Starved of oxygen embryos can be "programmed" for heart disease

15:59
Starved of oxygen embryos can be "programmed" for heart disease -

The heart disease has long been rated the leading cause of death worldwide. Known as the silent killer, he tracks his prey from conception to adulthood, often striking without warning. A new study suggests that one of the risk factors can begin even before birth, showing how low oxygen in the uterus or fetal hypoxia can impair heart later in life.

fetal hypoxia can be caused by a variety of factors. Mothers living at high altitude, smoke or develop diabetes during pregnancy may starve their oxygen embryos. When fetal hypoxia is prolonged, the heart and the vessels of the embryo change: The walls of the heart and aorta grow thicker, and blood vessels may become less sensitive to signals to relax, making it difficult for blood to flow. Previous research had suggested that these modifications, even if they help the unborn baby survive, are rampant in adulthood, increasing the risk of cardiovascular disease.

But it is not clear how this happens. Physiologist Dino Giussani and colleagues at the University of Cambridge in the UK hypothesized that hypoxia promotes injury in the uterus caused mainly by stress when the low oxygen molecules creates a highly overload reactive called free radicals.

To test this idea, the team conducted an experiment with four groups of pregnant rats: two sets undergoing hypoxic pregnancy and two controls. To create hypoxia, they placed pregnant rats in a room that kept their oxygen levels to 13%, rather than the norm of 21% for the majority of their pregnancy. Some rodents (those in one of two groups and hypoxia in one of the two control groups) received vitamin C water daily to its antioxidant effects.

When puppies are born, the researchers noted significant differences between the groups. Rats born to the hypoxic pregnancy without treatment with vitamin C showed a thickening of the walls of the aorta up to 170% above normal and molecular markers of disease, an increase such as increased protein heat shock the heart, cardiac oxidative stress signal. When the puppies have grown to adulthood in about 4 months, their hearts pumped always harder and faster than normal, which in the long term is a known predictor of eventual heart failure. The pups also showed blockages in their major arteries, just as people in development of cardiovascular diseases are. These changes are not visible in the offspring of newborns and adults hypoxic pregnancies treated with vitamin C, reports the online team today PLoS ONE .

Giussani said the results show that fetal hypoxia programs at both the heart and circulation in adulthood by oxidative stress in the womb. "Although the link between adverse conditions during pregnancy and cardiovascular disease in later life, has been established for many years," he said, "which explains the link had remained an enigma."

The research is "fascinating," says physiologist David Barker of the University of Southampton in the UK and Oregon Health and Science University in Portland, who some consider the father of fetal origins of the field of adult diseases, an offshoot of the so-called development programming. Much of the emphasis in the past has been on long-term consequences of nutrition. The work of the team of Giussani, he said, "highlights the importance of one of the other challenges that the human fetus is facing, which is getting enough oxygen." Adds John Challis from the University of Toronto in Canada, "These results are very interesting taking us several steps forward. ... Now that we understand the mechanism, we are much closer to being able to intervene. " A leading researcher in development programming, Challis said that this study opens the door to thinking about the fight against fetal hypoxia in humans with antioxidant treatment.

Giussani agreed that the ultimate goal is to identify a clinical intervention to prevent heart disease. He is quick to add, however, that vitamin C may not be the antioxidant of choice for the man because of its effects on the human fetal tissue has not been well studied. The next step, he said, is to take research on the human level, specifically looking at the high altitude effect of pregnancy, where there is less oxygen in all the uterus and heart conditions later in life.

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