The aim of the present study was to determine the effect of dexmedetomidine on hemodynamic changes and inflammatory responses in patients undergoing off-pump coronary artery bypass grafting (OPCABG). A total of 300 patients about to receive OPCABG were randomized evenly into the control group (n=116) and study group (n=123). Intravenous dexmedetomidine pump infusion was administered to patients in the study group at a rate of 0.4 µg.kg-1 .h-1. The control group received physiological saline at the same infusion speed. Changes in hemodynamic parameters and inflammatory indices were compared between the two groups. Hemodynamic parameters, such as the heart rate and mean arterial pressure, were lower in patients from the study group, compared with that in the control group (both P<0.05). The levels of pro-inflammatory factors, such as interleukin (IL)-6, tumor necrosis factor-α and C-reactive protein, were also reduced in the study group (P<0.05). The observed levels of IL-10 were lower in the control group compared with that in the study group, although a statistically significant difference was not achieved. Thus, the administration of dexmedetomidine in patients undergoing OPCABG stabilized hemodynamics and reduced inflammation. The present study was registered at the Chinese Clinical Trial Registry, under the trial registration number ChiCTR-OOC-15005978 (2015).

Heart (right) failure is the most frequent cause of death in patients with pulmonary arterial hypertension. Although historically, increased right ventricular afterload has been considered the main contributor to right heart failure in such patients, recent evidence has suggested a potential role of load-independent factors. Here, we tested the hypothesis that resistin–like molecule α (RELMα), which has been implicated in the pathogenesis of vascular remodeling in pulmonary artery hypertension, also contributes to cardiac metabolic remodeling, leading to heart failure. Recombinant RELMα (rRELMα) was generated via a Tet-On expression system in the T-REx 293 cell line. Cultured neonatal rat cardiomyocytes were treated with purified rRELMα for 24 h at a dose of 50 nM. Treated cardiomyocytes exhibited decreased mRNA and protein expression of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) and transcription factors PPARα and ERRα, which regulate mitochondrial fatty acid metabolism, whereas genes that encode for glycolysis-related proteins were significantly upregulated. Cardiomyocytes treated with rRELMα also exhibited a decreased basal respiration, maximal respiration, spare respiratory capacity, ATP-linked OCR, and increased glycolysis, as assessed with a microplate-based cellular respirometry apparatus. Transmission electron microscopy revealed abnormal mitochondrial ultrastructure in cardiomyocytes treated with rRELMα. Our data indicate that RELMα affects cardiac energy metabolism and mitochondrial structure, biogenesis, and function by downregulating the expression of the PGC-1α/PPARα/ERRα axis.