CARDIOVASCULAR SUSCEPTIBILITY TO ISCHEMIC MYOCARDIAL INJURY IN MALE AND FEMALE RAT OFFSPRING BORN GROWTH RESTRICTED

2016 ◽  
Vol 32 (10) ◽  
pp. S276-S277
Author(s):  
A. Shah ◽  
N. Matsumura ◽  
A. Quon ◽  
J.S. Morton ◽  
J.R. Dyck ◽  
...  
2017 ◽  
Vol 131 (17) ◽  
pp. 2303-2317 ◽  
Author(s):  
Amin Shah ◽  
Nobutoshi Matsumura ◽  
Anita Quon ◽  
Jude S. Morton ◽  
Jason R.B. Dyck ◽  
...  

Intrauterine growth restriction (IUGR) following prenatal hypoxia exposure leads to a higher risk of developing cardiovascular disease (CVD) in later life. Our aim was to evaluate cardiac susceptibility and its pathophysiological mechanisms following acute myocardial infarction (MI) in adult rat offspring exposed to prenatal hypoxia. Male and female rat offspring, which experienced normoxia (21% O2) or hypoxia (11% O2) in utero underwent sham or MI surgery at 12 weeks of age. Echocardiographic data revealed that both sexes had systolic dysfunction following MI surgery, independent of prenatal hypoxia. Male offspring exposed to prenatal hypoxia, however, had left ventricular dilatation, global dysfunction, and signs of diastolic dysfunction following MI surgery as evident by increased left ventricular internal diameter (LVID) during diastole (MI effect, P<0.01), Tei index (MI effect, P<0.001), and E/E′ ratio (prenatal hypoxia or MI effect, P<0.01). In contrast, diastolic dysfunction in female offspring was not as evident. Cardiac superoxide levels increased only in prenatal hypoxia exposed male offspring. Cardiac sarcoendoplasmic reticulum Ca2+-ATPase2a (SERCA2a) levels, a marker of cardiac injury and dysfunction, decreased in both male and female MI groups independent of prenatal hypoxia. Prenatal hypoxia increased cardiac ryanodine receptor 2 (RYR2) protein levels, while MI reduced RYR2 in only male offspring. In conclusion, male offspring exposed to prenatal hypoxia had an increased susceptibility to ischemic myocardial injury involving cardiac phenotypes similar to heart failure involving diastolic dysfunction in adult life compared with both offspring from healthy pregnancies and their female counterparts.


2020 ◽  
Vol 718 ◽  
pp. 134700 ◽  
Author(s):  
John T. Madden ◽  
Shannon M. Thompson ◽  
Christy M. Magcalas ◽  
Jennifer L. Wagner ◽  
Derek A. Hamilton ◽  
...  

2003 ◽  
Vol 28 (5) ◽  
pp. 385-394 ◽  
Author(s):  
Masako YAMAMOTO ◽  
Mitsuyuki SHIRAI ◽  
Kana SUGITA ◽  
Naoko NAGAI ◽  
Yumi MIURA ◽  
...  

2020 ◽  
Vol 158 (6) ◽  
pp. S-165-S-166
Author(s):  
Urszula Glowacka ◽  
Kinga Gawlinska ◽  
Dawid Gawlinski ◽  
Marcin Magierowski ◽  
Zbigniew Sliwowski ◽  
...  

2002 ◽  
Vol 24 (6) ◽  
pp. 522-530 ◽  
Author(s):  
Josephine M. Johns ◽  
Deborah A. Lubin ◽  
Jeffrey A. Lieberman ◽  
Jean M. Lauder

2019 ◽  
Vol 82 (10) ◽  
pp. 603-615 ◽  
Author(s):  
Clément Rosique ◽  
Dalila Lebsir ◽  
Philippe Lestaevel ◽  
Sheherazade Benatia ◽  
Pierre Guigon ◽  
...  

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Janice Dye ◽  
Erica Stewart ◽  
Mette Schladweiler ◽  
Lisa Copeland ◽  
Urmila Kodavanti ◽  
...  

2002 ◽  
Vol 174 (3) ◽  
pp. 411-418 ◽  
Author(s):  
D Swolin-Eide ◽  
J Dahlgren ◽  
C Nilsson ◽  
K Albertsson Wikland ◽  
A Holmang ◽  
...  

Events occurring early in life or prenatally are able to play important roles in the pathogenesis of diseases in adult life. Different sorts of stress or hormonal influences, during particular periods of pregnancy, may result in persisting or transient changes in physiology. Glucocorticoids are used for the treatment of a variety of diseases, to promote organ maturation and to prevent preterm delivery. Glucocorticoids are also known to affect skeletal growth and adult bone metabolism. The aim of the present study was to investigate whether exposure to dexamethasone (Dex) during fetal life has any effect on skeletal growth and/or bone mineral density in adult rat offspring. Pregnant rats were given injections of either Dex (100 micro g/kg) or vehicle on days 9, 11 and 13 of gestation. Dex-exposed male but not female rat offspring showed transient increases in crown-rump length and tibia and femur lengths at 3-6 weeks of age. In contrast, the cortical bone dimensions were altered in 12-week-old female but not male Dex-exposed offspring. The areal bone mineral densities of the long bones and the spine, as determined by dual X-ray absorptiometry, and trabecular as well as cortical volumetric bone mineral density, as measured using peripheral quantitative computerized tomography, were unchanged in both male and female Dex-exposed offspring. In conclusion, prenatal Dex exposure affects skeletal growth in a gender-specific manner, while the mineralization of bones is unaffected in both male and female offspring.


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