2006
DOI: 10.1097/01.gme.0000196593.44335.eb
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Medroxyprogesterone acetate inhibits the cardioprotective effect of estrogen in experimental ischemia-reperfusion injury

Abstract: In this study, we showed that the administration of MPA can inhibit the effects of E that lead to protection of the myocardium from reperfusion injury and that this involves both neutrophil-dependent and neutrophil-independent mechanisms.

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Cited by 22 publications
(15 citation statements)
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“…Progesterone significantly increases nitric oxide synthesis, whereas medroxyprogesterone acetate (MPA) impairs E 2 signaling both in vitro in human endothelial cells and in vivo in rats (30). In addition, MPA can inhibit the protective effect of E 2 on the rat myocardium after reperfusion injury (31). Drospirenone possesses characteristics closer to natural P than other synthetic progestins, and may provide certain advantages due to its effect on cardiovascular disease risk factors (32).…”
Section: Estrogenic Cardiovascular Protectionmentioning
confidence: 99%
“…Progesterone significantly increases nitric oxide synthesis, whereas medroxyprogesterone acetate (MPA) impairs E 2 signaling both in vitro in human endothelial cells and in vivo in rats (30). In addition, MPA can inhibit the protective effect of E 2 on the rat myocardium after reperfusion injury (31). Drospirenone possesses characteristics closer to natural P than other synthetic progestins, and may provide certain advantages due to its effect on cardiovascular disease risk factors (32).…”
Section: Estrogenic Cardiovascular Protectionmentioning
confidence: 99%
“…In contrast, numerous studies including the WHI have found the use of a synthetic progestin will result in an increase in cardiovascular risk factors, including worsening of lipid profiles, [124][125][126][127][128][129][130][131][132][133][134][135][136][137][138][139] prevention of normal vasodilation and promotion of coronary artery vasospasm, 126,127,130,134,139 increasing hypercoagulability, 13,140,141 worsening insulin resistance, 132,142-144 and promotion of cardiovascular plaque formation. 131,135,137,138,[145][146][147] In addition, synthetic progestin is proven to increase the actual incidence of myocardial infarction and stroke.…”
Section: Cardiovascular: Bioidentical Progesterone Versus Synthetic Pmentioning
confidence: 85%
“…131,135,137,138,[145][146][147] In addition, synthetic progestin is proven to increase the actual incidence of myocardial infarction and stroke. 2,139 Conversely, bioidentical progesterone has been shown not to have negative effects on the aforementioned cardiac risk factors in the short term in small studies. Unfortunately, these studies cannot be compared in scope and duration to the WHI study, leaving the question of whether bioidentical progesterone can actually protect from myocardial infarction or stroke in need of a more definitive answer.…”
Section: Cardiovascular: Bioidentical Progesterone Versus Synthetic Pmentioning
confidence: 98%
“…Infarct size is of pivotal importance for the extent of cardiac remodeling and chronic HF following MI. Booth and Lucchesi (2007) and Jeanes et al (2006) previously reported that an acute addition of MPA to an E2 treatment resulted in an extension of the necrotic zone after a cardiac ischemic effect. Nonetheless, those findings were limited to the events occurring during the first 4 hours after reperfusion injury.…”
Section: Discussionmentioning
confidence: 99%