Document Detail


Myofilament calcium sensitization delays decompensated hypertrophy differently between the sexes following myocardial infarction.
MedLine Citation:
PMID:  21106909     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Contractile dysfunction is common to many forms of cardiovascular disease. Approaches directed at enhancing cardiac contractility at the level of the myofilaments during heart failure (HF) may provide a means to improve overall cardiovascular function. We are interested in gender-based differences in cardiac function and the effect of sarcomere activation agents that increase contractility. Thus, we studied the effect of gender and time on integrated arterial-ventricular function (A-V relationship) following myocardial infarction (MI). In addition, transgenic mice that overexpress the slow skeletal troponin I isoform were used to determine the impact of increased myofilament Ca(2+) sensitivity following MI. Based on pressure-volume (P-V) loop measurements, we used derived parameters of cardiovascular function to reveal the effects of sex, time, and increased myofilament Ca(2+) sensitivity among groups of post-MI mice. Analysis of the A-V relationship revealed that the initial increase was similar between the sexes, but the vascular unloading of the heart served to delay the decompensated stage in females. Conversely, the vascular response at 6 and 10 wk post-MI in males contributed to the continuous decline in cardiovascular function. Increasing the myofilament Ca(2+) sensitivity appeared to provide sufficient contractile support to improve contractile function in both male and female transgenic mice. However, the improved contractile function was more beneficial in males as the concurrent vascular response contributed to a delayed decompensated stage in female transgenic mice post-MI. This study represents a quantitative approach to integrating the vascular-ventricular relationship to provide meaningful and diagnostic value following MI. Consequently, the data provide a basis for understanding how the A-V relationship is coupled between males and females and the enhanced ability of the cardiovascular system to tolerate pathophysiological stresses associated with HF in females.
Authors:
Krystyna M Shioura; Mariam Farjah; David L Geenen; R John Solaro; Paul H Goldspink
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-11-24
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  300     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-02-03     Completed Date:  2011-04-05     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R361-8     Citation Subset:  IM    
Affiliation:
Department of Medicine, Section of Cardiology, University of Illinois at Chicago, Chicago, Illinois, USA.
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MeSH Terms
Descriptor/Qualifier:
Actin Cytoskeleton / physiology*
Animals
Calcium / physiology*
Cardiac Output / physiology
Cardiomegaly / etiology,  pathology,  physiopathology*
Female
Heart / physiopathology
Heart Failure / etiology,  pathology,  physiopathology*
Heart Rate / physiology
Hemodynamics / physiology
Male
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
Mice, Transgenic
Myocardial Contraction / physiology*
Myocardial Infarction / complications,  pathology,  physiopathology*
Myocardium / pathology
Protein Isoforms / genetics
Sex Characteristics*
Stroke Volume / physiology
Troponin I / genetics
Vascular Resistance / physiology
Ventricular Dysfunction, Left / physiopathology
Grant Support
ID/Acronym/Agency:
P01-HL-62426/HL/NHLBI NIH HHS; R01-HL-090523/HL/NHLBI NIH HHS; T32-HL-07692/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Protein Isoforms; 0/Troponin I; 7440-70-2/Calcium
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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