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1 Departments of Biology, and Chemistry and Physics, Asbury College, Wilmore 40390-1198; 2 Department of Physiology, University of Kentucky College of Medicine, Lexington 40536-0298; 3 Center for Biomedical Engineering, Wenner-Gren Laboratory, University of Kentucky, Lexington 40506-0070; 4 Cardinal Hill Rehabilitation Hospital, Lexington, Kentucky 40504; and 5 Department of Behavioral Science, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033
This experiment quantified the initial disruption and subsequent adaptation of the blood pressure (BP)-heart rate (HR) relationship after spinal cord transection (SCT). BP and HR were recorded for 4 h via an implanted catheter in neurally intact, unanesthetized rats. The animals were then anesthetized, and their spinal cords were severed at T1-T2 (n = 5) or T4-T5 (n = 6) or sham lesioned (n = 4). BP was recorded for 4 h daily over the ensuing 6 days. The neurally intact rat showed a positive cross correlation, with HR leading BP at the peak by 1.8 ± 0.8 (SD) s. The cross correlation in unanesthetized rats (n = 2) under neuromuscular blockade was also positive, with HR leading. After SCT at T1-T2, the cross correlation became negative, with BP leading HR, and did not change during the next 6 days. The cross correlation also became negative 1-3 days after SCT at T4-T5, but in four rats by day 6 and thereafter the cross correlation progressively reverted to a positive value. We propose that the positive cross correlation with HR leading BP in the intact rat results from an open-loop control that depends on intact supraspinal input to sympathetic preganglionic neurons in the spinal cord. After descending sympathetic pathways were severed at T1-T2, the intact vagal pathway to the sinoatrial node dominated BP regulation via the baroreflex. We suggest that reestablishment of the positive correlation after SCT at T4-T5 was attributable to the surviving sympathetic outflow to the heart and upper vasculature reasserting some effective function, perhaps in association with decreased spinal sympathetic hyperreflexia. The HR-BP cross correlation may index progression of sympathetic dysfunction in pathological processes.
sympathetic; parasympathetic; dysautonomia; cross correlation; baroreflex
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