Key result
Insulin increases LV dP/dt max up to ~48% in isolated rat hearts.
Why the study?
Insulin exerts positive inotropic effects on cardiac muscle, but the relationship between cardiac contractility and PI3K/Akt activation remains unclear.
Does insulin improve cardiac contractility via the PI3K/Akt pathway in isolated rat hearts?
Population
Excised hearts from rats under pentobarbital anesthesia (n = 8 in each group)
Comparison
Insulin doses (0, 0.5, 5, 50 IU/L) with vs without wortmannin
Design
Randomized ex vivo animal study
Authors
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Should not change clinical practice; leaves open translation of rat heart inotropy to humans.
Does insulin improve cardiac contractility via the PI3K/Akt pathway in isolated rat hearts?
p-value: p=<0.05
Insulin exerts a dose-dependent, temporary positive inotropic effect on cardiac tissue mediated by the PI3K/Akt pathway, which can lead to tachyphylaxis at high doses.
Nakadate et al. (2022) studied Normal isolated rat hearts (n=64). Insulin (with or without wortmannin) vs. Insulin 0 IU/L (Control) was evaluated on Maximum left ventricular derivative of pressure development (LV dP/dt max) at 3 minutes (p=<0.05). Insulin at 5 and 50 IU/L increased maximum left ventricular derivative of pressure development by 14% and 48%, respectively, at 3 minutes compared with baseline in isolated rat hearts.
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