Mechanically induced changes in action potential duration and left ventricular segment length in acute regional ischaemia in the in situ porcine heart

1994 ◽  
Vol 28 (4) ◽  
pp. 528-534 ◽  
Author(s):  
S M Horner ◽  
M J Lab ◽  
C F Murphy ◽  
D J Dick ◽  
B Zhou ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Left Ventricular ◽  
Segment Length ◽  
Porcine Heart ◽  
Left Ventricular Segment ◽  
Induced Changes

Ability of Activation Recovery Intervals to Assess Action Potential Duration During Acute No-Flow Ischemia in the In Situ Porcine Heart

1998 ◽  
Vol 9 (8) ◽  
pp. 832-844 ◽  
Author(s):  
JUNICHI EJIMA ◽  
DAVID MARTIN ◽  
CONNIE ENGLE ◽  
ZOE SHERMAN ◽  
SATOSHI KUNIMOTO ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Porcine Heart

scholarly journals Sympathomimetic modulation of load-dependent changes in the action potential duration in the in situ porcine heart

1996 ◽  
Vol 32 (1) ◽  
pp. 148-157 ◽  
Author(s):  
S.M. Horner ◽  
C.F. Murphy ◽  
B. Coen ◽  
D.J. Dick ◽  
M.J. Lab
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Porcine Heart

Hypertensive-diabetic cardiomyopathy in rats

1990 ◽  
Vol 258 (3) ◽  
pp. H793-H805 ◽  
Author(s):  
F. S. Fein ◽  
B. E. Zola ◽  
A. Malhotra ◽  
S. Cho ◽  
S. M. Factor ◽  
...  
Keyword(s):  
Action Potential ◽  
Right Ventricular ◽  
Action Potential Duration ◽  
Stimulus Frequency ◽  
Negative Inotropic Effect ◽  
Left Ventricular ◽  
Resting Membrane Potential ◽  
Contraction And Relaxation ◽  
And Control ◽  
Myocardial Pathology

Left ventricular papillary muscle function, transmembrane action potentials, myosin adenosinetriphosphatase (ATPase) and isoenzyme distribution, and myocardial pathology were studied in hypertensive (H), diabetic (D), hypertensive-diabetic (HD), and control (C) rats. There was approximately 50% relative left ventricular hypertrophy in H and HD rats. Relative lung and liver weights were greater in HD rats. Peak velocity of shortening tended to decrease progressively in H, D, and HD rats. The duration of contraction and relaxation was markedly prolonged in Ds and HDs. The length-developed tension relation was blunted in HDs. The negative inotropic effect of verapamil was similar in all groups. Resting membrane potential and amplitude were decreased in D and HD rats. Action potential duration was increased in H, D, and especially HD rats. The shortening of action potential duration with increased stimulus frequency was greater in H, D, and especially HD rats than in Cs. Left ventricular myosin ATPase and V1 isoenzyme content decreased progressively in H, D, and HD rats. Right ventricular V1 isoenzyme content was not affected in H rats but was markedly decreased in D and HD rats. Left (and right) ventricular pathology was unchanged in rats with diabetes but was increased in rats with hypertension. These data suggest that the combination of myocardial pathology (due to hypertension) and cellular dysfunction (caused mainly by diabetes) may result in cardiomyopathy and congestive heart failure in the HD rat.

Regression of LV hypertrophy with captopril normalizes membrane currents in rabbits

1998 ◽  
Vol 275 (4) ◽  
pp. H1216-H1224 ◽  
Author(s):  
Seth J. Rials ◽  
Xiaoping Xu ◽  
Ying Wu ◽  
Roger A. Marinchak ◽  
Peter R. Kowey
Keyword(s):  
Cell Membrane ◽  
Action Potential ◽  
Renal Artery ◽  
Current Density ◽  
Action Potential Duration ◽  
Left Ventricular ◽  
Membrane Current ◽  
Membrane Capacitance ◽  
Membrane Currents ◽  
Cell Membrane Capacitance

Recent studies indicate that regression of left ventricular hypertrophy (LVH) normalizes the in situ electrophysiological abnormalities of the left ventricle. This study was designed to determine whether regression of LVH also normalizes the abnormalities of individual membrane currents. LVH was induced in rabbits by renal artery banding. Single ventricular myocytes from rabbits with LVH at 3 mo after renal artery banding demonstrated increased cell membrane capacitance, prolonged action potential duration, decreased inward rectifier K+ current density, and increased transient outward K+ current density compared with myocytes from age-matched controls. Additional rabbits were randomized at 3 mo after banding to treatment with either vehicle or captopril for an additional 3 mo. Myocytes from LVH rabbits treated with vehicle showed persistent membrane current abnormalities. However, myocytes isolated from LVH rabbits treated with captopril had normal cell membrane capacitance, action potential duration, and membrane current densities. Captopril had no direct effect on membrane currents of either control or LVH myocytes. These data support the hypothesis that the action potential prolongation and membrane current abnormalities of LVH are reversed by regression. Normalization of membrane currents probably explains the reduced vulnerability to ventricular arrhythmia observed in this LVH model after treatment with captopril.

scholarly journals Key pathways associated with heart failure development revealed by gene networks correlated with cardiac remodeling

2008 ◽  
Vol 35 (3) ◽  
pp. 222-230 ◽  
Author(s):  
Zhong Gao ◽  
Andreas S. Barth ◽  
Deborah DiSilvestre ◽  
Fadi G. Akar ◽  
Yanli Tian ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Action Potential ◽  
Action Potential Duration ◽  
Expression Patterns ◽  
Left Ventricular ◽  
Ventricular Pacing ◽  
Extracellular Matrix Components ◽  
Transcriptional Changes ◽  
Rapid Ventricular Pacing

Heart failure (HF) is the leading cause of morbidity and mortality in the industrialized world. While the transcriptomic changes in end-stage failing myocardium have received much attention, no information is available on the gene expression patterns associated with the development of HF in large mammals. Therefore, we used a well-controlled canine model of tachycardia-induced HF to examine global gene expression in left ventricular myocardium with Affymetrix canine oligonucleotide arrays at various stages after initiation of rapid ventricular pacing ( days 3, 7, 14, and 21). The gene expression data were complemented with measurements of action potential duration, conduction velocity, and left ventricular end diastolic pressure, and dP/d t(max) over the time course of rapid ventricular pacing. As a result, we present a phenotype-centered gene association network, defining molecular systems that correspond temporally to hemodynamic and electrical remodeling processes. Gene Ontology analysis revealed an orchestrated regulation of oxidative phosphorylation, ATP synthesis, cell signaling pathways, and extracellular matrix components, which occurred as early as 3 days after the initiation of ventricular pacing, coinciding with the early decline in left ventricular pump function and prolongation of action potential duration. The development of clinically overt left ventricular dysfunction was associated with few additional changes in the myocardial transcriptome. We conclude that the majority of tachypacing-induced transcriptional changes occur early after initiation of rapid ventricular pacing. As the transition to overt HF is characterized by few additional transcriptional changes, posttranscriptional modifications may be more critical in regulating myocardial structure and function during later stages of HF.

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