Arterial and left ventricular pressures illude transient alternans of contractility during postextrasystolic potentiation.

Autor: Iribe G; Department of Cardiovascular Physiology, Okayama University Graduate School of Medicine and Dentistry, Okayama 700-8558, Japan. pepper@xa2.so-net.ne.jp, Shimizu J, Mohri S, Syuu Y, Imaoka T, Kiyooka T, Araki J, Kanmura Y, Kajiya F, Suga H
Jazyk: angličtina
Zdroj: The Japanese journal of physiology [Jpn J Physiol] 2004 Aug; Vol. 54 (4), pp. 373-83.
DOI: 10.2170/jjphysiol.54.373
Abstrakt: We have previously found that the postextrasystolic (PES) potentiation (PESP) of the left ventricular (LV) contractility (Emax) decays typically in transient alternans even in the normally ejecting canine heart. This contradicted the general expectation that arterial pressure (AP) and LV pressure (LVP) usually decay exponentially during PESP. We hypothesized this contradiction to be due to the different cardiodynamic behaviors of AP and LVP from LV Emax during PESP. We tested this hypothesis by measuring AP, LVP, LV volume, Emax, effective arterial elastance (Ea) as an index of afterload, and pulse pressure (PP) during PESP in eight anesthetized open-chest dogs by using the conductance catheter system. We changed Ea by changing the total peripheral resistance (TPR) with methoxamine hydrochloride (iv) and repeated the measurements. Although the Emax alternans patterns during PESP were comparable between the normal and high afterloads, LVP and PP were slightly potentiated and alternated under the normal afterload, whereas LVP and PP were obviously potentiated and alternated under the high afterload. We also simulated the effects of Ea/Emax on the transient alternans of AP and LVP on a computer. Despite the same alternans pattern of Emax, a higher Ea/Emax, which is typical in heart failure, caused a larger PP alternans, whereas a lower Ea/Emax, which is typical in normal hearts, almost eliminated it. These results suggest that a transient alternans of LV contractility during PESP could be overlooked when AP and LVP are monitored in in situ normal hearts.
Databáze: MEDLINE