Yu-juan Zhao1, Feng-qi Liu2, Chun-hong Xiu2, Jie Jiang2, Jian-hua Wang2, Yan-song Xu2, Shi-ying Fu2, Qi Huang3. 1. Department of Cardiology, First Clinical Medical College of Harbin Medical University,. Electronic address: zhaoyujuan2008@yahoo.cn. 2. Department of Cardiology, First Clinical Medical College of Harbin Medical University. 3. Centre for Cellular Morphology, Harbin Medical University, Harbin, China.
Abstract
OBJECTIVE: To evaluate the effect of high thoracic epidural analgesia (HTEA) in congestive heart failure (CHF). DESIGN: Rat model of CHF. SETTING: Harbin Medical University, Harbin, Heilongjiang, China. PARTICIPANTS: One hundred thirty-five rats. INTERVENTIONS: HTEA involved 5 times daily injections of 0.1% lidocaine at the T3-T4 level. MEASUREMENTS AND MAIN RESULTS: The authors examined myocardial norepinephrine (NE), angiotensin II (Ang II), endothelin-1 (ET1), and tumor necrosis factor-α (TNF-α) concentrations 2, 4, and 6 weeks after the start of HTEA. They also examined histologic changes in heart tissue and myocardial expression of apoptosis-inducing factor (AIF) and poly (ADP-ribose) polymerase (PARP). Sham rats were used as a control. In the time course, myocardial NE, Ang II, ET1, and TNF-α concentrations were significantly higher in the CHF group compared with the HTEA and sham groups (p< 0.05). Similarly, PARP and AIF protein expression levels were significantly higher in the CHF group compared with the HTEA and sham groups (p< 0.05). Microscopy revealed pronounced damage to myocardial cell structures in the CHF group; this damage clearly was reduced in the HTEA group. In addition, cardiac function evaluation indicated treatment with HTEA resulted in similar heart function as animals that did not have surgically induced CHF. CONCLUSIONS: The findings suggest that HTEA induces changes in sympathetic nervous system, renin-angiotensin system, endothelial, and inflammatory process activity involved in CHF.
OBJECTIVE: To evaluate the effect of high thoracic epidural analgesia (HTEA) in congestive heart failure (CHF). DESIGN:Rat model of CHF. SETTING: Harbin Medical University, Harbin, Heilongjiang, China. PARTICIPANTS: One hundred thirty-five rats. INTERVENTIONS: HTEA involved 5 times daily injections of 0.1% lidocaine at the T3-T4 level. MEASUREMENTS AND MAIN RESULTS: The authors examined myocardial norepinephrine (NE), angiotensin II (Ang II), endothelin-1 (ET1), and tumor necrosis factor-α (TNF-α) concentrations 2, 4, and 6 weeks after the start of HTEA. They also examined histologic changes in heart tissue and myocardial expression of apoptosis-inducing factor (AIF) and poly (ADP-ribose) polymerase (PARP). Sham rats were used as a control. In the time course, myocardial NE, Ang II, ET1, and TNF-α concentrations were significantly higher in the CHF group compared with the HTEA and sham groups (p< 0.05). Similarly, PARP and AIF protein expression levels were significantly higher in the CHF group compared with the HTEA and sham groups (p< 0.05). Microscopy revealed pronounced damage to myocardial cell structures in the CHF group; this damage clearly was reduced in the HTEA group. In addition, cardiac function evaluation indicated treatment with HTEA resulted in similar heart function as animals that did not have surgically induced CHF. CONCLUSIONS: The findings suggest that HTEA induces changes in sympathetic nervous system, renin-angiotensin system, endothelial, and inflammatory process activity involved in CHF.
Authors: Tamás Bárány; Andrea Simon; Gergő Szabó; Rita Benkő; Zsuzsanna Mezei; Levente Molnár; Dávid Becker; Béla Merkely; Endre Zima; Eszter M Horváth Journal: Oxid Med Cell Longev Date: 2017-11-09 Impact factor: 6.543