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.
Keywords: apoptosis; congestive heart failure; cytokines; high thoracic epidural analgesia; neurohumoral factors.
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