Journal of cardiac failure · 2007
Cardiac alterations in furosemide-treated thiamine-deprived rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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da Cunha Sergio, Cunha Bastos Jayme, Salles João Bosco, Silva Maria Cristina Costa, Cunha Bastos Vera Lúcia Freire, Mandarim-de-Lacerda Carlos Alberto
Аннотация
BACKGROUND: Chronic administration of furosemide may induce thiamine deficiency and cause or aggravate myocardial dysfunction.
METHODS AND RESULTS: Wistar rats were divided into four groups according to food and treatment: (1) thiamine standard chow with intraperitoneal furosemide administration; (2) thiamine standard chow with intraperitoneal saline administration; (3) thiamine-deficient chow with intraperitoneal furosemide administration; and (4) thiamine-deficient chow with intraperitoneal saline administration. Thiamine status was evaluated by high-performance liquid chromatography determination in plasma, erythrocytes, and myocardium, and by erythrocyte transketolase activity and the thiamine pyrophosphate effect to recover transketolase activity. Left ventricular mass index, intramyocardial arteries-to-cardiomyocyte ratio, cardiomyocyte cross-sectional area, and cardiomyocyte nuclei number were estimated. Myocardial structure was also studied by transmission electronic microscopy. Group 3 showed significantly lower blood and myocardial thiamine levels, which was not observed in group 1. Left ventricular mass index, cardiomyocyte cross-sectional area, and intramyocardial arteries-to-cardiomyocyte ratio were smaller in thiamine-deficient and furosemide-treated rats. However, no significant variation was found in the number of cardiomyocyte nuclei among the groups. Transmission electronic microscopy showed mitochondrial alterations in the thiamine-deficient groups.
CONCLUSION: The present results indicate that furosemide administration is not the primary cause of thiamine deficiency in rats with adequate thiamine intake. Furosemide aggravates thiamine deficiency only in situations associated with insufficient thiamine intake, causing cardiac structural alterations, such as myocardial fiber hypotrophy, poor microvascularization, and mitochondrial degeneration.
METHODS AND RESULTS: Wistar rats were divided into four groups according to food and treatment: (1) thiamine standard chow with intraperitoneal furosemide administration; (2) thiamine standard chow with intraperitoneal saline administration; (3) thiamine-deficient chow with intraperitoneal furosemide administration; and (4) thiamine-deficient chow with intraperitoneal saline administration. Thiamine status was evaluated by high-performance liquid chromatography determination in plasma, erythrocytes, and myocardium, and by erythrocyte transketolase activity and the thiamine pyrophosphate effect to recover transketolase activity. Left ventricular mass index, intramyocardial arteries-to-cardiomyocyte ratio, cardiomyocyte cross-sectional area, and cardiomyocyte nuclei number were estimated. Myocardial structure was also studied by transmission electronic microscopy. Group 3 showed significantly lower blood and myocardial thiamine levels, which was not observed in group 1. Left ventricular mass index, cardiomyocyte cross-sectional area, and intramyocardial arteries-to-cardiomyocyte ratio were smaller in thiamine-deficient and furosemide-treated rats. However, no significant variation was found in the number of cardiomyocyte nuclei among the groups. Transmission electronic microscopy showed mitochondrial alterations in the thiamine-deficient groups.
CONCLUSION: The present results indicate that furosemide administration is not the primary cause of thiamine deficiency in rats with adequate thiamine intake. Furosemide aggravates thiamine deficiency only in situations associated with insufficient thiamine intake, causing cardiac structural alterations, such as myocardial fiber hypotrophy, poor microvascularization, and mitochondrial degeneration.