DeVeau Kathryn M, Martin Emily K, King Nicholas T, Shum-Siu Alice, Keller Bradley B, West Christopher R, Magnuson David S K
Anatomical Sciences & Neurobiology, University of Louisville, Louisville, KY, United States; Department of Neurological Surgery, University of Louisville, Louisville, KY, United States.
Department of Neurological Surgery, University of Louisville, Louisville, KY, United States.
Auton Neurosci. 2018 Jan;209:19-24. doi: 10.1016/j.autneu.2016.12.005. Epub 2016 Dec 23.
There is general consensus that spinal cord injuries (SCI) above T6 result in altered sympathetic control of the heart, which negatively influences cardiac structure and function. To by-pass disrupted circuitry and investigate cardiac responses under enhanced sympathetic activity we utilized dobutamine (DOB) stress echocardiography. Animals were divided into a T2, 25g-cm contusive SCI (SCI) or an uninjured control (CON) group. Echocardiography was performed pre-SCI and at 1, 2 and 6weeks post-SCI. Increasing doses of DOB (5, 10 & 20μg/min/kg) were infused intravenously pre-SCI and at 1 and 6weeks post-SCI. Parasternal-short axis images were used to compare group differences in systolic function and track changes in response to SCI and DOB over time. One week post-SCI, stroke volume (SV), end diastolic volume (EDV), cardiac output (CO) and ejection fraction (EF) were all reduced compared to CON and these deficits persisted to 6weeks. We also found an increase in collagen deposition at 6weeks post SCI. Pre-SCI, DOB elicited a decrease in EDV and increases in CO, EF and HR but not SV. At 6weeks following SCI, in addition to increases in CO, EF and HR, DOB also induced increases in SV. This is the first report, to our knowledge, of DOB responses in a contusive SCI model with persistent cardiac impairments. The return of CO to pre-SCI levels and the substantial increase in SV at low DOB dosages shows that impaired descending control of the heart is directly contributing to reduced resting SV after SCI.
普遍共识是,T6以上的脊髓损伤(SCI)会导致心脏交感神经控制改变,这对心脏结构和功能产生负面影响。为了绕过受损的神经回路并研究交感神经活动增强时的心脏反应,我们使用了多巴酚丁胺(DOB)负荷超声心动图。将动物分为T2、25g-cm挫伤性脊髓损伤(SCI)组或未受伤的对照组(CON)。在脊髓损伤前以及脊髓损伤后1、2和6周进行超声心动图检查。在脊髓损伤前以及脊髓损伤后1和6周静脉内输注递增剂量的多巴酚丁胺(5、10和20μg/min/kg)。使用胸骨旁短轴图像比较收缩功能的组间差异,并跟踪脊髓损伤和多巴酚丁胺随时间变化的反应。脊髓损伤后1周,与对照组相比,每搏输出量(SV)、舒张末期容积(EDV)、心输出量(CO)和射血分数(EF)均降低,这些缺陷持续至6周。我们还发现脊髓损伤后6周胶原沉积增加。脊髓损伤前,多巴酚丁胺引起舒张末期容积降低,心输出量、射血分数和心率增加,但每搏输出量未增加。脊髓损伤后6周,除了心输出量、射血分数和心率增加外,多巴酚丁胺还诱导每搏输出量增加。据我们所知,这是关于具有持续性心脏损伤的挫伤性脊髓损伤模型中多巴酚丁胺反应的首次报告。心输出量恢复到脊髓损伤前水平以及低剂量多巴酚丁胺时每搏输出量大幅增加表明,脊髓损伤后心脏下行控制受损直接导致静息每搏输出量降低。