The protective effects of 17beta-estradiol against ischemia–reperfusion injury and its effect on pacing postconditioning protection to the heart

Abstract

The role of pacing postconditioning (PPC) in the heart protection against ischemia-reperfusion injury is not completely understood. The aim of this study was to investigated if 17-β-estradiol (estrogen, E2), endogenous atrial natriuretic peptide (ANP), endogenous brain natriuretic peptide (BNP), and tumor necrosis factor-alpha (TNF-α) are involved in PPC-mediated protection. Langendorff perfused female Wistar rat hearts were used for this study. Hearts challenged with regional ischemia for 30 min subjected to no further treatment served as a control. The PPC protocol was 3 cycles of 30 s pacing alternated between the right atrium and left ventricle (LV). Protection was assessed by recovery of LV contractility and coronary vascular-hemodynamics. Ischemia induced a significant (P < 0.05) deterioration in the heart function compared with baseline data. PPC alone or in combination with short-term E2 treatment (E2 infusion at the beginning of reperfusion) significantly (P < 0.05) improved the heart functions. Short-term E2 treatment post-ischemically afforded protection similar to that of PPC. However, long-term E2 substitution for 6 weeks completely attenuated the protective effects of PPC. Although no changes were noted in endogenous ANP levels, PPC significantly increased BNP expression level and decreased TNF-α in the cardiomyocyte lysate and coronary effluent compared to ischemia and controls. Our data suggested a protective role for short-term E2 treatment similar to that of PPC mediated by a pathway recruiting BNP and downregulating TNF-α. Our study further suggested a bad influence for long-term E2 substitution on the heart as it completely abrogated the protective effects of PPC.

Discrepancy in calcium release from the sarcoplasmic reticulum and intracellular acidic stores for the protection of the heart against ischemia/reperfusion injury

“…Moreover, PPC induced a remarkable reduction in the CK and LDH levels. Although evaluations of hemodynamics have seldom been conducted, the protective effects of PPC were reported by us and other researchers [1,2,30,34]. However, the pathways involved in PPC-mediated protection and the interaction between PPC and body homeostasis have not been completely elucidated.…”

“…Anesthesia was administered to the rats via intraperitoneal injection of sodium pentobarbital (60 mg/kg), and the anticoagulant heparin (a dose of 1000 U/kg body weight) was delivered via the femoral vein. Heart cannulation and perfusion were performed as described previously [1]. Briefly, the isolated heart was retrogradely perfused with freshly prepared KrebsHensleit buffer (117.86 mM NaCl, 5 Oxygenation was performed using a mixture of CO 2 (5 %) and O 2 (95 %) at a pH range of 7.35 to 7.45 and at a temperature of 37.0 ± 0.5°C.…”

“…Coronary vascular dynamics were evaluated by assessing coronary flow (CF) and coronary vascular resistance (CVR). Cardiovascular functions were measured as previously described [1,3]. Briefly, a waterfilled latex balloon was placed and secured in the LV cavity.…”

The Expanding Complexity of Estrogen Receptor Signaling in the Cardiovascular System

“…Premenopausal women have reduced cardiovascular disease and the occurrence increases after menopause 1, 2 . Furthermore, many studies in animal models have reported less hypertrophy and less ischemia-reperfusion (I/R) injury in females compared to males 3, 4 . Additional studies with ovariectomized females have also shown that addition of estrogen reduces hypertrophy and I/R injury 5 (Figure 1 summarize the cardiovascular effects associated with estrogen).…”

Remifentanil functions in the adaptive protection of cardiac function following ischemia

“…A previous study has indicated that opioid receptor agonists can protect diastolic and systolic function following ischemia-reperfusion (19). Kin et al (20) revealed that an opioid receptor agonist had no effect on myocardial diastolic and systolic function prior to ischemia, but that the left ventricular end-diastolic pressure (LVEDP) of the agonist group prior to ischemia increased more slowly and that cardiac spasmodic contraction occurred later than in the control group.…”