17β-Estradiol Prevents Dysfunction of Canine Coronary Endothelium and Myocardium and Reperfusion Arrhythmias After Brief Ischemia/Reperfusion

Circulation ◽  
1996 ◽  
Vol 94 (11) ◽  
pp. 2901-2908 ◽  
Author(s):  
Young D. Kim ◽  
Barbara Chen ◽  
John Beauregard ◽  
Peter Kouretas ◽  
George Thomas ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Reperfusion Arrhythmias ◽  
17Β Estradiol ◽  
Coronary Endothelium

scholarly journals Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats

2001 ◽  
Vol 91 (4) ◽  
pp. 1828-1835 ◽  
Author(s):  
Nicole Stupka ◽  
Peter M. Tiidus
Keyword(s):  
Muscle Damage ◽  
Ischemia Reperfusion Injury ◽  
Serum Insulin ◽  
Ischemia Reperfusion ◽  
Neutrophil Infiltration ◽  
Female Rats ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
17Β Estradiol

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17β-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater ( P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats ( P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower ( P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater ( P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower ( P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower ( P< 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content ( P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

Intraluminal-restricted 17β-estradiol exerts the same myocardial protection against ischemia/reperfusion injury in vivo as free 17β-estradiol

Steroids ◽  
2008 ◽  
Vol 73 (5) ◽  
pp. 528-538 ◽  
Author(s):  
Arturo Rodriguez-Hernandez ◽  
Ivan Rubio-Gayosso ◽  
Israel Ramirez ◽  
Israel Ita-Islas ◽  
Eduardo Meaney ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Protection ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
17Β Estradiol

NO produced by endothelial NO synthase is a mediator of delayed preconditioning-induced endothelial protection

2003 ◽  
Vol 284 (6) ◽  
pp. H2053-H2060 ◽  
Author(s):  
Karine Laude ◽  
Julie Favre ◽  
Christian Thuillez ◽  
Vincent Richard
Keyword(s):  
Ischemia Reperfusion ◽  
No Synthase ◽  
Cardiac Ischemia ◽  
Sham Surgery ◽  
Nos Inhibitor ◽  
Coronary Endothelial Cells ◽  
Cardiac Preconditioning ◽  
Coronary Endothelium ◽  
Inos Inhibition

Preconditioning with brief periods of ischemia-reperfusion (I/R) induces a delayed protection of coronary endothelial cells against reperfusion injury. We assessed the possible role of nitric oxide (NO) produced during prolonged I/R as a mediator of this endothelial protection. Anesthetized rats were subjected to 20-min cardiac ischemia/60-min reperfusion, 24 h after sham surgery or cardiac preconditioning (1 × 2-min ischemia/5-min reperfusion and 2 × 5-min ischemia/5-min reperfusion). The nonselective NO synthase (NOS) inhibitor l-NAME, the selective inhibitors of neuronal (7-nitroindazole) or inducible (1400W) NOS, or the peroxynitrite scavenger seleno-l-methionine were administered 10 min before prolonged ischemia. Preconditioning prevented the reperfusion-induced impairment of coronary endothelium-dependent relaxations to acetylcholine (maximal relaxation: sham 77 ± 3; I/R 44 ± 6; PC 74 ± 5%). This protective effect was abolished by l-NAME (41 ± 7%), whereas 7-NI, 1400W or seleno-l-methionine had no effect. The abolition of preconditioning by l-NAME, but not by selective nNOS or iNOS inhibition, suggests that NO produced by eNOS is a mediator of delayed endothelial preconditioning.

Cellular and molecular mechanisms of 17β-estradiol postconditioning protection against gastric mucosal injury induced by ischemia/reperfusion in rats

Life Sciences ◽  
2010 ◽  
Vol 86 (1-2) ◽  
pp. 30-38 ◽  
Author(s):  
Dongshu Du ◽  
Xiaobo Ma ◽  
Jianfu Zhang ◽  
Yongmei Zhang ◽  
Xiaoyan Zhou ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Mucosal Injury ◽  
Gastric Mucosal Injury ◽  
17Β Estradiol

scholarly journals Cardioprotective Effects of Quercetin Against Ischemia-Reperfusion Injury Are Age-Dependent

2016 ◽  
pp. S101-S107 ◽  
Author(s):  
M. BARTEKOVA ◽  
J. RADOSINSKA ◽  
D. PANCZA ◽  
M. BARANCIK ◽  
T. RAVINGEROVA
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reperfusion Arrhythmias ◽  
Beneficial Effects ◽  
Adult Rat ◽  
Rat Hearts ◽  
Age Dependent ◽  
Old Rats ◽  
Contraction And Relaxation ◽  
Quercetin Treatment

Quercetin, a polyphenolic compound present in various types of food, has been shown to exert beneficial effects in different cardiac as well as non-cardiac ischemia/reperfusion (I/R) models in adult animals. However, there is no evidence about the effects of quercetin on I/R injury in non-mature animals, despite the fact that efficiency of some interventions against I/R is age-dependent. This study was aimed to investigate the effects of chronic quercetin treatment on I/R injury in juvenile and adult rat hearts. Juvenile (4-week-old) as well as adult (12-week-old) rats were treated with quercetin (20 mg/kg/day) for 4 weeks, hearts were excised and exposed to 25-min global ischemia followed by 40-min reperfusion. Functional parameters of hearts and occurrence of reperfusion arrhythmias were registered to assess the cardiac function. Our results have shown that quercetin improved post-ischemic recovery of LVDP, as well as recovery of markers of contraction and relaxation, +(dP/dt)max and –(dP/dt)max, respectively, in juvenile hearts, but not in adult hearts. Quercetin had no impact on incidence as well as duration of reperfusion arrhythmias in animals of both ages. We conclude that the age of rats plays an important role in heart response to quercetin treatment in the particular dose and duration of the treatment. Therefore, the age of the treated subjects should be taken into consideration when choosing the dose of quercetin and duration of its application in prevention and/or treatment of cardiovascular diseases.

Acute effects of 17β-estradiol on myocardial pH, Na+, and Ca2+ and ischemia-reperfusion injury

2005 ◽  
Vol 288 (1) ◽  
pp. C57-C64 ◽  
Author(s):  
Steven E. Anderson ◽  
Dawn M. Kirkland ◽  
Andrea Beyschau ◽  
Peter M. Cala
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Ovariectomized Rats ◽  
Functional Coupling ◽  
Cytosolic Ph ◽  
Thermodynamic Effect ◽  
17Β Estradiol ◽  
Developed Pressure

Evidence suggests that 1) ischemia-reperfusion injury is due largely to cytosolic Ca2+ accumulation resulting from functional coupling of Na+/Ca2+ exchange (NCE) with stimulated Na+/H+ exchange (NHE1) and 2) 17β-estradiol (E2) stimulates release of NO, which inhibits NHE1. Thus we tested the hypothesis that acute E2 limits myocardial Na+ and therefore Ca2+ accumulation, thereby limiting ischemia-reperfusion injury. NMR was used to measure cytosolic pH (pHi), Na+ (Na[Formula: see text]), and calcium concentration ([Ca2+]i) in Krebs-Henseleit (KH)-perfused hearts from ovariectomized rats (OVX). Left ventricular developed pressure (LVDP) and lactate dehydrogenase (LDH) release were also measured. Control ischemia-reperfusion was 20 min of baseline perfusion, 40 min of global ischemia, and 40 min of reperfusion. The E2 protocol was identical, except that 1 nM E2 was included in the perfusate before ischemia and during reperfusion. E2 significantly limited the changes in pHi, Na[Formula: see text] and [Ca2+]i during ischemia ( P < 0.05). In control OVX vs. OVX+E2, pHi fell from 6.93 ± 0.03 to 5.98 ± 0.04 vs. 6.96 ± 0.04 to 6.68 ± 0.07; Na[Formula: see text] rose from 25 ± 6 to 109 ± 14 meq/kg dry wt vs. 25 ± 1 to 76 ± 3; [Ca2+]i changed from 365 ± 69 to 1,248 ± 180 nM vs. 293 ± 66 to 202 ± 64 nM. E2 also improved recovery of LVDP and diminished release of LDH during reperfusion. Effects of E2 were diminished by 1 μM Nω-nitro-l-arginine methyl ester. Thus the data are consistent with the hypothesis. However, E2 limitation of increases in [Ca2+]i is greater than can be accounted for by the thermodynamic effect of reduced Na[Formula: see text] accumulation on NCE.

17β-Estradiol Accelerated Renal Tubule Regeneration in Male Rats After Ischemia/Reperfusion-Induced Acute Kidney Injury

Shock ◽  
2016 ◽  
Vol 46 (2) ◽  
pp. 158-163 ◽  
Author(s):  
Chia-Chun Wu ◽  
Chia-Yu Chang ◽  
Sheng-Tsung Chang ◽  
Sheng-Hsien Chen
Keyword(s):  
Acute Kidney Injury ◽  
Renal Tubule ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Male Rats ◽  
17Β Estradiol

scholarly journals Postischemic Cerebral Blood Flow Recovery in the Female: Effect of 17β-Estradiol

1995 ◽  
Vol 15 (4) ◽  
pp. 666-672 ◽  
Author(s):  
Patricia D. Hurn ◽  
Marguerite T. Littleton-Kearney ◽  
Jeffrey R. Kirsch ◽  
A. M. Dharmarajan ◽  
Richard J. Traystman
Keyword(s):  
Blood Flow ◽  
Ischemia Reperfusion ◽  
Brain Regions ◽  
Reproductive Hormones ◽  
Global Cerebral Ischemia ◽  
Atherosclerotic Vascular Disease ◽  
Estradiol Treatment ◽  
Vessel Occlusion ◽  
Regional Flow ◽  
17Β Estradiol

Female reproductive hormones are considered to be protective agents in atherosclerotic vascular disease and stroke. The present study determined if there are unique cerebrovascular responses in female animals to global cerebral ischemia and if 17β-estradiol is important to postischemic outcome in brain. Three groups of anesthetized, sexually mature rabbits were treated with normotensive four-vessel occlusion (6 min) and 3 h of reperfusion: females chronically instrumented with 17β-estradiol implants (EFEM; n = 8, plasma estradiol level = 365 ± 48 pg/ml), untreated females (FEM; n = 8, estradiol = 13 ± 3 pg/ml), and untreated males (M; n = 8, estradiol < limit of radioimmunoassay). CBF (microspheres) and somatosensory evoked potential (SEP) amplitude were measured during ischemia/reperfusion. Baseline hemispheric blood flow and regional flow distribution were not altered by chronic estradiol treatment. Hemispheric blood flow was equivalently reduced during ischemia in FEM and M (6 ± 1 and 9 ± 2 ml min−1 100 g−1 respectively); however postischemic hyperemia was greater in FEM than M (CBF = 257 ± 27 and 183 ± 27 ml min−1 100 g−1. However, EFEM experienced higher CBF during ischemia (e.g., 13 ± 2 ml min−1 100 g−1) and less hyperemia (134 ± 4 ml min−1 100 g−1 in hemispheres) in numerous brain regions than FEM. CBF at 3 h reperfusion was not different among the groups. Recovery of SEPs was incomplete and similar in all groups. We conclude that chronic exogenous 17β-estradiol treatment increases CBF during global incomplete ischemia and ameliorates postischemic hyperemia in the female animal.

Sign in / Sign up

Export Citation Format

Share Document