Nishimura H, Yoshikawa T, Anzai T, Baba A, Kobayashi N, Wainai Y, Ogawa S
Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
Jpn Circ J. 1998 Oct;62(10):773-8. doi: 10.1253/jcj.62.773.
This study focused on the role of the baroreceptor-mediated control during the compensatory process after acute left ventricular overloading induced by aortic regurgitation (AR). Baroreceptor-heart rate sensitivity was measured using a phenylephrine-induced increase in blood pressure according to the steady state method before, 1 day, 1 week and 4 weeks after production of AR in 7 rabbits, and compared with 6 other rabbits that underwent a sham operation. Blood pressure was monitored noninvasively using Finapres in the unanesthetized state. Four weeks after the procedure, the left ventricular diameters of both end-diastole and end-systole were larger in the rabbits with AR than in the sham-operated rabbits. There was no difference in the left ventricular end-diastolic pressure or cardiac output. Left ventricular weight was higher in the rabbits with AR than in the sham-operated rabbits. Myocardial beta-adrenergic receptor density and norepinephrine content were comparable between the two groups. Baroreceptor-heart rate sensitivity significantly decreased 1 week after production of AR, and this alteration in sensitivity was partially restored 4 weeks after production of AR. These findings suggested that the altered baroreceptor-heart rate sensitivity was reversible, relating to the compensatory process after acute left ventricular overloading, and that these changes had some role in its pathophysiology.
