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Figure 1 | Critical Care

Figure 1

From: Phosphodiesterase 4D disruption causes β2 adrenergic receptors to behave like β1 adrenergic receptors in vivo

Figure 1

Starling axis. Measurements of LVEDV and stroke volume were obtained using electrocardiogram-gated MRI and plotted on a Starling axis. By 8 months of age the β1/PDE4D DKO mice demonstrated left ventricular dilatation similar to that experienced by β2KO mice during continuous catecholamine (isoprotenerol) administration. In β2KO mice, the dilatation has been attributed to cardiac remodeling caused by continuous β1 adrenergic receptor activation in the absence of β2 adrenergic receptor-mediated protective effects. The absence of the β1 adrenergic receptor in the β1/PDE4D DKO mice suggests that the PDE4D disruption causes β2 adrenergic receptors to behave like β1 adrenergic receptors in vivo, a phenomenon that has been shown to occur in vitro.

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