Identification of the length and location of the A1 pulley combining palpation technique with palm landmarks: a cadaveric study.

Through anatomical morphology, to accumulate the relevant parameters of the A1 pulley of each adult finger. A total of 100 fingers were selected, dissected layer by layer, and the A1 pulley and neurovascular of each finger were observed. Measure the length of the A1 pulley, the distance between the needle knife insertion point and the proximal edge of A1 pulley, and the nerves and blood vessels on both sides. (1) The length of A1 pulleys of each finger is 6.18 ± 0.33 mm, 6.58 ± 0.73 mm, 5.98 ± 0.67 mm, 5.36 ± 1.08 mm, 5.63 ± 1.09 mm. (2) The distances between the needle knife entry point of each finger and the volar proper nerve of the ulnar finger are 7.00 ± 1.55 mm, 8.29 ± 1.46 mm, 5.10 ± 0.25 mm, 5.30 ± 0.24 mm, 0 mm; the distances from the volar proper nerve of the radial finger are 9.08 ± 0.87 mm, 4.70 ± 1.10 mm, 7.03 ± 0.72 mm, 6.81 ± 0.22 mm, 7.81 ± 0.57 mm. (3) The distances between the needle knife entry point of each finger and the proper volar artery of the ulnar finger are 10.40 ± 0.75 mm, 8.89 ± 0.53 mm, 6.35 ± 0.44 mm, 7.26 ± 0.16 mm, 0 mm, respectively; The distances from the volar proper artery of the radial finger are 8.75 ± 1.07 mm, 6.10 ± 0.35 mm, 11.44 ± 0.41 mm, 8.19 ± 0.60 mm, 9.78 ± 0.68 mm, respectively. The landmarks of the needle entry points are located at the position corresponding to the highest point of the metacarpal heads, except the tail finger. From the needle knife entry point to distal, cut the proximal edge of the A1 pulley longitudinally along the midline until the patient can flex autonomously, and pay attention to the distance between the two sides of 3.60-11.85 mm neurovascular bundle.

The Efficacy and Safety of Telerehabilitation for Fibromyalgia: Systematic Review and Meta-analysis of Randomized Controlled Trials.

BACKGROUND: Fibromyalgia is a chronic pain syndrome characterized by persistent and widespread musculoskeletal pain. Telerehabilitation is a promising treatment for patients with fibromyalgia through long-term monitoring, intervention, supervision, consultation, and education. OBJECTIVE: This study aimed to perform a comprehensive systematic review and meta-analysis of the efficacy and safety of telerehabilitation in patients with fibromyalgia. METHODS: Randomized controlled trials (RCTs) related to fibromyalgia and telerehabilitation were systematically searched in the PubMed, PEDro, Cochrane Library, ScienceDirect, Ovid MEDLINE, Embase, and Web of Science databases from inception to November 13, 2022. Two independent researchers screened the literatures and evaluated the methodological quality using the Cochrane Risk of Bias Tool. The outcome measures included the Fibromyalgia Impact Questionnaire scale, pain intensity, depression, pain catastrophizing, quality of life (QoL), and adverse events. Pooled effect sizes were calculated by Stata SE 15.1; a fixed effects model was used when I2<50%, whereas a random effects model was used when I2≥50%. RESULTS: A total of 14 RCTs with 1242 participants were included in this meta-analysis. The pooled results indicated that the telerehabilitation improved the Fibromyalgia Impact Questionnaire score (weighted mean difference -8.32, 95% CI -11.72 to -4.91; P<.001), pain intensity (standardized mean difference [SMD] -0.62, 95% CI -0.76 to -0.47; P<.001), depression levels (SMD -0.42, 95% CI -0.62 to -0.22; P<.001), pain catastrophizing (weighted mean difference -5.81, 95% CI -9.40 to -2.23; P=.001), and QoL (SMD 0.32, 95% CI 0.18 to 0.47; P<.001) in patients with fibromyalgia compared to control interventions. Only 1 RCT reported a mild adverse event of telerehabilitation; the other 13 RCTs did not mention this. CONCLUSIONS: Telerehabilitation can improve the symptoms and QoL of fibromyalgia. However, the safety of telerehabilitation remains uncertain due to the lack of sufficient evidence for the management of fibromyalgia. More rigorously designed trials are needed in the future to verify the safety and efficacy of telerehabilitation in fibromyalgia. TRIAL REGISTRATION: PROSPERO CRD42022338200; https://tinyurl.com/322keukv.

Morphometric study of percutaneous A1 pulley of thumb release.

Through anatomy, microscope, histopathology, and simulating needle knife operation on specimens, to accumulate the relevant parameters of the A1 pulley of thumb, and to provide an anatomical evidence for the needle knife therapy of stenosing flexor tenosynovitis. A total of 20 fingers were selected from 20 intact adult upper limb specimens, a small amount of emerald green waterproof dye was injected from the needle insertion point, dissected layer by layer, and the A1 pulley and neurovascular bundle were observed. Observe the loosening of the thumb A1 pulley after 5 and 10 times of simulated needle knife cutting on the specimen; observe the relationship between the needle knife entry point and the A1 pulley under the thumb extension and abduction, and the thumb extension neutral position respectively; further observe the histological characteristics, and the relationship between needle entry point and A1 pulley by microscope. ① In general observation, the A1 pulleys of each finger were transverse fibers perpendicular to the flexor tendon, tough in texture, connected with synovial fibers at the proximal end. It is difficult to distinguish, and connected with oblique fibers at the distal end. ② The release rate of the thumb A1 pulley after 5 and 10 times of simulated needle knife cutting on the specimen were (40.46 ± 2.22)% and (63.52 ± 4.49)%, respectively. ③ In the neutral position of the thumb straightening, the needle entry point is 3.06 ± 0.14 mm from the proximal side of the proximal edge of the A1 pulley, which overlaps with the needle entry point where the thumb is straight and abducted. ④ Observed under a microscope, the A1 pulley is a dense transverse fiber with a pale yellow dense connective tissue, both ends are continuous with the synovial fibers. It is thin and translucent, and loose connective tissue. The A1 pulley is a dense transverse fiber with a pale yellow dense connective tissue. The anatomical key points of the needle knife therapy lie in the extended and abducted position of the thumb. Currently, it is believed that cutting the proximal edge of the A1 pulley is sufficient, and there is no need to cut the entire A1 pulley.

Capsaicin ameliorates intermittent high glucose-mediated endothelial senescence via the TRPV1/SIRT1 pathway.

BACKGROUND: Patients with diabetes have accelerated vascular aging when compared with healthy individuals. Hyperglycemia, especially intermittent high glucose (IHG), is the main cause of vascular endothelial senescence. Capsaicin, a major component of chili pepper is thought to contribute to cardiovascular protection by spicy food. OBJECTIVE: To investigate the pathway related with the effects of capsaicin on endothelial cell senescence induced by IHG. METHODS: HUVECs were exposed to IHG (5 mM or 33 mM glucose, alternating every 12 hours for 3 days) and treated with capsaicin at 0.3, 1 and 3 µM. To determine endothelial cell senescence, we examined the senescence-related ß-galactosidase staining, cell cycle arrest, cell viability, as well as production of reactive oxygen species (ROS). To evaluate the involvement of TRPV1/[Ca2+]i/CaMKII/AMPK/SIRT1 pathway in anti- senescence effects of capsaicin, HUVECs were treated with CAPZ (a TRPV1 antagonist), BAPTA-AM (an intracellular calcium chelator), KN62 (a CaMKII antagonist), compound C (an AMPK inhibitor), or EX527 (a SIRT1 inhibitor). To knockdown TRPV1, HUVECs were transfected with shRNA lentivirus targeting TRPV1. The levels of SIRT1, p21, TRPV1, AMPK and phospho-AMPK were evaluated by western blotting. RESULTS: IHG suppressed the levels of SIRT1 and enhanced endothelial senescence. Capsaicin upregulated SIRT1 expression and downregulated the senescence marker, p21, thereby protecting endothelial cells from IHG-induced senescence as indicated by relieved G0/G1 phase arrest, improved cell viabilities, and reduced counts of senescent cells and ROS production. Pre-treatment with CAPZ, BAPTA-AM, KN62 or compound C abrogated the anti-senescence effects of capsaicin. Capsaicin restored AMPK phosphorylation and IHG-inhibited TRPV1 expression. Moreover, TRPV1 silencing suppressed SIRT1 expression and abolished the anti-senescence effects of capsaicin. CONCLUSION: Capsaicin elevates SIRT1 levels through TRPV1/[Ca2+]i/CaMKII/AMPK pathway and suppresses IHG-mediated endothelial cell senescence. This study provides initial evidence that capsaicin is a potential candidate for the prevention of vascular aging in diabetes.

Rutaecarpine Prevents High Glucose-Induced Endothelial Cell Senescence Through Transient Receptor Potential Vanilloid Subtype 1/ SIRT1 Pathway.

ABSTRACT: SIRT1 functions as a longevity factor to counteract vascular aging induced by high glucose. Our previous study revealed that rutaecarpine, the natural agonist of transient receptor potential vanilloid subtype 1 (TRPV1), prevented high glucose-induced endothelial dysfunction. The present study aims to evaluate the effects of rutaecarpine on endothelial cell senescence induced by high glucose, and focus on the regulatory effect on SIRT1 expression. In cultured human umbilical vein endothelial cell (HUVEC), exposure to 33 mM high glucose for 72 hours induced cellular senescence, demonstrated as cell cycle arrest at G0/G1 phase, decreased cell viability, and increased number of senescence-associated ß-galactosidase positive senescence cells and ROS production, which were effectively attenuated by treatment with rutaecarpine (0.3, 1, and 3 µM). Furthermore, rutaecarpine upregulated longevity protein SIRT1 expression in HUVECs, accompanied by decreased level of senescence marker p21. In addition, rutaecarpine increased intracellular calcium level in HUVECs, and pretreatment with TRPV1 antagonist capsazepine, intracellular Ca2+ chelator BAPTA-AM or CaM antagonist W-7 abolished the effects of rutaecarpine on SIRT1 expression. In summary, this study shows that rutaecarpine upregulates SIRT1 expression and prevents high glucose-induced endothelial cell senescence, which is related to activation of TRPV1/[Ca2+]i/CaM signal pathway. Our findings provide evidence that rutaecarpine may be a promising candidate with a novel mechanism in prevention vascular aging in diabetes.

Rutaecarpine Reverses the Altered Connexin Expression Pattern Induced by Oxidized Low-density Lipoprotein in Monocytes.

Adhesion of monocytes to the vascular endothelium is crucial in atherosclerosis development. Connexins (Cxs) which form hemichannels or gap junctions, modulate monocyte-endothelium interaction. We previously found that rutaecarpine, an active ingredient of the Chinese herbal medicine Evodia, reversed the altered Cx expression induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells, and consequently decreases the adhesive properties of endothelial cells to monocytes. This study further investigated the effect of rutaecarpine on Cx expression in monocytes exposed to ox-LDL. In cultured human monocytic cell line THP-1, ox-LDL rapidly reduced the level of atheroprotective Cx37 but enhanced that of atherogenic Cx43, thereby inhibiting adenosine triphosphate release through hemichannels. Pretreatment with rutaecarpine recovered the expression of Cx37 but inhibited the upregulation of Cx43 induced by ox-LDL, thereby improving adenosine triphosphate-dependent hemichannel activity and preventing monocyte adhesion. These effects of rutaecarpine were attenuated by capsazepine, an antagonist of transient receptor potential vanilloid subtype 1. The antiadhesive effects of rutaecarpine were also attenuated by hemichannel blocker 18α-GA. This study provides additional evidence that rutaecarpine can modulate Cx expression through transient receptor potential vanilloid subtype 1 activation in monocytes, which contributes to the antiadhesive properties of rutaecarpine.

Rutaecarpine prevented dysfunction of endothelial gap junction induced by Ox-LDL via activation of TRPV1.

Gap junctions, which is formed by connexins, has been proved to play an important role in the atherogenesis development. Rutaecarpine was reported to inhibited monocyte migration, which indicates its potential for anti-atherosclerosis activity. This study evaluated the effect of rutaecarpine on endothelial dysfunction, and focused on the regulation of connexin expression in endothelial cells by rutaecarpine. Endothelia damage was induced by exposing HUVEC-12 to Ox-LDL (100mg/l) for 24h, which decreased the expression of protective proteins Cx37 and Cx40, but induced atherogenic Cx43 expression, in both mRNA and protein levels, concomitant with the impaired propidium iodide diffusion through the gap junctions. Pretreatment with rutaecarpine effectively recovered the expression of Cx37 and Cx40, but inhibited Cx43 expression, thereby improving gap junction communication and significantly prevented the endothelial dysfunction. Consequently, the cell viability and nitric oxide production were increased, lactate dehydrogenase production was decreased and monocyte adhesion was inhibited. These protective effects of rutaecarpine were remarkably attenuated by pretreatment with capsazepine, a competitive antagonist of transient receptor potential vanilloid subtype 1 (TRPV1). In summary, this study is the first to report that rutaecarpine prevents endothelial injury and gap junction dysfunction induced by Ox-LDL in vitro, which is related to regulation of connexin expression patterns via TRPV1 activation. These results suggest that rutaecarpine has the potential for use as an anti-atherosclerosis agent with a novel mechanism.

Bisphenol A regulates the estrogen receptor alpha signaling in developing hippocampus of male rats through estrogen receptor.

Bisphenol A (BPA), one of the most common environmental endocrine disruptors, has been recognized to have wide adverse effects on the brain development and behavior. These adversities are related to its ability to bind estrogen receptor (ER) with subsequent alteration of its expression in the target areas. However, very little is known about whether BPA exposure also affects ER phosphorylation and its translocation to nucleus during postnatal development, two critical steps for its function. Here, we found that during development from postnatal day 7 (P7) to P21, the alpha subtype of ER (ERα) in the hippocampus of male rats experienced remarkable alterations in terms of its expression, phosphorylation and translocation to nucleus. Exposure to low level of BPA had bidirectional, development-dependent effects on the expression of ERα mRNA and protein, but decreased ERα phosphorylation and impaired its translocation to nucleus throughout the period investigated. Treatment with low dose of ICI 182,780 (ICI), an ER antagonist to block the binding of ER with BPA, reversed the altered ERα following BPA exposure, highlighting critical involvement of ER. Moreover, ICI treatment rescued the hippocampus-dependent behavioral deficits in the adult rats experiencing early-life BPA exposure. Overall, our results indicate that BPA interferes with the ERα signaling in the developing hippocampus in an ER-dependent manner, which may underlie its adverse behavioral and cognitive outcomes in adult animals.

Chronic stress impairs GABAergic control of amygdala through suppressing the tonic GABAA receptor currents.

BACKGROUND: Chronic stress is generally known to exacerbate the development of numerous neuropsychiatric diseases such as fear and anxiety disorders, which is at least partially due to the disinhibition of amygdala subsequent to the prolonged stress exposure. GABA receptor A (GABAAR) mediates the primary component of inhibition in brain and its activation produces two forms of inhibition: the phasic and tonic inhibition. While both of them are critically engaged in limiting the activity of amygdala, their roles in the amygdala disinhibition subsequent to chronic stress exposure are largely unknown. RESULTS: We investigated the possible alterations of phasic and tonic GABAAR currents and their roles in the amygdala disinhibition subsequent to chronic stress. We found that both chronic immobilization and unpredictable stress led to long lasting loss of tonic GABAAR currents in the projection neurons of lateral amygdala. By contrast, the phasic GABAAR currents, as measured by the spontaneous inhibitory postsynaptic currents, were virtually unaltered. The loss of tonic inhibition varied with the duration of daily stress and the total days of stress exposure. It was prevented by pretreatment with metyrapone to block corticosterone synthesis or RU 38486, a glucocorticoid receptor antagonist, suggesting the critical involvement of glucocorticoid receptor activation. Moreover, chronic treatment with corticosterone mimicked the effect of chronic stress and reduced the tonic inhibition in lateral amygdala of control mice. The loss of tonic inhibition resulted in the impaired GABAergic gating on neuronal excitability in amygdala, which was prevented by metyrapone pretreatment. CONCLUSIONS: Our study suggests that enduring loss of tonic but not phasic GABAAR currents critically contributes to the prolonged amygdala disinhibition subsequent to chronic stress. We propose that the preferential loss of tonic inhibition may account for the development of stress-related neuropsychiatric diseases.

A role for diallyl trisulfide in mitochondrial antioxidative stress contributes to its protective effects against vascular endothelial impairment.

Persistent hyperglycemia increases a systemic oxidative stress, causing the onset of vascular endothelial dysfunction and atherosclerosis. Diallyl trisulfide (DAT), a natural organosulfur compound in garlic, has been reported to have actions of dilating blood vessels and antibacteria, etc. In this study, models of obese diabetic rat in vivo and high glucose concentration (HG)-induced endothelial cell injury in vitro were used to investigate the protective effects of DAT on vascular endothelial injury and its underlying mechanisms. In the in vivo model, the obese diabetic rats were injected venously with DAT (5.0 mg kg(-1)d(-1)) and Vitamin E (1.0 mg kg(-1)d(-1)) respectively, once daily for 7 consecutive days. In the in vitro model, HG-injured HUVEC were treated with or without DAT (25 µmol L(-1), 50 µmol L(-1), 100 µmol L(-1)) or Vitamin E (25 µmol L(-1)) respectively for 24h. The extents of vascular endothelial injury and protective effects of DAT were evaluated. The results both in vivo and in vitro displayed that DAT-treatment significantly attenuated the endothelial cell impairments. Besides, DAT-treatment markedly decreased the levels of malondialdehyde (MDA) and reactive oxygen species, whereas elevated the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in mitochondrium. Moreover, DAT-treatment considerably improved mitochondrial respiration function. Taken together, our results suggest that DAT protects vascular endothelium from HG or hyperglycemia induced-injury by reducing mitochondrial oxidative stress. The findings provide a novel insight for DAT to potentially treat the oxidative stress diseases, i.e., atherosclerosis, diabetes, and neurodegenerative diseases.

Involvement of anion exchanger-2 in apoptosis of endothelial cells induced by high glucose through an mPTP-ROS-Caspase-3 dependent pathway.

Excess apoptosis of endothelial cells (EC) plays crucial roles in the onset and progression of vasculopathy in diabetes mellitus. Anion exchanger-2 (AE2) might be involved in the vasculopathy. However, little is known about the molecular mechanisms that AE2 mediated the apoptosis of EC. The purpose of this study was to explore the role of AE2 in the apoptosis of HUVECs induced by high glucose (HG) and its possible mechanisms. First, HUVECs were exposed to different glucose concentrations (5.5, 17.8, 35.6, 71.2 and 142.4 mmol/l, respectively, pH = 7.40) for different time points (12, 24, 48, 72, 120, and 168 h, respectively). Intracellular Cl(-) concentration ([Cl(-)]i), AE2 expression and the apoptosis were assayed. Then, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), Cl(-)-free media or specific RNA interference (RNAi) for AE2 was used to confirm whether AE2 could mediate the apoptosis induced by HG. Finally, the mechanisms of the AE2-mediated apoptosis were investigated by detecting mitochondrial permeability transition pore (mPTP, DeltaPsim) openings, reactive oxygen species (ROS) levels and Caspase-3 activity. We found that HG upregulated the AE2 expression and activity, increased [Cl(-)]i and induced the apoptosis in a time- and concentration-dependent manner. The apoptosis of HUVECs by HG was possibly mediated by AE2 through an mPTP-ROS-Caspase-3 dependent pathway. These findings suggested that AE2 was likely to be a glucose-sensitive transmembrane transporter and a novel potential therapeutic target for diabetic vasculopathy.

Transient receptor potential vanilloid 1-mediated expression and secretion of endothelial cell-derived calcitonin gene-related peptide.

Calcitonin gene-related peptide (CGRP), the principal transmitter in sensory nerves, could also be expressed in vascular endothelium. Transient receptor potential vanilloid 1(TRPV1), which modulates the synthesis and release of CGRP in sensory nerves, is also present in endothelial cells. The present study tested whether TRPV1 modulates the release and synthesis of CGRP in endothelial cells, and evaluated the protective effect of endothelial cell-derived CGRP. Human umbilical vein endothelial cells (HUVECs) were treated with capsaicin or hyperthermia. The level of CGRP mRNA was detected by RT-PCR, and protein level was measured by radioimmunoassay. Endothelial cell injury was induced by lysophosphatidylcholine, and evaluated by cell viability and lactate dehydrogenase activity. HUVECs expressed CGRP, both alpha- and beta-subtype. Capsaicin increased the level of CGRP in the culture medium, and up-regulated the expression of CGRP in endothelial cells. Hyperthermia also increased the level of CGRP mRNA. These effects were abolished by capsazepine, a competitive antagonist of TRPV1. Capsaicin significantly attenuated the endothelial cell damage induced by LPC, which was prevented and aggravated by capsazepine or CGRP(8-37,) antagonist of CGRP receptor. These results indicate that TRPV1 also regulates the expression and secretion of endothelial cell-derived CGRP, which affords protective effects on endothelial cells.

Asymmetric dimethylarginine is not involved in ovariectomy-induced osteopenia in rats.

Previous studies have indicated that the plasma concentration of nitric oxide synthase inhibitor, asymmetric dimethylarginine (ADMA), was increased in postmenopausal women. In the study reported here, we tested the relationship between the decrease of bone mineral density (BMD) and ADMA concentration in ovariectomized (OVX) rats. Ovariectomized rats at 8 months of age were treated with 17beta-estradiol (10 or 30 microg/kg of body weight/day, s.c.) or L-arginine (300 mg/kg/day, i.p.) for 12 weeks (n = 10 for each group). Pre- and posttreatment total BMD, posttreatment plasma nitrite/nitrate and ADMA concentrations, and posttreatment BMD in the lumbar part of the spine (L4-L6), femurs, and tibias were examined. Ovariectomy caused a significant decrease in several BMD indexes, which was reversed by estrogen treatment (P < 0.05). Plasma nitrite/nitrate concentration was significantly decreased in OVX rats, but was restored by estrogen treatment (P < 0.05). There were no differences in the plasma concentration of ADMA in OVX or estrogen-treated rats. L-Arginine had no effect on plasma nitrite/nitrate concentration and BMD in OVX rats. These results suggest that ovariectomy does not influence the plasma concentration of ADMA, and that ADMA is not involved in ovariectomy-induced osteopenia in rats.

Delayed preconditioning by cardiac ischemia involves endogenous calcitonin gene-related peptide via the nitric oxide pathway.

Previous investigations have shown separately that calcitonin gene-related peptide (CGRP) or nitric oxide (NO) is involved in mediation of ischemic preconditioning. In the present study, we tested interactions of CGRP with NO in mediation of delayed preconditioning. In Sprague-Dawley rats, ischemia-reperfusion injury was induced by 45-min occlusion followed by 3-h reperfusion of coronary artery, and preconditioning was induced by four cycles of 3-min ischemia and 5-min reperfusion. Infarct size, plasma creatine kinase activity, the plasma level of NO and CGRP, and the expression of CGRP mRNA in dorsal root ganglion were measured. Pretreatment with preconditioning significantly reduced infarct size and the release of creatine kinase during reperfusion, and caused a significant increase in the expression of CGRP mRNA, concomitantly with an elevation in the plasma level of CGRP and NO. The effects of preconditioning were completely abolished by administration of L-nitroarginine methyl ester (L-NAME, 10 mg/kg, i.p.), an inhibitor of NO synthase. Pretreatment with capsaicin (50 mg/kg, s.c.), which depletes transmitters in capsaicin-sensitive sensory nerves, also blocked the cardioprotection of preconditioning and reduced the synthesis and release of CGRP, but did not affect the concentration of NO. The present results suggest the delayed protection afforded by ischemic preconditioning is also mediated by endogenous CGRP via the NO pathway in rat heart.

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

In the present study, we tested the effects of long-term estrogen replacement treatment on myocardial ischemia-reperfusion injury and on the cardioprotection of ischemic preconditioning in isolated hearts from ovariectomized rats. Ovariectomized rats were treated with 17beta-estradiol (30 micro g/kg/d, s.c.) for 12 weeks. Isolated rat hearts were perfused in the Langendorff mode. Heart rate, coronary flow, left ventricular pressure and its first derivative (+/-LVdp/dtmax) were recorded. Fifteen-min global ischemia and 30-min reperfusion caused a significant decrease of cardiac mechanical function, which were not affected by ovariectomy or estrogen replacement treatment. The isolated hearts in all groups could be preconditioned, and the cardioprotection afforded by preconditioning in the sham-operated rats was greater compared with ovariectomized rats with or without estrogen treatment. These results suggest that long-term estrogen replacement treatment exerts no effect on the inhibition of mechanical function after ischemia-reperfusion, and this study also suggests that estrogen does not affect ischemic preconditioning in isolated hearts of ovariectomized rats.