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Articles in PresS, published online ahead of print April 18, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00003.2002
Submitted on January 7, 2002
Accepted on April 8, 2002
1 Departments of Biology, and Chemistry and Physics, Asbury College, Wilmore, KY, USA
2 Departments of Physiology, University of Kentucky College of Medicine, Lexington, KY, USA
3 Center for Biomedical Engineering, Wenner-Gren Lab, University of Kentucky, Lexington, KY, USA
4 Departments of Physiology, University of Kentucky College of Medicine, Lexington, KY, USA; Cardinal Hill Rehabilitation Hospital, Lexington, KY, USA
5 Departments of Behavioral Science, Pennsylvania State University College of Medicine, Hershey, PA, USA
6 Departments of Physiology, University of Kentucky College of Medicine, Lexington, KY, USA; Center for Biomedical Engineering, Wenner-Gren Lab, University of Kentucky, Lexington, KY, USA
* To whom correspondence should be addressed. E-mail: randall{at}uky.edu.
This experiment quantified the initial disruption and subsequent adaptation of the relationship between blood pressure (BP) and heart rate (HR) after spinal cord transection. Blood pressure and HR were recorded for 4 hours via an implanted catheter in neurally-intact, unanesthetized rats. The animals were then anesthetized and their spinal cords severed at T1-T2 (n=5) or at T4-T5 (n=6) or sham lesioned (n=4). BP was recorded for 4 hours 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 sec. (mean ± SD). The cross-correlation in unanesthetized rats (n=2) under neuromuscular blockade was also positive with HR leading. After the T1-T2 transection 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 to 3 days after the T4-T5 lesion, but in 4 rats by 
day 6 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 upon intact supra-spinal input to sympathetic preganglionic neurons in the spinal cord. After descending sympathetic pathways were severed between T1-T2, the intact vagal pathway to the SA-node dominated BP regulation via the baroreflex. We suggest that the re-establishment of the positive correlation following T4-T5 lesion was attributable to the surviving sympathetic outflow to the heart and upper vasculature reasserting some effective function, perhaps in association with decreased spinal sympathetic hyper-reflexia. The HR-BP cross-correlation may index progression of sympathetic dysfunction in pathological processes.
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