Medical Express

ISSN (print): 2318-8111

ISSN (online): 2358-0429

Author's Articles

2 result(s) for: Eliete Bouskela

Protective microcirculatory and anti-inflammatory effects of heparin on endotoxemic hamsters

Marcos L. Miranda; Luiz Felipe M. Prota; Maria Júlia B. Silva; Fernando L. Sicuro; Eliane S. Furtado; Ana Olimpia M. T. Santos; Eliete Bouskela

MEDICALEXPRESS 2014;1(3):127-134 - ORIGINAL RESEARCH

Abstract PDF

OBJECTIVE: Apart from its anticoagulant properties, heparin has vasodilator and anti-inflammatory effects that could assist in the reversal of septic microcirculatory changes. This paper investigates the effects of heparin on endotoxemia-related microcirculatory changes and compares them to those observed with the use of recombinant human activated protein C.
METHODS: After skinfold chamber implantation procedures and endotoxemia induction by intravenous Escherichia coli lipopolysaccharide administration (2 mg.kg-1), male golden Syrian hamsters were treated with intravenous unfractionated heparin (0.2 mg.kg-1). Intravital microscopy of skinfold chamber preparations allowed quantitative analysis of microvascular variables and venular leukocyte rolling and adhesion. Macrohemodynamic parameters were also analyzed. Endotoxemic hamsters treated with recombinant human activated protein C and non-treated animals served as controls.
RESULTS: Heparin decreased lipopolysaccharide-induced leukocyte rolling and arteriolar vasoconstriction; it also increased survival when compared with non-treated animals, while recombinant human activated protein C decreased leukocyte adhesion. Administration of heparin plus recombinant human activated protein C was associated with a significant attenuation of lipopolysaccharide-induced capillary perfusion deficits.
CONCLUSIONS: Heparin yields protective effects on endotoxemic animals' microcirculation. Those benefits were potentiated when heparin was administered in conjunction with recombinant human activated protein C.



Keywords: sepsis; endotoxemia; microcirculation; heparin; recombinant human activated protein C.

Low dose of green tea catechins improves endothelial function and vascular smooth muscle cell reactivity in obese women

Daniel Alexandre Bottino; Débora Cherfan Goulart Nogueira; Ana Cláudia Lourenço; Vanessa Silveira Fortes; Andresa A. Berretta; Eliete Bouskela

MEDICALEXPRESS 2014;1(5):262-267 - ORIGINAL RESEARCH

Abstract PDF

BACKGROUND: The high prevalence of obesity in the world is associated with several health problems, with endothelial dysfunction figuring as a frequent feature. We investigated whether low dose consumption of green tea extract (catechins < 200 mg/day) could modify endothelial function, lipid profile, fasting glucose and insulin, post load plasma glucose, inflammatory/oxidative stress biomarkers and blood pressure in obese women.
METHODS: Sixteen obese women with body mass index (BMI) between 30 and 40 Kg/m2, mean age 38 [33-40] years, consumed 600 ml green tea (3 × 200 ml) per day, containing 153.3 mg of catechins and 72.5 mg of caffeine, during three months. Endothelial function was evaluated through venous occlusion plethysmography by increment of peak forearm blood flow (FBF), after 5 min ischemia, during the reactive hyperemia response/baseline FBF. Endothelium-independent vasodilation was analyzed through peak FBF after 0.4 mg sublingual nitroglycerin/baseline FBF.
RESULTS: After 3 months, this consumption of green tea reduced BMI from 34.02 to 33.13, and diastolic blood pressure by 4 mmHg. The reactive hyperemia response/baseline FBF improved by 27%, and the endothelium-independent vasodilation by 12%. The blood biochemical profile, where all parameters were within the normal range, remained unaltered.
CONCLUSIONS: A low dose of green tea ameliorated the endothelial dysfunction present in obesity, indicating that its consumption should be encouraged in these patients, because endothelial dysfunction is an early marker of atherosclerosis.



Keywords: Obesity; green tea; microcirculation; venous occlusion plethysmography; endothelial function.