Data on cardiac and vascular functionality in ex vivo and in vivo models following acute administration of trimethylamine N-oxide

This dataset provides information on cardiac, vascular and mitochondrial functionality in ex vivo and in vivo models after acute treatment with trimethylamine N-oxide (TMAO). The accumulation of TMAO in tissue was assessed after performing heart perfusion or incubating aortic tissue in a buffer solution with or without TMAO. To test the effects of TMAO on mitochondrial substrate oxidation, the aortic rings and heart homogenates of Wistar rats were incubated with or without TMAO in buffer solution containing [9,10-3H] palmitate (5 µCi/ml) or D-[U-14C] glucose (0.625 µCi/ml). The effects of TMAO on vascular reactivity were tested in isolated rat conductance and resistance vessels. The impact of elevated TMAO levels on cardiac function and infarct size was evaluated in an isolated rat heart infarction model. The outcomes after single and 7-day administration of TMAO (120 mg/kg) on normal or forced heart function (administration of isoproterenol, 10 µg/mouse) in CD-1 mice were evaluated by echocardiography. The data presented here provide information on measurements in experimental models of cardiac and vascular function and energy metabolism under acutely increased TMAO levels. Additionally, the data could be used further in the planning of future in vitro, ex vivo, and in vivo studies focused on clarifying molecular mechanisms targeted by elevated TMAO levels.