Heart rate-arterial blood pressure relationship in conscious rat before vs. after spinal cord transection

2002 ◽  
Vol 283 (3) ◽  
pp. R748-R756 ◽  
Author(s):  
Bobby R. Baldridge ◽  
Don E. Burgess ◽  
Ethan E. Zimmerman ◽  
Jonathan J. Carroll ◽  
Aletia G. Sprinkle ◽  
...  

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.

1989 ◽  
Vol 257 (6) ◽  
pp. R1506-R1511 ◽  
Author(s):  
L. C. Weaver ◽  
R. D. Stein

Previous experiments in our laboratory have shown that discharge of splenic, mesenteric, and splanchnic nerves is well maintained after spinal cord transection in chloralose-anesthetized cats (8, 9, 11). The primary purpose of this investigation was to determine if maintained sympathetic discharge could be observed after spinal transection in the absence of chloralose anesthesia. In cats anesthetized with alphaxalone-alphadolone, changes in splanchnic discharge, blood pressure, and heart rate caused by decerebration and removal of the forebrain were observed. This procedure decreased blood pressure, increased heart rate, and had no immediate effect on sympathetic discharge or its rhythm (assessed by power density spectral analysis). One hour after decerebration and termination of anesthesia, splanchnic discharge had increased by approximately 36%. Next, effects of spinal cord transection on discharge of splanchnic, mesenteric, and renal nerves were observed in the decerebrate-unanesthetized cats. Splanchnic discharge decreased by 50%, mesenteric nerve discharge was unchanged, and renal nerve discharge decreased by 97%. Therefore, splanchnic nerve discharge was not as well maintained in decerebrate-unanesthetized cats as it had been in chloralose-anesthetized animals, and the remaining splanchnic discharge appeared to affect mesenteric nerves preferentially. Finally, spectral analysis of the splanchnic discharge demonstrated that before cord transection, most of the signal was in the 0- to 6-Hz frequency range, whereas after transection the proportion of signal in this frequency range was significantly reduced and the proportion in higher frequencies (7-25 Hz) was significantly increased. This loss of low-frequency rhythmicity is consistent with findings in our previous studies in chloralose-anesthetized cats.


2007 ◽  
Vol 5;10 (9;5) ◽  
pp. 677-685
Author(s):  
David M. Schultz

Background: Several animal studies support the contention that thoracic spinal cord stimulation (SCS) might decrease arterial blood pressure. Objective: To determine if electrical stimulation of the dorsal spinal cord in humans will lower mean arterial pressure (MAP) and heart rate (HR). Design: Case Series Methods: Ten normotensive subjects that were clinically indicated for SCS testing were studied. Two of the 10 patients who underwent testing were excluded from the analysis because they did not respond to the Cold Pressor Test (CPT). Systolic blood pressure, diastolic blood pressure, and heart rate were measured continuously at the wrist (using the Vasotrac device). SCS was administered with quadripolar leads implanted into the epidural space under fluoroscopic guidance. SCS was randomly performed either in the T1-T2 or T5-T6 region of the spinal cord during normal conditions as well as during transient stress induced by CPT. The CPT was conducted by immersing the non-dominant hand in ice-cold water for 2 minutes. Results: There were moderate decreases in MAP and HR during SCS at the T5-T6 region compared to baseline that did not reach statistical significance. However, SCS at the T1-T2 region tended to increase MAP and HR compared to baseline but the change did not reach statistical significance. Arterial blood pressure was transiently elevated by 9.4 ± 3.8 mmHg using CPT during the control period with SCS turned off and also during SCS at either the T1-T2 region or T5-T6 region of the spinal cord (by 9.2 ± 5 mmHg and 10.7 ± 8.4 mmHg, respectively). During SCS at T5-T6, the CPT significantly increased MAP by 5.9±7.1 mmHg compared to control CPT (SCS off). Conclusion: This study demonstrated that SCS at either the T1-T2 or T5-T6 region did not significantly alter MAP or HR compared to baseline (no SCS). However, during transcient stress (elevated sympathetic tone) induced by CPT, there was a significant increase in MAP and moderate decrease in HR during SCS at T5-T6 region, which is not consistent with previous data in the literature. Acute SCS did not result in adverse cardiovascular responses and proved to be safe. Key words: Spinal cord stimulation, mean arterial pressure, heart rate, cold pressor test


2005 ◽  
Vol 99 (1) ◽  
pp. 53-58 ◽  
Author(s):  
A. William Sheel ◽  
Andrei V. Krassioukov ◽  
J. Timothy Inglis ◽  
Stacy L. Elliott

Autonomic dysreflexia (AD) can occur during penile vibratory stimulation in men with spinal cord injury, but this is variable, and the association with lesion level is unclear. The purpose of this study was to characterize the cardiovascular responses to penile vibratory stimulation in men with spinal cord injury. We hypothesized that those with cervical injuries would demonstrate a greater degree of AD compared with men with thoracic injuries. We also questioned whether the rise in blood pressure could be attenuated by sildenafil citrate. Participants were classified as having cervical ( n = 8) or thoracic ( n = 5) injuries. While in a supine position, subjects were instrumented with an ECG, and arterial blood pressure was determined beat by beat. Subjects reported to the laboratory twice and received an oral dose of sildenafil citrate (25–100 mg) or no medication. Penile vibratory stimulation was performed using a handheld vibrator to the point of ejaculation. At ejaculation during the nonmedicated trials, the cervical group had a significant decrease in heart rate (−5–10 beats/min) and increase in mean arterial blood pressure (+70–90 mmHg) relative to resting conditions, whereas the thoracic group had significant increases in both heart rate (+8–15 beats/min) and mean arterial pressure (+25–30 mmHg). Sildenafil citrate had no effect on the change in heart rate or mean arterial pressure in either group. In summary, men with cervical injuries had more pronounced AD during penile vibratory stimulation than men with thoracic injuries. Administration of sildenafil citrate had no effect on heart rate or blood pressure during penile vibratory stimulation in men with spinal cord injury.


1975 ◽  
Vol 228 (4) ◽  
pp. 1288-1292 ◽  
Author(s):  
RD Wurster ◽  
WC Randall

Arterial blood pressure, heart rate, and cutaneous volume pulses were recorded during controlled elevation of urinary bladder pressure in a group of seven patients with spinal cord transsection above vertebral level T5 and in another group of four patients below T5. Profound elevations in systolic blood pressure and pulse pressure were induced by bladder distension when the lesion was situated above T5. Lesser elevations occurred in patients with lesions below T5. Marked vasoconstriction characterized skin areas innervated by the "isolated" spinal cord, while passive dilatation occurred in areas supplied by the proximal cord. Only three of seven patients with lesions above T5 level had decreased heart rate during marked elevations in arterial blood pressure. The marked elevations in pulse pressure in patients with lesions above T5 could not be explained solelyby increased vasoconstriction and decreased heart rate, but involves also inotropic cardiac responses. These inotropic responses are mediated by cardiac sympathetic nerves which leave the spinal cord above the T5 level.


1997 ◽  
Vol 273 (4) ◽  
pp. R1361-R1366 ◽  
Author(s):  
Giorgio R. Sansone ◽  
Ralph Bianca ◽  
Rafael Cueva-Rolón ◽  
Lisbeth E. Gómez ◽  
Barry R. Komisaruk

The present study ascertained whether increases in heart rate (HR) and systolic blood pressure (SBP) produced by vaginocervical stimulation (VS; 500 g force) persist in the unanesthetized rat after chronic spinal cord transection at selected levels. Three groups were used: spinal cord transection at T7 ( n = 10) or L5 ( n = 10) or a sham-operated control group (Sh, n = 10). In the Sh group, VS increased significantly both HR, by 95 ± 14.3 beats/min (bpm) (22 ± 3.7% above baseline), and BP, by 37 ± 5.7 mmHg (37 ± 7.7% above baseline), confirming earlier findings. In the T7 group, VS significantly decreased HR by 107 ± 21.4 bpm (27 ± 4.1% below baseline) and increased BP by 41.3 ± 12.9 mmHg (32 ± 8.3% above baseline). In response to VS, HR increased in every rat in the Sh group and decreased in every rat in the T7 group. In the L5 group, VS failed to significantly affect HR or BP. In the present study, specific levels of spinal cord transection produced differential HR and BP responses to VS in the rat. A model is presented addressing the component responses of autonomic dysreflexia that can occur, contingent on the level of spinal cord injury, in women during parturition or sexual intercourse.


2007 ◽  
Vol 292 (4) ◽  
pp. R1502-R1509 ◽  
Author(s):  
Paolo Castiglioni ◽  
Marco Di Rienzo ◽  
Arsenio Veicsteinas ◽  
Gianfranco Parati ◽  
Giampiero Merati

It is still unclear whether the low-frequency oscillation in heart rate is generated by an endogenous neural oscillator or by a baroreflex resonance. Our aim was to investigate this issue by analyzing blood pressure and heart rate variability and the baroreflex function in paraplegic subjects with spinal cord injury below the fourth thoracic vertebra. These subjects were selected because they represent a model of intact central neural drive to the heart, with a partially impaired autonomic control of the vessels. In our study, arterial blood pressure and ECG were recorded in 33 able-bodied controls and in 33 subjects with spinal cord lesions between the fifth thoracic and the fourth lumbar vertebra 1) during supine rest (lowest sympathetic activation), 2) sitting on a wheelchair (light sympathetic activation), and 3) during exercise (moderate sympathetic activation). Blood pressure and heart rate spectra, coherence, and baroreflex function (sequence technique) were estimated in each condition. Compared with controls, paraplegic subjects showed a reduction of the low-frequency power of blood pressure and heart rate, and, unlike controls, a 0.1-Hz peak did not appear in their spectra. Sympathetic activation increased the 0.1-Hz peak of blood pressure and heart rate and the coherence at 0.1 Hz in controls only. Paraplegic subjects also had significantly lower baroreflex effectiveness and greater blood pressure variability. In conclusion, the disappearance of the 10-s oscillation of heart rate and blood pressure in subjects with spinal cord lesion supports the hypothesis of the baroreflex nature of this phenomenon.


2020 ◽  
Vol 128 (3) ◽  
pp. 554-564
Author(s):  
Heidi L. Lujan ◽  
Stephen E. DiCarlo

A wide range of spinal cord levels (cervical 8–thoracic 6) project to the stellate ganglia (which provides >90% of sympathetic supply to the heart), with a peak at the thoracic 2 (T2) level. We hypothesize that despite the proximity of the lesions, high thoracic spinal cord injuries (i.e., T2–3 SCI) do not closely mimic the hemodynamic responses recorded with cervical SCI (i.e., C6–7 SCI). To test this hypothesis, rats were instrumented with an intra-arterial telemetry device (Data Sciences International PA-C40) for recording arterial pressure, heart rate, and locomotor activity as well as a catheter within the intraperitoneal space. After recovery, rats were subjected to complete C6–7 spinal cord transection ( n = 8), sham transection ( n = 4), or T2–3 spinal cord transection ( n = 7). After the spinal cord transection or sham transection, arterial pressure, heart rate, and activity counts were recorded in conscious animals, in a thermoneutral environment, for 20 s every minute, 24 h/day for 12 consecutive weeks. After 12 wk, chronic reflex- and stress-induced cardiovascular and hormonal responses were compared in all groups. C6–7 rats had hypotension, bradycardia, and reduced physical activity. In contrast, T2–3 rats were tachycardic. C6–7 rats compared with T2–3 and spinal intact rats also had reduced cardiac sympathetic tonus, reduced reflex- and stress induced cardiovascular responses, and reduced sympathetic support of blood pressure as well as enhanced reliance on angiotensin to maintain arterial blood pressure. Thus injuries above and below the peak level (T2) of spinal cord projections to the stellate ganglia have remarkably different outcomes. NEW & NOTEWORTHY Twelve consecutive weeks of resting hemodynamic data as well as chronic reflex- and stress-induced cardiovascular, autonomic, and hormonal responses were compared in spinal intact and C6–7 and T2–3 spinal cord-transected rats. C6–7 rats compared with T2–3 and spinal intact rats had reduced cardiac sympathetic tonus, reduced reflex- and stress-induced cardiovascular responses, and reduced sympathetic support of blood pressure as well as enhanced reliance on angiotensin to maintain arterial blood pressure. Thus injuries above and below the peak level (T2) of spinal cord projections to the stellate ganglia have remarkably different outcomes.


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