Birth Weight and Its Relationship with the Cardiac Autonomic Balance in Healthy Children

Several studies indicate that the fetal environment plays a significant role in the development of cardiometabolic disease later in life. However, a few studies present conflicting data about the correlation between birth weight and the impairment of cardiac autonomic modulation. The purpose of the present study was to provide further knowledge to elucidate this contradictory relationship. One hundred children aged 5 and 14 years had anthropometric parameters, body composition and blood pressure levels determined. Heart rate variability (HRV) was evaluated by heart rate monitoring, including measurements of both the time and frequency domains. The results showed inverse correlation between the HRV parameters with BMI (RMSSD: P = 0.047; PNN50: P = 0.021; HF: P = 0.041), systolic (RMSSD: P = 0.023; PNN50: P = 0.032) and diastolic (PNN50: P = 0.030) blood pressure levels. On the other hand, there were consistent positive correlations between the HRV parameters and birth weight (RMSSD: P = 0.001; PNN50: P = 0.001; HF: P = 0.002). To determine the effect of birth weight on HRV parameters, we perform multivariate linear regression analysis adjusted for potentially confounding factors (prematurity, gender, age, BMI, physical activity index and SBP levels). These findings were preserved even after adjusting for these confounders. Our results suggested that impaired cardiac autonomic modulation characterized by a reduction in the parasympathetic activity occurs in children with low birth weight. One possible interpretation for these data is that a vagal withdrawal, rather than a sympathetic overactivity, could precede the development of hypertension and other cardiometabolic diseases in children with low birth weight. However, long-term studies should be performed to investigate this possibility.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Univ Fed Sao Paulo, Div Nephrol, Sao Paulo, BrazilUniv Fed Alagoas, Dept Nutr, Alagoas, BrazilUniv Fed Sao Paulo, Dept Pediat, Sao Paulo, BrazilUniv Fed Sao Paulo, Div Nephrol, Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Pediat, Sao Paulo, BrazilFAPESP: 2013/03139-0Web of Scienc

NADPH oxidase and enhanced superoxide generation in intrauterine undernourished rats: involvement of the renin-angiotensin system

Objective: We previously reported that intrauterine undernutrition increased the oxidative stress by decreasing superoxide dismutase activity. in the present study, we tested whether NADPH oxidase, xanthine oxidase, cyclooxygenase or nitric oxide synthase are responsible for the increased O-2(-) generation observed in rats submitted to intrauterine undernutrition. in addition, we investigated the 2 effect of angiotensin II (ANG II on O-2(-) production via activation of NADPH oxidase. Methods: Female pregnant Wistar rats were fed either normal or 50% of the normal intake diets, during the whole gestational period. At 16 weeks of age, the rats were used for the study of intravital fluorescence microscopy; microvascular reactivity, local ANG II concentration and AT(1), p22(phox) and gp91(phox) gene expression. in this study only the male offspring was used. Results: Treatment of mesenteric arterioles with the xanthine oxidase inhibitor oxypurinol, the nitric oxide synthase inhibitor L-NAME or the cyclooxygenase, inhibitor diclofenac did not significantly change superoxide production. Thus, these vascular sources of superoxide were not responsible for the increased superoxide concentration. in contrast, treatment with the NADPH oxidase inhibitor apocynin significantly decreased superoxide generation and improved vascular function. On the other hand, intrauterine undernutrition did not alter the gene expression for p22(phox) and gp91(phox). the fact that the local ANG II concentration was increased and the attenuation of oxidative stress by blocking AT, receptor with losartan, led us to suggest that ANG II induces O-2 generation in intrauterine undernourished rats. Conclusion: Our study shows that NADPH oxidase inhibition attenuated superoxide anion generation and ameliorated vascular function in rats submitted to intrauterine undernutrition. Although it is not clear which mechanisms are responsible for the increase in NADPH oxidase activity, a role for ANG II-mediated superoxide production via activation of NADPH oxidase is suggested. (C) 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.Univ São Paulo, Inst Biomed Sci, Dept Pharmacol, Lab Hypertens, BR-05508900 São Paulo, SP, BrazilUNIFESP, Lab Nephrol, São Paulo, SP, BrazilUNIFESP, Lab Nephrol, São Paulo, SP, BrazilWeb of Scienc

Cystatin C and renal function in pediatric kidney transplant recipients

In clinical practice, the glomerular filtration rate (GFR) is often determined with serum creatinine. However, studies have shown cystatin C to be a better parameter for the diagnosis of impaired renal function. We compared GFR estimated by plasma cystatin C with GFR estimated by serum creatinine in a sample of 50 pediatric renal transplant recipients and 24 healthy children. The correlation between GFR estimated by serum creatinine and by cystatin C was significant (r = 0.75; P < 0.001, Person’s correlation); however, in pediatric kidney transplant recipients, the GFR was 6.7 mL/min lower when determined using cystatin C rather than serum creatinine. Moreover, using GFR estimated by cystatin C we found that 42% of the pediatric kidney transplant recipients had an estimated GFR <60 mL·min-1·1.73 (m²)-1, whereas when GFR was estimated by the serum creatinine formula only 16% of the children had values below this cutoff point indicative of chronic kidney disease (P < 0.001). We conclude that, in pediatric kidney transplant recipients, estimation of GFR yields lower values when cystatin C is used rather than serum creatinine.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Universidade Federal de São Paulo (UNIFESP) Departamento de Medicina Disciplina de NefrologiaUniversidade Federal de São Paulo (UNIFESP) Departamento de PediatriaUNIFESP, Depto. de Medicina Disciplina de NefrologiaUNIFESP, Depto. de PediatriaFAPESP: 04/10342-7SciEL

COVID-19: Impact in endothelial function and therapy with Mesenchymal Stromal Cells

The new pandemic of SARS-CoV-2 Betacoronavirus, has spread worldwide, and infected millions of individuals causing the disease denominated of COVID-19. Further on flu symptoms, due to the high tropism of virus, has most been observed in the COVID-19 pathophysiology: acute heart failure, thromboembolism events, acute renal failure, neurological and liver damage, and multiple organ failure, with special attention to endothelial disfunction. Hence, elucidate whether virus target the endothelium is a crucial step to understand COVID-19 pathogenesis. However, the permissiveness of blood vessels during SARS-CoV-2 infection remains unclear, but regardless endothelial infection, the vascular disfunction may occurred in response to molecular inflammatory signaling triggered by immune cells that attempt to limit infection. Thus, alternative therapies using mesenchymal stromal cells (MSCs) can change this scenario and help critically ill patients. In this reflection, we attempt to discuss COVID-19 pathophysiology with impact in endothelial function and explore the applicability of MSC-based therapies as alternative treatment.

COVID-19: Impact in endothelial function and therapy with Mesenchymal Stromal Cells

The new pandemic of SARS-CoV-2 Betacoronavirus, has spread worldwide, and infected millions of individuals causing the disease denominated of COVID-19. Further on flu symptoms, due to the high tropism of virus, has most been observed in the COVID-19 pathophysiology: acute heart failure, thromboembolism events, acute renal failure, neurological and liver damage, and multiple organ failure, with special attention to endothelial disfunction. Hence, elucidate whether virus target the endothelium is a crucial step to understand COVID-19 pathogenesis. However, the permissiveness of blood vessels during SARS-CoV-2 infection remains unclear, but regardless endothelial infection, the vascular disfunction may occurred in response to molecular inflammatory signaling triggered by immune cells that attempt to limit infection. Thus, alternative therapies using mesenchymal stromal cells (MSCs) can change this scenario and help critically ill patients. In this reflection, we attempt to discuss COVID-19 pathophysiology with impact in endothelial function and explore the applicability of MSC-based therapies as alternative treatment.

COVID-19: Impact in endothelial function and therapy with Mesenchymal Stromal Cells

The new pandemic of SARS-CoV-2 Betacoronavirus, has spread worldwide, and infected millions of individuals causing the disease denominated of COVID-19. Further on flu symptoms, due to the high tropism of virus, has most been observed in the COVID-19 pathophysiology: acute heart failure, thromboembolism events, acute renal failure, neurological and liver damage, and multiple organ failure, with special attention to endothelial disfunction. Hence, elucidate whether virus target the endothelium is a crucial step to understand COVID-19 pathogenesis. However, the permissiveness of blood vessels during SARS-CoV-2 infection remains unclear, but regardless endothelial infection, the vascular disfunction may occurred in response to molecular inflammatory signaling triggered by immune cells that attempt to limit infection. Thus, alternative therapies using mesenchymal stromal cells (MSCs) can change this scenario and help critically ill patients. In this reflection, we attempt to discuss COVID-19 pathophysiology with impact in endothelial function and explore the applicability of MSC-based therapies as alternative treatment