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Researchers found that high blood sugar (glucose) causes stronger contraction of blood vessels and also identified a protein associated with this increased contraction. The findings could lead to new treatments to improve outcomes after heart attack or stroke, the study authors said.
A heart attack occurs when an artery that provides blood to the heart is blocked. High blood sugar at the time of a heart attack could make this blockage more severe by causing the artery to contract, resulting in a higher risk of complications, according to the research team at the University of Leicester in England.
"We have shown that the amount of sugar, or glucose, in the blood changes the behavior of blood vessels, making them contract more than normal. This could result in higher blood pressure, or could reduce the amount of blood that flows through vital organs," Richard Rainbow, a lecturer in cardiovascular cell physiology, said in a university news release.
"This was an experimental lab study, which means that we can draw conclusions about cause and effect in a controlled environment," he added.
"Here, we have identified a known signaling protein family, protein kinase C, is a key part of this enhanced contractile response, and have also shown in our experiments that we can restore the normal level of contractile response and reverse the effects on the heart, with inhibitors of these proteins," Rainbow said.
"This is the first study to show direct evidence of blood vessel contraction to glucose, and the potential mechanism behind this contractile response. In the experimental models we used in this study, including human blood vessels, increasing glucose to the levels that could be reached after a large meal altered vascular contraction," Rainbow said.
"A large number of people who suffer a heart attack will have high glucose due to the 'stress response'. This means that even people who are not diabetic may [have high blood sugar] during a heart attack," he explained.
The study was published online recently in the British Journal of Pharmacology.
-- Robert Preidt
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SOURCE: University of Leicester, news release, Jan. 5, 2016