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ABSTRACT: Endogenous oestrogen deficiency after menopause is associated with high risk of acute cardiac events and the protection of exogenous oestrogen supplements remains uncertain. This study investigates whether oestrogen therapy protects the heart from ischemic injury in oophorectomised rats.
Sexually mature female Sprague-Dawley rats (6 for each group) with bilateral oophorectomy underwent selective ligation (occlusion) of left coronary artery for 4 weeks. 17β-oestradiol (E2) supplements (10 μg, i.m., every other day) were started before (preventive-therapeutic supplement) or after coronary occlusion (therapeutic supplement).
In oophorectomised rats plasma levels of E2 declined from 1301 ± 80 to 196 ± 48 pmol/L (p<0.01) and cardiac expression of oestrogen receptors (ER) decreased by ∼60%. E2 supplements recovered the ER expression. Selective ligation of left coronary led myocardial infarction in the left ventricle, with an increase in plasma cardiac troponin I (cTn-I), decrease in systolic blood pressure (SBP), and reduction of left ventricular pressures. Preventive-therapeutic but not therapeutic E2 supplement reduced cTn-I levels (from 21.9 ± 2.0 to 6.0 ± 0.3 ng/mL, p<0.01), minimised infarction (from 37.0 ± 1.2% to 18.1 ± 2.3%, p<0.05), increased SBP (from 82 ± 4.2 to 97 ± 4.4mm Hg, p<0.05), and improved left ventricular end pressures in the oophorectomised rats following coronary occlusion.
Postmenopausal (ooporectomised) oestrogen supplement commenced before establishment of myocardial ischemia minimises myocardial infarction and ventricular dysfunction following the coronary artery occlusion. Cellular and molecular mechanisms underlying the cardiac protection of oestrogen therapy remain unclear, in which activation of cardiac ER expression and increasing in circulating CD90(+) stem cells may be involved.
International journal of cardiology 09/2011; 151(3):290-5. · 7.08 Impact Factor
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Sen Zhu,
Rui Xue,
Pan Zhao, Fen-Ling Fan,
Xiaomu Kong,
Senfeng Zheng,
Qifei Han,
Yi Zhu,
Nanping Wang,
Jichun Yang,
Youfei Guan
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ABSTRACT: Restenosis after angioplasty remains a major clinical problem. Prostaglandin E(2) (PGE(2)) plays an important role in vascular homeostasis. The PGE(2) receptor E-prostanoid 2 (EP2) is involved in the proliferation and migration of various cell types. We aimed to determine the role of EP2 in the pathogenesis of neointimal formation after vascular injury.
Wire-mediated vascular injury was induced in the femoral arteries of male wild-type (EP2+/+) and EP2 gene-deficient (EP2-/-) mice. In EP2+/+ mice, EP2 mRNA expression was increased in injured vessels for at least 4 weeks after vascular injury. Neointimal hyperplasia was markedly accelerated in EP2-/- mice, which was associated with increased proliferation and migration of vascular smooth muscle cells (VSMCs) and increased cyclin D1 expression in the neointima layer. Platelet-derived growth factor-BB (PDGF-BB) treatment resulted in more significant cell proliferation and migration in VSMCs of EP2-/- mice than in those of EP2+/+ mice. Activation and overexpression of EP2 attenuated PDGF-BB-elicited cell proliferation and migration, induced G(1)→S-phase arrest and reduced PDGF-BB-stimulated extracellular signal-regulated kinase phosphorylation in EP2+/+ VSMCs.
These findings reveal a novel role of the EP2 receptor in neointimal hyperplasia after arterial injury. The EP2 receptor may represent a potential therapeutic target for restenosis after angioplasty.
Arteriosclerosis Thrombosis and Vascular Biology 06/2011; 31(8):1739-47. · 6.37 Impact Factor
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ABSTRACT: 1. Patent ductus arteriosus (PDA) is a common congenital heart defect in premature infants. The present study was designed to determine the role of the prostaglandin (PG) E(2) pathway in the process of ductus arteriosus (DA) maturation and functional closure. 2. Changes in PGE(2) pathway-related enzymes and receptors in DA in preterm and term rabbits were examined at both the mRNA and protein levels. In addition, responses of DA rings to Po(2) and PGE(2) were determined. 3. Circulating PGE(2) levels remained high until 2 h after birth. High levels of the EP(4) receptor were found in preterm DA. These tissues were sensitive to PGE(2), which caused vessel dilation, but were insensitive to increased Po(2). In contrast, DA tissues from term rabbits exhibited an immediate contractile response to increased Po(2) and PGE(2) treatment resulted in vasoconstriction, which was associated with increased EP(3) and decreased EP(4) receptor expression in term DA. 4. In conclusion, the preterm PDA is maintained by high levels of PGE(2), which mainly binds to the EP(4) receptor under conditions of hypoxia. In contrast, in the term DA, in which levels of the EP(3) receptor are higher than in preterm DA, exposure to PGE(2) resulted in vasoconstriction under normoxic conditions. These findings suggest that blocking the EP(4) receptor may represent a more selective treatment for the preterm PDA, whereas activating the EP(3) receptor may be more suitable for the treatment of the term PDA.
Clinical and Experimental Pharmacology and Physiology 05/2010; 37(5-6):574-80. · 1.85 Impact Factor
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ABSTRACT: Summary1. Patent ductus arteriosus (PDA) is a common congenital heart defect in premature infants. The present study was designed to determine the role of the prostaglandin (PG) E2 pathway in the process of ductus arteriosus (DA) maturation and functional closure.2. Changes in PGE2 pathway-related enzymes and receptors in DA in preterm and term rabbits were examined at both the mRNA and protein levels. In addition, responses of DA rings to Po2 and PGE2 were determined.3. Circulating PGE2 levels remained high until 2 h after birth. High levels of the EP4 receptor were found in preterm DA. These tissues were sensitive to PGE2, which caused vessel dilation, but were insensitive to increased Po2. In contrast, DA tissues from term rabbits exhibited an immediate contractile response to increased Po2 and PGE2 treatment resulted in vasoconstriction, which was associated with increased EP3 and decreased EP4 receptor expression in term DA.4. In conclusion, the preterm PDA is maintained by high levels of PGE2, which mainly binds to the EP4 receptor under conditions of hypoxia. In contrast, in the term DA, in which levels of the EP3 receptor are higher than in preterm DA, exposure to PGE2 resulted in vasoconstriction under normoxic conditions. These findings suggest that blocking the EP4 receptor may represent a more selective treatment for the preterm PDA, whereas activating the EP3 receptor may be more suitable for the treatment of the term PDA.
Clinical and Experimental Pharmacology and Physiology 01/2010; 37(5‐6):574 - 580. · 1.85 Impact Factor
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ABSTRACT: To explore the treatment of heparin-induced thrombocytopenia (HIT) in venous thromboembolism.
A total of 202 patients with venous thromboembolism without anticoagulation contraindications were enrolled. All of them were treated with low molecular weight heparin (LMWH) and/or unfractionated heparin (UFH). The peripheral blood cells were examined regularly.
HIT occurred in 6 patients. And argatroban was used to treat HIT. The overall incidence rate of HIT in this study was 2.97%. The time of occurrence of HIT was about Days 3 - 9 after using heparin. The platelet recovered to the basic level at Days 3 - 7 after withdrawing heparin and initiating argatroban.
The count of platelet should be measured in the patients receiving regular LMWH and/or UFH therapy. And the above regimen should be discontinued timely when the platelet count declined progressively by over 50%. Argatroban was effective.
Zhonghua yi xue za zhi 06/2009; 89(20):1405-7.
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Sheng li ke xue jin zhan [Progress in physiology] 02/2009; 40(1):71-4.
