scholarly journals Arterial and Left Ventricular Pressures Illude Transient Alternans of Contractility during Postextrasystolic Potentiation

2004 ◽  
Vol 54 (4) ◽  
pp. 373-383 ◽  
Author(s):  
G. Iribe ◽  
J. Shimizu ◽  
S. Mohri ◽  
Yi Syuu ◽  
T. Imaoka ◽  
...  
1984 ◽  
Vol 247 (3) ◽  
pp. H371-H379 ◽  
Author(s):  
P. A. Anderson ◽  
K. L. Glick ◽  
A. Manring ◽  
C. Crenshaw

Developmental changes in contractility were sought in the fetal and postnatal sheep heart by using postextrasystolic potentiation and force, pressure, and wall-motion measures. Two different preparations were used, isolated myocardium and the chronically instrumented lamb. In the isolated muscle, the following increased significantly with age: force of contraction, the maximum rate of rise of force, and postextrasystolic potentiation. In the intact heart prior to birth [period of study, 20 +/- 4 (SD) days] heart rate (HR) fell significantly, and the following increased significantly: postextrasystolic potentiation [measured with the maximum rate of rise of left ventricular (LV) pressure (Pmax)], LV peak systolic pressure (LVP), end-diastolic dimension (EDD), end-systolic dimension (ESD), and aortic diastolic pressure. After birth, LVP, Pmax, HR, LVEDP, EDD, and ESD increased and postextrasystolic potentiation fell. The latter fall was not found in vitro and probably demonstrates a transient change in contractility, related to hormonal or neural stimulation. Over the subsequent postnatal days (6-122 days), HR fell while potentiation, EDD, and ESD increased significantly. Both in vitro and in vivo, the overall increase in postextrasystolic potentiation demonstrates a similar long-term change in contractility. The similarity of this change to that induced by mild hypertrophy suggests that development and mild hypertrophy alter myocardial contractility through a common mechanism.


2000 ◽  
Vol 278 (5) ◽  
pp. H1464-H1472 ◽  
Author(s):  
Shinyu Lee ◽  
Junichi Araki ◽  
Takeshi Imaoka ◽  
Masaki Maesako ◽  
Gentaro Iribe ◽  
...  

Postischemic myocardial stunning halved left ventricular contractility [end-systolic maximum elastance ( E max)] and doubled the O2 cost of E max in excised cross-circulated canine heart. We hypothesized that this increased O2 cost derived from energy-wasteful myocardial Ca2+ handling consisting of a decreased internal Ca2+ recirculation, some futile Ca2+ cycling, and a depressed Ca2+ reactivity of E max. We first calculated the internal Ca2+ recirculation fraction (RF) from the exponential decay component of postextrasystolic potentiation. Stunning significantly accelerated the decay and decreased RF from 0.63 to 0.43 on average. We then combined the decreased RF with the halved E maxand its doubled O2 cost and analyzed total Ca2+handling using our recently developed integrative method. We found a decreased total Ca2+ transport and a considerable shift of the relation between futile Ca2+ cycling and Ca2+ reactivity in an energy-wasteful direction in the stunned heart. These changes in total Ca2+ handling reasonably account for the doubled O2 cost of E max in stunning, supporting the hypothesis.


1983 ◽  
Vol 51 (3) ◽  
pp. 583-590 ◽  
Author(s):  
John D. Carroll ◽  
Rene Widmer ◽  
Otto M. Hess ◽  
Heinz O. Hirzel ◽  
Hans P. Krayenbuehl

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