morphology of their mitochondria, nuclei, lysosomes, basal and apical membranes. Interestingly, in addition to the nuclei, inclusion bodies were found in the cytoplasm and in mitochondria. The epithelial cell structure modifications included an early loss of the apical microvillae, followed by a decrement of the luminal space and the respective apposition and proximity of apical membranes, resulting in the formation of atypical intercellular contacts and adhesion structures. Similar but less marked alterations were observed in subacute lead intoxication as well. Our work contributes in the understanding of the physiopathology of lead intoxication on the structure of renal tubular epithelial cell-cell contacts in vivo.