Navegando por Palavras-chave "vascular reactivity"

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    The balloon catheter induces an increase in contralateral carotid artery reactivity to angiotensin II and phenylephrine
    (Nature Publishing Group, 2004-05-01) Accorsi-Mendonca, D.; Correa, FMA; Paiva, Therezinha B. [UNIFESP]; Souza, H. P. de; Laurindo, FRM; Oliveira, A. M. de; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    1 the effects of balloon injury on the reactivity of ipsilateral and contralateral carotid arteries were compared to those observed in arteries from intact animals (control arteries).2 Carotid arteries were obtained from Wistar rats 2, 4, 7, 15, 30 or 45 days after injury and mounted in an isolated organ bath. Reactivity to angiotensin II (Ang II), phenylephrine (Phe) and bradykinin (BK) was studied. Curves were constructed in the absence or presence of endothelium or after incubation with 10 muM indomethacin, 500 muM valeryl salicylate or 0.1 muM celecoxib.3 Phe, Ang II and BK maximum effects (Emax) were decreased in ipsilateral arteries when compared to control arteries. No differences were observed among pD2 or Hill coefficient.4 Emax to Phe (4 and 7 days) and to Ang II (15 and 30 days) increased in the contralateral artery. in addition, Phe or Ang II reactivity was not significantly different in aorta rings from control or carotid-injured animals.5 the increased responsiveness of contralateral artery was not due to changes in carotid blood flow or resting membrane potential. the endothelium-dependent inhibitory component is not present in the contraction of contralateral arteries and it is not related to superoxide anion production.6 Indomethacin decreased contralateral artery responsiveness to Phe and Ang II. Valeryl salicylate reduced the Ang II response in contralateral and control arteries. Celecoxib decreased the Phe Emax of contralateral artery.7 in conclusion, decreased endothelium-derived factors and increased prostanoids appear to be responsible for the increased reactivity of contralateral arteries after injury.
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    Preserved flow-mediated dilation but delayed time-to-peak diameter in individuals with metabolic syndrome
    (Wiley-Blackwell, 2014-07-01) Fernandes, Igor A.; Sales, Allan R. K.; Rocha, Natalia G.; Silva, Bruno M. [UNIFESP]; Vianna, Lauro C.; Nobrega, Antonio C. L. da; Universidade Federal Fluminense (UFF); Universidade Federal de São Paulo (UNIFESP)
    Introduction: Inconsistent evidences of the metabolic syndrome (MetS) impact on vascular reactivity raise questions on flow-mediated dilation (FMD) discriminatory power for disturbances induced by this clustering of risk factors. Previous reports, however, suggest that covariates such as the follow-up of the artery diameter changes, the arterial size and shear stress affect FMD responses and consequently its discriminatory power for distinctive clinical profiles.Objective: To determine the impact of MetS on traditional, arterial size-and shear-rate-adjusted FMD, the follow-up-derived time-to-peak diameter (TP), as well as their power for discriminating subjects with this clustering of risk factors from a sample of healthy individuals.Methods: Twenty-one MetS and ten healthy subjects underwent an assessment of endothelial function via FMD.Results: Traditional and allometrically scaled FMD did not differ between groups (P>0.05) as well as the approach in which the covariate was the peak diameter shear rate. in the existence of MetS, TP was longer (67.7 +/- 16.4 s versus healthy 42.1 +/- 16.3 s, P = 0.001). ROC curve analysis indicated that TP (AUC = 0.871 [95% CI, 0.718-1.000]) had greater power of discrimination for MetS than FMD approaches. in addition, TP presented a moderate and significant association with sE-selectin (r = 0.458, P = 0.048).Conclusion: Time-to-peak diameter (TP) rather than FMD distinguished MetS from a healthy profile. Therefore, at least in subjects with MetS, TP may provide insights into the impact of this clustering of risk factors on the vascular phenotype.