| Summary: | Diastolic dysfunction is the hemodynamic hallmark of hypertensive heart disease. Tau (τ) has been used to describe left ventricle relaxation. The relationship between τ and afterload has been controversial. Our goal was to demonstrate this relationship in mice, because genetically-modified mouse models have been used extensively for studies in cardiovascular diseases.Increased arterial load was produced by phenylephrine administration (50 µg/kg iv) (n = 10). A series of pressure-volume loops was recorded with a Millar conductance catheter in vivo as the left ventricle pressure reached the maximum. The arterial load was expressed as Ea (effective arterial elastance). Tau values were computed using three mathematical methods: τWeiss, τGlantz, and τLogistic.A correlation plot between τ and Ea showed a biphasic relationship a flat phase I and an inclined phase II. The existence of an inflection point was proved mathematically with biphasic linear regression. Pressure-volume area (PVA), a parameter linearly related to myocardial O2 consumption (MVO2), was found to be directly proportional to Ea. The plot of τ versus PVA was also biphasic.We concluded that a small increase of the arterial load by phenylephrine increased PVA (index of MVO2) but had little effect on τ. However, after an inflection point, further increase of arterial load and PVA resulted in the linear increase of τ.
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