Intrinsic resistance of female hearts to an ischemic insult is abrogated in primary cardiac hypertrophy

Bell, James R., Porrello, Enzo R., Huggins, Catherine E., Harrap, Stephen B. and Delbridge, Lea M.D 2008, Intrinsic resistance of female hearts to an ischemic insult is abrogated in primary cardiac hypertrophy, American journal of physiology : heart and circulatory physiology, vol. 294, no. 4, pp. 514-522.

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Title Intrinsic resistance of female hearts to an ischemic insult is abrogated in primary cardiac hypertrophy
Author(s) Bell, James R.
Porrello, Enzo R.
Huggins, Catherine E.
Harrap, Stephen B.
Delbridge, Lea M.D
Journal name American journal of physiology : heart and circulatory physiology
Volume number 294
Issue number 4
Start page 514
End page 522
Publisher American Physiological Society
Place of publication Bethesada, Md.
Publication date 2008-04
ISSN 0363-6135
1522-1539
Keyword(s) sex differences
intracellular signaling
cardiac function
ischemia-reperfusion
Summary Important sex differences in cardiovascular disease outcomes exist, including conditions of hypertrophic cardiomyopathy and cardiac ischemia. Studies of sex differences in the extent to which load-independent (primary) hypertrophy modulates the response to ischemia-reperfusion (I/R) damage have not been characterized. We have previously described a model of primary genetic cardiac hypertrophy, the hypertrophic heart rat (HHR). In this study the sex differences in HHR cardiac function and responses to I/R [compared to control normal heart rat (NHR)] were investigated ex vivo. The ventricular weight index was markedly increased in HHR female (7.82 ± 0.49 vs. 4.80 ± 0.10 mg/g; P < 0.05) and male (5.76 ± 0.22 vs. 4.62 ± 0.07 mg/g; P < 0.05) hearts. Female hearts of both strains exhibited a reduced basal contractility compared with strain-matched males [maximum first derivative of pressure (dP/dtmax): NHR, 4,036 ± 171 vs. 4,258 ± 152 mmHg/s; and HHR, 3,974 ± 160 vs. 4,540 ± 259 mmHg/s; P < 0.05]. HHR hearts were more susceptible to I/R (I = 25 min, and R = 30 min) injury than NHR hearts (decreased functional recovery, and increased lactate dehydrogenase efflux). Female NHR hearts exhibited a significantly greater recovery (dP/dtmax) post-I/R relative to male NHR (95.0 ± 12.2% vs. 60.5 ± 9.4%), a resistance to postischemic dysfunction not evident in female HHR (29.0 ± 5.6% vs. 25.9 ± 6.3%). Ventricular fibrillation was suppressed, and expression levels of Akt and ERK1/2 were selectively elevated in female NHR hearts. Thus the occurrence of load-independent primary cardiac hypertrophy undermines the intrinsic resistance of female hearts to I/R insult, with the observed abrogation of endogenous cardioprotective signaling pathways consistent with a potential mechanistic role in this loss of protection.
Notes Checked Ulrich's - Pamh, 09/09/09
Language eng
Field of Research 110201 Cardiology (incl Cardiovascular Diseases)
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
HERDC collection year 2008
Copyright notice ©2008, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30018617

Document type: Journal Article
Collection: School of Exercise and Nutrition Sciences
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Created: Wed, 09 Sep 2009, 16:55:48 EST

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