Key result
Spontaneously hypertensive rats exhibited lower stroke volume and a 4-fold reduction in the efficiency of the Frank-Starling mechanism compared to normotensive controls.
Why the study?
Does spontaneous hypertension impair cardiohemodynamics and the Frank-Starling mechanism in a rat model?
Does spontaneous hypertension impair cardiohemodynamics and the Frank-Starling mechanism in a rat model?
Answers are grounded in this paper and cite their sources.
Spontaneously hypertensive rats exhibit reduced cardiac efficiency, increased arterial stiffness, and an impaired Frank-Starling mechanism, leading to higher myocardial oxygen consumption.
We studied cardiohemodynamics and efficiency Frank-Starling mechanism in 6-month-old spontaneously hypertensive rats (SHR) and age-matched Wistar rats, using pressure-volume (PV) conductance catheter system (Millar Instruments, Houston, TX) to evaluate systolic and diastolic function in vivo. Rats were anesthetized with urethane. Cardiohemodynamics analyzed using PVAN 3.6 (Millar Instruments). We found that systolic and diastolic function of the heart in spontaneously hypertensive rats were lower, than in controls. We have shown, inhibition of the efficiency Frank-Starling mechanism, increasing arterial stiffness in spontaneously hypertensive rats. It's shown, less efficiency heart work, with more energy and more oxygen consumption in spontaneously hypertensive rats, may be associated with increasing arterial stiffness and decrease functional reserve of the heart.
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Dorofeieva et al. (2012) studied Spontaneous hypertension (n=16). Spontaneous hypertension vs. Normotensive Wistar rats was evaluated on Stroke volume (µl) (p=<0.001). Spontaneously hypertensive rats exhibited lower stroke volume and a 4-fold reduction in the efficiency of the Frank-Starling mechanism compared to normotensive controls.
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