Effect of estrogen replacement treatment on ischemic preconditioning in isolated rat hearts

Peng, Wei; Yu, Jing; Deng, Sheng; Jiang, Jun-Ling; Deng, Han-Wu; Li, Yuan‐Jian

doi:10.1139/y04-024

Cited by 12 publications

(6 citation statements)

References 30 publications

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“…In our study, the microcirculatory manifestations of reduced efficacy of IPC after OVX were demonstrated for the first time, but similar reactions were observed with other manifestations of postischemic tissue injury in other organs by others (i.e., cardiac dysfunction) . The consequences of E2 supplementation in these scenarios, however, are not at all clear.…”

Section: Discussionsupporting

confidence: 78%

“…The results are somewhat controversial, as the protective effects of IPC were present in OVX rabbits . Also, E2 did not exert any alleviating effects in other studies where IPC was combined with OVX . Furthermore, long‐ and short‐term estrogen administration produced different effects, and inter‐species and inter‐organ differences and dissimilarities cannot be ruled out either .…”

Section: Discussionmentioning

confidence: 92%

“…Other studies have shown that the positive cardiac effects of IPC are lost when the endogenous estrogen levels are reduced by ovariectomy (OVX), but cardioprotection could be re‐established by estrogen supplementation . So far, available data on the effects of estrogen replacement during IPC appear to conflict . We showed earlier that OVX per se did not predispose female rats to more severe inflammatory reactions, but estrogen supplementation reduced the harmful consequences of limb IR .…”

mentioning

confidence: 79%

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Estrogen‐dependent efficacy of limb ischemic preconditioning in female rats

Pócs

Janovszky

Garab

et al. 2017

Journal Orthopaedic Research

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ABSTRACT:Our aim was to examine the effects of ischemic preconditioning (IPC) on the local periosteal and systemic inflammatory consequences of hindlimb ischemia-reperfusion (IR) in Sprague-Dawley rats with chronic estrogen deficiency (13 weeks after ovariectomy, OVX) in the presence and absence of chronic 17beta-estradiol supplementation (E2, 20 mg kg À1 , 5 days/week for 5 weeks); sham-operated (non-OVX) animals served as controls. As assessed by intravital fluorescence microscopy, rolling and the firm adhesion of polymorphonuclear neutrophil leukocytes (PMNs) gave similar results in the Sham þ IR and OVX þ IR groups in the tibial periosteal microcirculation during the 3-h reperfusion period after a 60-min tourniquet ischemia. Postischemic increases in periosteal PMN adhesion and PMN-derived adhesion molecule CD11b expressions, however, were significantly reduced by IPC (two cycles of 10 0 /10 0 ) in Sham animals, but not in OVX animals; neither plasma free radical levels (as measured by chemiluminescence), nor TNF-alpha release was affected by IPC. E2 supplementation in OVX animals restored the IPC-related microcirculatory integrity and PMN-derived CD11b levels, and TNF-alpha and free radical levels were reduced by IPC only with E2. An enhanced estrogen receptor beta expression could also be demonstrated after E2 in the periosteum. Overall, the beneficial periosteal microcirculatory effects of limb IPC are lost in chronic estrogen deficiency, but they can be restored by E2 supplementation. This suggests that the presence of endogenous estrogen is a necessary facilitating factor of the anti-inflammatory protection provided by limb IPC in females. The IPC-independent effects of E2 on inflammatory reactions should also be taken into account in this model. ß

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 79%

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Estrogen‐dependent efficacy of limb ischemic preconditioning in female rats

Pócs

Janovszky

Garab

et al. 2017

Journal Orthopaedic Research

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“…Surgical ovariectomy has been shown to exacerbate myocardial oxidative stress-induced damage caused by anthracycline administration (50), and estrogen administration protects against ischemia-reperfusion injury (6,57). This suggests that the cardiac dysfunction observed in hearts from chemically ovariectomized rats in the present study may be attributed to compromised antioxidant status.…”

Section: Discussionmentioning

confidence: 58%

Effects of voluntary wheel running on cardiac function and myosin heavy chain in chemically gonadectomized rats

Hydock

Lien²,

Schneider³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Reducing testosterone and estrogen levels with a luteinizing hormone-releasing hormone agonist such as Zoladex (i.e., chemical gonadectomy) is a common treatment for many prostate and breast cancer patients, respectively. There are reports of surgical gonadectomy inducing cardiac dysfunction, and exercise has been shown to be cardioprotective under these circumstances. Minimal research has been done investigating the effects of chemical gonadectomy and increased physical activity on cardiac function. The purpose of this investigation was to examine the effects of chemical gonadectomy and physical activity on cardiac function. Male (M) and female (F) Sprague-Dawley rats received either Zoladex treatment (Zol) that suppressed gonadal function for 8 wk or control implants (Con) and either were allowed unlimited access to voluntary running wheels (WR) or remained sedentary (Sed) throughout the treatment period. In vivo and ex vivo left ventricle (LV) function were then assessed, and myosin heavy chain (MHC) expression was analyzed to help explain LV functional differences. Hearts from M Sed+Zol exhibited significantly lower aortic blood flow velocity, developed pressure, and maximal rate of pressure development and higher beta-MHC expression than M Sed+Con. Hearts from F Sed+Zol exhibited significantly lower LV wall thicknesses, fractional shortening, and developed pressure and higher beta-MHC expression than F Sed+Con. This cardiac dysfunction was not evident in hearts from M or F WR+Zol, and this was associated with a preservation of the MHC isoform distribution. Thus an 8-wk chemical gonadectomy with Zoladex promoted cardiac dysfunction in male and female rats, and voluntary wheel running protected against this cardiac dysfunction.

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“… 8 – 12 Likewise, the data regarding whether chronic oestrogen depletion interferes with the development of IPC have not been entirely consistent. 20 – 22 The apparent discrepancy in the previous reports might be due, at least in part, to different experimental models ( in vivo vs. ex vivo ), different I/R or IPC protocols, different parameters used to assess myocardial damage, and, possibly, species differences. Song et al .…”

Section: Discussionmentioning

confidence: 97%

Loss of ischaemic preconditioning in ovariectomized rat hearts: possible involvement of impaired protein kinase C phosphorylation

Shinmura

Nagai

Tamaki

et al. 2008

Cardiovascular Research

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AimsThe aims of this study were to determine whether chronic oestrogen withdrawal influences the development of ischaemic preconditioning (IPC) in female hearts, to investigate the mechanism whereby IPC is impaired, and to assess whether direct activation of protein kinase C (PKC) can mimic IPC in female hearts with chronic oestrogen depletion.Methods and resultsWe performed Sham-operation (Sham) or bilateral ovariectomy on 16-week-old Sprague–Dawley female rats. Ovariectomized rats were randomized to subcutaneous implantation of 17β-estradiol (OxE) or placebo (OxP) pellets. Four weeks later, isolated, perfused hearts were subjected to 30 min of ischaemia followed by 120 min of reperfusion with or without three cycles of 5 min ischaemia/5 min reperfusion. The cardioprotective effect of IPC was completely lost in the OxP group. Western immunoblots revealed that in the OxP group, IPC failed to translocate PKCε to the membranous fraction and that phosphorylation of PKCε (Ser729) and phosphoinositide-dependent kinase (PDK) 1 (Ser241) was impaired. Oestrogen replacement restored the IPC effect, the translocation and phosphorylation of PKCε, and the phosphorylation of PDK1. In the OxP group, pre-treatment with a PKCε selective activator peptide (Ψ–εRACK) mimicked the IPC effect. Pre-treatment with a phosphatidylinositol-3 kinase inhibitor before IPC abrogated the translocation and phosphorylation of PKCε in the Sham group.ConclusionsThe cardioprotective effect of IPC is lost in female hearts with chronic oestrogen withdrawal and this is due, at least in part, to impaired translocation and phosphorylation of PKCε. Selective activation of PKCε-mediated signalling can fully restore the IPC effect in a manner analogous to oestrogen replacement.

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Effect of estrogen replacement treatment on ischemic preconditioning in isolated rat hearts

Cited by 12 publications

References 30 publications

Estrogen‐dependent efficacy of limb ischemic preconditioning in female rats

Estrogen‐dependent efficacy of limb ischemic preconditioning in female rats

Effects of voluntary wheel running on cardiac function and myosin heavy chain in chemically gonadectomized rats

Loss of ischaemic preconditioning in ovariectomized rat hearts: possible involvement of impaired protein kinase C phosphorylation

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