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  • Title: Effects of vasoactive drugs upon haemodynamic power and input impedance in normal rats.
    Author: Wright G.
    Journal: Cardiovasc Res; 1991 Nov; 25(11):923-9. PubMed ID: 1813120.
    Abstract:
    STUDY OBJECTIVE: The objectives were (a) to describe the effects of vasoactive drugs in normal rats upon cardiovascular function assessed by computing aortic haemodynamic power and input impedance, each separated into their component parts, and (b) to study the relationship between left ventricular pulsatile power output and the vascular impedance. DESIGN: Haemodynamic power and input impedance were computed from measurements of aortic blood pressure and flow in normal rats. The rats were then given an infusion of a vasoconstrictor drug (methoxamine) followed by a vasodilator drug (hydralazine) in order to study the effects of changes in vascular impedance upon haemodynamic power. EXPERIMENTAL MATERIAL: The measurements were made on pentobarbitone anaesthetised male Wistar rats of approximately 400 g body weight (10 infused with Hartmann's solution as controls and 10 infused with the drugs). MEASUREMENTS AND MAIN RESULTS: Aortic total haemodynamic power was between 9.96 mW and 10.37 mW during the control period and reached a maximum of 11.36 mW during the methoxamine infusion, but this difference was not statistically significant. It then decreased significantly to 4.32 mW by the end of the hydralazine infusion. Pulsatile power was only 0.32(SEM 0.08) mW (2.8% of the total power) in the control state and decreased to 0.12(0.1) mW (1.7%) during the methoxamine infusion, but increased to 0.59(0.15) mW (12.5%) by the end of the hydralazine infusion. The vascular effects were complex and involved all four of the input impedance parameters--peripheral resistance, characteristic resistance, arterial compliance, and inertance. Reflex responses of the vascular wall were apparent as temporal changes in characteristic resistance and arterial compliance. CONCLUSIONS: Changes in cardiovascular function can be described by computing haemodynamic power and input impedance and then separating these into their component parts. Administration of the vasoactive drugs affected left ventricular mean and pulsatile power output and all four components of the input impedance. The frequency distribution of left ventricular pulsatile power output may be matched to the vascular impedance in order to optimise tissue perfusion.
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