PMID- 17993597
OWN - NLM
STAT- MEDLINE
DCOM- 20080228
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 294
IP  - 1
DP  - 2008 Jan
TI  - Susceptibility to systolic dysfunction in the myocardium from chronically 
      infarcted spontaneously hypertensive rats.
PG  - H372-8
AB  - We explored whether the hypertensive heart is susceptible to myocardial 
      dysfunction in viable noninfarcted tissue post-myocardial infarction (MI), the 
      potential mechanisms thereof, and the impact of these changes on pump function. 
      Six to seven months after the ligation of the left anterior descending coronary 
      artery, left ventricular (LV) myocardial systolic function, as assessed from the 
      percent shortening of the noninfarcted lateral wall segmental length determined 
      over a range of filling pressures (ultrasonic transducers placed in the lateral 
      wall in anaesthetized, open-chest, ventilated rats) and the percent thickening of 
      the posterior wall (echocardiography), was reduced in infarcted spontaneous 
      hypertensive rats (SHR-MI) (P < 0.05) but not in normotensive Wistar-Kyoto 
      (WKY-MI) animals compared with corresponding controls [SHR-sham operations (Sham) 
      and WKY-Sham]. This change in the regional myocardial function in SHR-MI, but not 
      in WKY-MI, occurred despite a similar degree of LV dilatation (increased LV 
      end-diastolic dimensions and volume intercept of the LV end-diastolic 
      pressure-volume relation) in SHR-MI and WKY-MI rats and a lack of difference in 
      LV relative wall thinning, LV wall stress, apoptosis [terminal deoxynucleotidyl 
      transferase biotin-dUTP nick-end labeling (TUNEL)], or necrosis (pathological 
      score) between SHR-MI and WKY-MI rats. Although the change in regional myocardial 
      function in the SHR-MI group was not associated with a greater reduction in 
      baseline global LV chamber systolic function [end-systolic elastance (LV E(es)) 
      and endocardial fractional shortening determined in the absence of an adrenergic 
      stimulus], in the presence of an isoproterenol challenge, noninfarct-zone LV 
      systolic myocardial dysfunction manifested in a significant reduction in LV E(es) 
      in SHR-MI compared with WKY-MI and SHR and WKY-Sham rats (P < 0.04). In 
      conclusion, these data suggest that with chronic MI, the hypertensive heart is 
      susceptible to the development of myocardial dysfunction, a change that cannot be 
      attributed to excessive chamber dilatation, apoptosis, or necrosis, but which in 
      turn contributes toward a reduced cardiac adrenergic inotropic reserve.
FAU - Norton, Gavin R
AU  - Norton GR
AD  - Cardiovascular Pathophysiology and Genomics Research Unit, School of Physiology, 
      University of the Witwatersrand Medical School, 7 York Road, Parktown 2193, 
      Johannesburg, South Africa. gavin.norton@wits.ac.za
FAU - Veliotes, Demetri G A
AU  - Veliotes DG
FAU - Osadchii, Oleg
AU  - Osadchii O
FAU - Woodiwiss, Angela J
AU  - Woodiwiss AJ
FAU - Thomas, D Paul
AU  - Thomas DP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071109
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Cardiotonic Agents)
RN  - L628TT009W (Isoproterenol)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cardiotonic Agents/pharmacology
MH  - Coronary Vessels/surgery
MH  - Disease Models, Animal
MH  - Hypertension/*complications/pathology/physiopathology
MH  - Isoproterenol/pharmacology
MH  - Ligation
MH  - Male
MH  - *Myocardial Contraction/drug effects
MH  - Myocardial Infarction/*complications/pathology/physiopathology
MH  - Myocardium/pathology
MH  - Necrosis
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Stress, Mechanical
MH  - *Systole
MH  - Time Factors
MH  - Ventricular Dysfunction, Left/*etiology/pathology/physiopathology
MH  - Ventricular Remodeling
EDAT- 2007/11/13 09:00
MHDA- 2008/02/29 09:00
CRDT- 2007/11/13 09:00
PHST- 2007/11/13 09:00 [pubmed]
PHST- 2008/02/29 09:00 [medline]
PHST- 2007/11/13 09:00 [entrez]
AID - 01024.2007 [pii]
AID - 10.1152/ajpheart.01024.2007 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2008 Jan;294(1):H372-8. doi: 
      10.1152/ajpheart.01024.2007. Epub 2007 Nov 9.