Cardiovascular susceptibility to in vivo ischemic myocardial injury in male and female rat offspring exposed to prenatal hypoxia

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.


2016 ◽  
Vol 32 (10) ◽  
pp. S276-S277
Author(s):  
A. Shah ◽  
N. Matsumura ◽  
A. Quon ◽  
J.S. Morton ◽  
J.R. Dyck ◽  
...  


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.



2017 ◽  
Vol 131 (23) ◽  
pp. 2791-2794 ◽  
Author(s):  
Michal Zeman ◽  
Monika Okuliarova

Cardiovascular diseases (CVDs) are the leading cause of mortality and hypertension contributes substantially to the incidence of stroke, coronary artery disease, heart failure, atrial fibrillation and peripheral vascular disease. The origin of hypertension is clearly multifactorial, and a complex and multifaceted approach is necessary to decrease its incidence. The most recognizable factors involved in reducing the incidence of hypertension are prevention, early diagnosis and treatment; however, the importance of the foetal environment and early postnatal development has recently been considered. In clinical practice, these factors are still frequently overlooked, probably because of a lack of knowledge about the underlying mechanisms and effective treatment or prevention. Pathophysiological mechanisms underlying the prenatal programming of CVDs were investigated in the study by Shah et al. published recently in Clinical Science (2017) 131(17), 2303–2317. The study explored cardiac susceptibility of adult male and female rat offspring to ischaemic myocardial injury due to prenatal exposure to hypoxia. The results demonstrated significant changes in global cardiac function and left ventricular dilatation following myocardial infarction in rat offspring prenatally exposed to hypoxia. The effects were gender specific and occurred only in males, whereas females were protected. These findings are important from several perspectives. First, they point to the fact that an inadequate foetal environment can increase susceptibility to death from myocardial infarction. Second, during their reproductive life, females are better protected from cardiovascular insult than males, but it is not known if they lose this advantage after menopause, and can be equally at risk as males.



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 ◽  
Author(s):  
Lisa Koshko ◽  
Lucas K. Debarba ◽  
Mikaela Sacla ◽  
Juliana M.B. de Lima ◽  
Olesya Didyuk ◽  
...  

SummaryEnvironmental chemicals play a significant role in the development of metabolic disorders, especially when exposure occurs early in life. We have recently demonstrated that benzene exposure, at concentrations relevant to a cigarette smoke, induces a severe metabolic imbalance in a sex-specific manner affecting male but not female mice. However, the roles of benzene in the development of aberrant metabolic outcomes following gestational exposure, remain largely unexplored. In this study, we exposed pregnant C57BL/6JB dams to benzene at 50 ppm or filtered air for 5 days/week (6h/day from gestational day 1 to birth) and studied male and female offspring metabolic phenotypes in their adult life. While no changes in body weight or body composition were observed between groups, 4-month-old male and female offspring exhibited reduced parameters of energy homeostasis (VO2, VCO2, and heat production). However, only male offspring from benzene-exposed dams were glucose intolerant and insulin resistant at this age. By six months of age, both male and female offspring displayed glucose and insulin intolerance, associated with elevated expression of hepatic gluconeogenesis and inflammatory genes. Additionally, this effect was accompanied by elevated insulin secretion and increased beta-cell mass only in male offspring. Thus, gestational benzene exposure can reprogram offspring for increased susceptibility to the metabolic imbalance in adulthood with differential sensitivity between sexes.



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 ◽  
...  


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