OBJETIVO: Avaliar os efeitos agudos de concentrações de glicose usadas para o diagnóstico do diabetes mellitus, na reatividade vascular (RV) de rim isolado de coelhos normais. METODOLOGIA: Rins isolados de coelhos normais foram agudamente expostos (3hs) a concentrações normais (5,5mM) e elevadas (7, 7,8 e 11,1mM) de glicose. A RV foi avaliada com acetilcolina. RESULTADO: Houve redução significativa na vasodilatação dependente do endotélio no grupo com glicose 11,1mM em comparação ao controle (redução máxima na pressão de perfusão de 24±3 vs. 41±4%; p<0,05), mas não ocorreram diferenças significativas entre os grupos com glicose 7 e 7,8mM e o controle (reduções máximas na pressão de perfusão de 39±4 e 34±3, respectivamente, vs. 41±4%, p>0,05). CONCLUSÃO: Níveis de glicose utilizados para o diagnóstico pós-TOTG de DM são capazes de provocar alterações agudas na RV. Estes efeitos não foram observados com os valores diagnósticos de jejum. Especulamos que a glicemia pós-TOTG possa estar mais relacionada com a presença de disfunção endotelial do que os níveis diagnósticos de jejum e, por isto, se correlacione melhor com o risco cardiovascular.

OBJECTIVE: To assess the acute effects of glucose levels used in diagnosis of diabetes mellitus on vascular reactivity in the isolated rabbit kidney. METHODS: Isolated rabbit kidneys were acutely exposed (3hs) to normal (5.5mM) and high (7, 7.8 and 11.1mM) glucose concentrations. Vascular reactivity was evaluated with acetylcholine. RESULTS: Kidneys perfused with glucose 11.1mM (maximal reduction in the perfusion pressure of 24±3 vs. 41±4%; p<0.05), but not with 7 and 7.8mM (maximal reduction in the perfusion pressures of 39±4 e 34±3%, respectively, vs. 41±4%, p>0.05) showed significantly decreased endothelium-dependent relaxations compared to control. CONCLUSIONS: High glucose levels typically observed after an oral glucose challenge can acutely alter vascular reactivity. We speculated that post-OTTG glucose levels are more strongly related to endothelial dysfunction and this is the reason why it is more correlated with cardiovascular disease.

OBJECTIVE: To assess the acute effects of high glucose concentrations on vascular reactivity in the isolated non diabetic rabbit kidney. METHODS: Rabbits were anaesthetized for isolation of the kidneys. Renal arteries and veins were cannulated for perfusion with Krebs-Henselleit solution and measurement of perfusion pressure. After 3 hours of perfusion with glucose 5,5 mM (control ) and 15 mM, the circulation was submitted to sub maximal precontraction (80% of maximal response) trough continuous infusion of noradrenaline 10 mM. Vascular reactivity was then assessed trough dose-responses curves with endothelium-dependent (acetylcholine) and independent (sodium nitroprusside) vasodilators. The influence of hyperosmolarity was analyzed with perfusion with mannitol 15mM. RESULTS: A significant reduction in the endothelium-dependent vasodilation in glucose 15mM group was observed compared to that in control, but there was no difference in endothelium-independent vasodilation. After perfusion with mannitol 15 mM, a less expressive reduction in endothelium-dependent vasodilation was observed, only reaching significance in regard to the greatest dose of acetylcholine. CONCLUSION: High levels of glucose similar to those found in diabetic patients in the postprandial period can cause significant acute changes in renal vascular reactivity rabbits. In diabetic patients these effects may also occur and contribute to diabetes vascular disease.

Para verificar a variabilidade do controle glicêmico em um estudo não controlado de diabéticos durante um ano de acompanhamento, nós avaliamos retrospectivamente 113 pacientes diabéticos. Com os valores das HBA1c (hemoglobina glicada) dosadas em 1998 calculamos um índice de controle que foi associado à idade, duração do diabetes, IMC e dose de insulina. A HBA1c foi maior em pacientes DM1 do que DM2, respectivamente [7,9 (4,4-13,3) vs. 7,0 (4,4-13,4)%; p= 0,007]. Nos 90 pacientes com no mínimo duas HBA1c, 68 (75,6%) mantiveram o controle: 51 (76,1%) em bom, 8 (11,1%) em regular e 9 (11,9%) em péssimo controle. Nenhum manteve todas as HBA1c na faixa da normalidade, sendo que 26 pacientes (28,9%) tiveram pelo menos uma HBA1c normal. No grupo geral, 44 pacientes (48,9%) apresentaram aumento da HBA1c, 41 (45,6%) diminuição e 5 pacientes (5,6%) mantiveram o mesmo valor, sem diferença entre DM1 e DM2 (p= 0,77). Observamos diferença na HBA1c e tempo de duração de diabetes entre os pacientes com DM2 que tratavam com dieta, hipoglicemiante oral, terapia combinada e monoterapia com insulina, respectivamente (5,4±0,5 vs. 6,3±1,3 vs. 7,6±1,4 vs. 8,4±2,0%; p= 0,001) e (8,5±9,9 vs. 5,3±4,2 vs. 14,1±9,6 vs. 16,9±8,1 anos; p= 0,003). O coeficiente de variação intraindividual da HBA1c foi de 11,6±7,4% (p= 0,0000), sendo de 12,8±7,6% (p= 0,0000) em DM1 e 10,4±7,2% em DM2 (p= 0,0000) sem diferença entre ambos. Concluímos que em nossa amostra a maioria dos pacientes manteve um bom controle apesar da variabilidade intraindividual e da dificuldade em normalizar os níveis de HBA1c.

To evaluate the variability of glicemic control in diabetic patients followed during one year, we conducted a retrospective study in which the record data of 113 diabetic patients were analyzed. The value of HBA1c (glycated hemoglobin) measured during a year were registered and an index of glicemic control was calculated. This index was associated with duration of diabetes, BMI and dose of insulin. HBA1c were higher in type 1 diabetes than type 2, respectively, [7.9 (4.4-13.3) vs. 7.0 (4.4-13.4)%; p= 0.007]. In 90 patients with at least two HBA1c measurements, 68 (75.6%) had no change in glicemic control: 51 (76.1%) had good, 8 (11.1%) regular and 9 (11.9%) poor control. None of them sustained all the HBA1c in the normal range: 26 (28.9%) had at least one normal HBA1c value. In general group, 44 patients (48.9%) showed increase, 41 (45.6%) decreased and 5 (5.6%) remained with the same level of HBA1c, without difference between DM1 and DM2 (p= 0,77). A difference in HBA1c and diabetes duration among patients with DM2 treated with diet, oral hipoglycemic agents, combined therapy and monotherapy with insulin, was noted respectively (5.4±0.5 vs. 6.3±1.3 vs. 7.6±1.4 vs. 8.4±2.0%; p= 0.001) and (8.5±9.9 vs. 5.3±4.2 vs. 14.1±9.6 vs. 16.9±8.1 years; p= 0,003). The intraindividual coefficient of variation of HBA1c was 11.6±7.4% (p= 0.0000) being 12.8±7.6 (p= 0.0000) in type 1 and 10.4±7.2% in type 2 (p= 0.0000) without difference between both groups. In conclusion: the majority of the patients in our study maintained a good control despite the intraindividual variability of HBA1c and the difficulty to keeping it in the normal range.