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Study design: Experimental laboratory investigation of spinal cord conductivity alterations in a rat model of ischemic spinal cord injury (SCI). Objective: To observe the epidural spinal cord stimulation-induced electromyography responses, and to investigate the possible alterations of spinal cord conduction velocity (SCCV) and compound muscle action potentials (CMAPs) after ischemic SCI in rats. Settings: Adnan Menderes University, Institute of Health Science, Aydin, Turkey. Methods: SCI was induced by transient occlusion of the abdominal aorta in male Sprague-Dawley rats. Spinal cord histopathology was examined to determine neuronal damage and Tarlov scale was used to grade locomotor functions. Epidural electrical stimulation of spinal cord was performed by monopolar needle electrodes sequentially at L1-L2 and L5-L6 levels, and CMAPs were recorded from the left gastrocnemius muscle by surface electrodes. Amplitudes and durations of CMAPs were evaluated and SCCVs were calculated by analyzing the latency difference of CMAPs. Results: Ischemia-induced SCI resulted in significant reduction of Tarlov scores and a significant decline in number of viable neurons. Similarly, a significant decrement was observed in SCCV following spinal cord ischemia. Conclusion: This study demonstrated that measurement of SCCV via epidural electrical stimulation is possible and displays a significant decline after spinal cord ischemia in rats. We suggest that this method can be beneficial to quantify neuronal damage after experimental ischemic SCI. Rats are commonly used in experimental studies owing to the firm analogy of spinal cord anatomy between these animals and humans. 2 Motor functions after SCI are generally evaluated by locomotor scales such as Basso Beattie and Bresnahan (BBB) and Tarlov scales. These qualitative assessment methods are performed by visual inspection and scoring of hind limb activity, and mainly determine fine locomotor skills. 3 However, there are difficulties in objective determination of neurological status following SCI in rats, which drive the attempts for developing more quantitative methods. 4,5 Various alternative methods have been developed for quantitative determination of motor deficits after SCI in rodents, which involve employment of video assistance such as single-frame motion analysis, 5 automated quantitative gait analysis 4 or robotic devices. 6

The present study showed that preoperative poor CCC is a powerful predictor of the development of AF after CABG surgery.

This study found that in patients with CAD, compliance with the traditional MD is related to decreased severity of coronary atherosclerosis.

Design of the study, acquisition and analysis of data, final approval. ORIGINAL ARTICLE Experimental SurgeryActa Cir Bras. 2020;35(2):e202000202 AbstractPurpose: To investigate the effects of adalimumab pretreatment on the lipopolysaccharide-mediated myocardial injury.Methods: Twenty-eight Wistar rats were randomized into four groups (n=7). Control (C) group animals were injected once a day with intraperitoneal (i.p) 0.9 % saline for two days. In the Adalimumab (Ada) group, adalimumab was injected at a dose of 10 mg/kg/ day (i.p) for two days. Lipopolysaccharide (Lps) group rats were injected with a dose of 5 mg/kg (i.p) lipopolysaccharide. Lipopolysaccharide + Adalimumab (Lps+Ada) group rats received adalimumab before the administration of lipopolysaccharide. The animals were sacrificed 24 h after the last injection and blood samples were obtained for determination of biochemical cardiac injury markers and circulating levels of TNF-α and interleukin-6 (IL-6). Hearts were harvested for histological examination.Results: Endotoxin exposure resulted in significant increases in serum cardiac injury markers, serum cytokines and histological myocardial injury scores in the Lps group. The levels of circulating cytokines, cardiac injury markers and histological injury scores for myocardial necrosis, perivascular cell infiltration, and inflammation were significantly reduced in Lps+Ada as compared to Lps group (p<0.05). Conclusions:Adalimumab pretreatment reduces endotoxin-induced myocardial damage in rats. This beneficial effect is thought to be related to the reduction of cytokine release.