Effects of spinal cord transection on sympathetic discharge in decerebrate-unanesthetized cats

1989 ◽  
Vol 257 (6) ◽  
pp. R1506-R1511 ◽  
Author(s):  
L. C. Weaver ◽  
R. D. Stein
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Spectral Analysis ◽  
Spinal Cord Transection ◽  
Renal Nerves ◽  
Frequency Range ◽  
Renal Nerve ◽  
Sympathetic Discharge ◽  
Nerve Discharge

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.

Cardiovascular responses to vaginocervical stimulation in the spinal cord-transected rat

1997 ◽  
Vol 273 (4) ◽  
pp. R1361-R1366 ◽  
Author(s):  
Giorgio R. Sansone ◽  
Ralph Bianca ◽  
Rafael Cueva-Rolón ◽  
Lisbeth E. Gómez ◽  
Barry R. Komisaruk
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Spinal Cord Injury ◽  
Cardiovascular Responses ◽  
Spinal Cord Transection ◽  
Autonomic Dysreflexia ◽  
Control Group ◽  
Cord Injury ◽  
Sh Group

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.

Effect of in vivo gene transfer of nNOS in the PVN on renal nerve discharge in rats

2002 ◽  
Vol 282 (2) ◽  
pp. H594-H601 ◽  
Author(s):  
Yi-Fan Li ◽  
Shyamal K. Roy ◽  
Keith M. Channon ◽  
Irving H. Zucker ◽  
Kaushik P. Patel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nadph Diaphorase ◽  
Sympathetic Outflow ◽  
Renal Nerve ◽  
Cultured Fibroblasts ◽  
Dose Dependent Increase ◽  
Nerve Discharge

The paraventricular nucleus (PVN) of the hypothalamus is known to be involved in the control of sympathetic outflow. Nitric oxide (NO) has been shown to have a sympathoinhibitory effect in the PVN. The goal of the present study was to examine the influence of overexpression of neuronal NO synthase (nNOS) within the PVN on renal sympathetic nerve discharge (RSND). Adenovirus vectors encoding either nNOS (Ad.nNOS) or β-galactosidase (Ad.β-Gal) were transfected into the PVN in vivo. Initially, the dose of adenovirus needed for infection was determined from in vitro infection of cultured fibroblasts. In Ad.nNOS-treated rats, the local expression of nNOS within the PVN was confirmed by histochemistry for NADPH-diaphorase-positive neurons. There was a robust increase in staining of NADPH-diaphorase-positive cells in the PVN on the side injected with Ad.nNOS. The staining peaked at 3 days after injection of the virus. In α-chloralose- and urethane-anesthetized rats, microinjection of N G-monomethyl-l-arginine (l-NMMA), a NO antagonist, into the PVN produced a dose-dependent increase in RSND, blood pressure, and heart rate. There was a potentiation of the increase in RSND, blood pressure, and heart rate due to l-NMMA in Ad.nNOS-injected rats compared with Ad.β-Gal-injected rats. These results suggest that the endogenous NO-mediated effect in the PVN of Ad.nNOS-treated rats is more effective in suppressing RSND compared with Ad.β-Gal-treated rats. These observations support the contention that an overexpression of nNOS within the PVN may be responsible for increased suppression of sympathetic outflow. This technique may be useful in pathological conditions know to have increased sympathetic outflow, such as hypertension or heart failure.

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 ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Cross Correlation ◽  
Open Loop ◽  
Spinal Cord Transection ◽  
Conscious Rat ◽  
Loop Control ◽  
Arterial Blood ◽  
The Cross

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.

Blood pressure power within frequency range ∼0.4 Hz in rat conforms to self-similar scaling following spinal cord transection

2005 ◽  
Vol 288 (3) ◽  
pp. R737-R741 ◽  
Author(s):  
David C. Randall ◽  
Bobby R. Baldridge ◽  
Ethan E. Zimmerman ◽  
Jonathan J. Carroll ◽  
Richard O. Speakman ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Transection ◽  
Frequency Range ◽  
Self Similarity ◽  
Intact State ◽  
Arterial Blood ◽  
Before And After ◽  
Self Similar ◽  
Lower Frequencies

This study quantified the effect of interrupting the descending input to the sympathetic preganglionic neurons on the dynamic behavior of arterial blood pressure (BP) in the unanesthetized rat. BP was recorded for ∼4-h intervals in six rats in the neurally intact state and in the same animals after complete spinal cord transection (SCT) between T4 and T5. In the intact state, power within the frequency range of 0.35–0.45 Hz was 1.53 ± 0.38 mmHg2/Hz (mean ± SD by fast Fourier transform). One week after SCT, power within this range decreased significantly ( P < 0.05) to 0.43 ± 0.62 mmHg2/Hz. To test for self-similarity before and after SCT, we analyzed data using a wavelet (i.e., functionally, a digital bandpass filter) tuned to be maximally sensitive to fluctuations with periods of ∼2, 4, 8, 16, 32, or 64 s. In the control state, all fluctuations with periods of ≥4 s conformed to a “self-similar” (i.e., fractal) distribution. In marked contrast, the oscillations with a period of ∼2 s (i.e., ∼0.4 Hz) were significantly set apart from those at lower frequencies. One day and seven days after the complete SCT, however, the BP fluctuations at ∼0.4 Hz now also conformed to the same self-similar behavior characteristic of the lower frequencies. We conclude that 1) an intact sympathetic nervous system endows that portion of the power spectrum centered around ∼0.4 Hz with properties (e.g., a periodicity) that differ significantly from the self-similar behavior that characterizes the lower frequencies and 2) even within the relatively high frequency range at 0.4 Hz self-similarity is the “default” condition after sympathetic influences have been eliminated.

Dorsal root afferent influences on tonic firing of renal and mesenteric sympathetic nerves in rats

1993 ◽  
Vol 264 (6) ◽  
pp. R1193-R1199 ◽  
Author(s):  
R. B. Taylor ◽  
L. C. Weaver
Keyword(s):  
Spinal Cord ◽  
Dorsal Root ◽  
Sympathetic Nerves ◽  
Renal Nerve ◽  
Dorsal Rhizotomy ◽  
Renal Nerve Activity ◽  
Afferent Discharge ◽  
High Cervical ◽  
Sympathetic Discharge ◽  
Nerve Discharge

After spinal cord transection in cats and rats, the activity of many sympathetic nerves is not entirely lost, and firing of other nerves continues unabated or is increased. This study was done to evaluate the importance of dorsal root afferent discharge on the generation of tonic sympathetic activity in renal and mesenteric postganglionic nerves in spinal rats and in rats with intact neuraxes. Sympathetic discharge was recorded in anesthetized rats, and peripheral afferent influences were eliminated by dorsal rhizotomy from T4 to L2. Activity of renal and mesenteric nerves was well maintained after high cervical and thoracic (T4) cord transections. Rhizotomy had no effect on sympathetic discharge in rats with intact neuraxes but decreased renal nerve activity significantly (-25%) in spinal rats. Because rhizotomy decreased mesenteric discharge in only three of six spinal rats, mean mesenteric nerve discharge was not decreased significantly. The decreased renal nerve discharge after dorsal rhizotomy could not be attributed to input from any specific spinal segment, and ipsilateral input was no greater than contralateral input. After rhizotomy, both renal and mesenteric nerves had substantial excitatory drive from the transected, deafferented spinal cord. These findings demonstrate that dorsal root afferent influences on spinal neurons can contribute to the generation of tonic discharge in some sympathetic nerves in spinal animals.

Effect of nitric oxide within the paraventricular nucleus on renal sympathetic nerve discharge: role of GABA

1998 ◽  
Vol 275 (3) ◽  
pp. R728-R734 ◽  
Author(s):  
Kun Zhang ◽  
Kaushik P. Patel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Sympathetic Nerve ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Sympathetic Nerve ◽  
Arterial Blood ◽  
Gaba System ◽  
Renal Sympathetic ◽  
Nerve Discharge

Both nitric oxide (NO) and GABA are known to provide inhibitory inputs to the paraventricular nucleus (PVN) of the hypothalamus and are involved in the control of sympathetic outflow. The purpose of the present study was to examine the interaction of NO and GABA in the regulation of renal sympathetic nerve activity in rats. The responses of renal nerve activity, blood pressure, and heart rate to microinjection of sodium nitroprusside (SNP), an NO donor, into the PVN were measured in the presence and absence of blockade of the GABA system (bicuculline; 2 nmol). Microinjection of SNP (50, 100, and 200 nmol) into the PVN elicited significant decreases in renal nerve discharge, arterial blood pressure, and heart rate, reaching −36.4 ± 9.7%, −11 ± 5 mmHg, and −34 ± 14 beats/min, respectively, at the highest dose. These responses were eliminated by blockade of the GABA system. Conversely, microinjection of N ω-nitro-l-arginine methyl ester (l-NAME; 50, 100, and 200 nmol) elicited significant increases in the renal sympathetic nerve discharge, arterial blood pressure, and heart rate, reaching 88.9 ± 16.6%, 9 ± 1 mmHg, and 29 ± 9 beats/min, respectively, at the highest dose. These sympathoexcitatory responses were masked by prior blockade of the GABA system with bicuculline. The sympathoexcitatory effect of l-NAME was also eliminated by activation of the GABA system with muscimol. In conclusion, our data indicate that the inhibitory effect of endogenous NO within the PVN on the renal sympathetic nerve activity is mediated by GABA.

Diurnal Blood Pressure Variation in Quadriplegic Chronic Spinal Cord Injury Patients

1991 ◽  
Vol 80 (3) ◽  
pp. 271-276 ◽  
Author(s):  
Henry Krum ◽  
William J. Louis ◽  
Douglas J. Brown ◽  
Graham P. Jackman ◽  
Laurence G. Howes
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Heart Rate ◽  
Spinal Cord Injury ◽  
Ambulatory Monitoring ◽  
Pressure Variation ◽  
Night Time ◽  
Cord Injury ◽  
Blood Pressure Variation ◽  
Neurologically Intact

1. Measurement of blood pressure and heart rate over a 24 h period was peformed in 10 quadriplegic spinal cord injury patients and 10 immobilized, neurologically intact orthopaedic subjects by using the Spacelabs 90207 automated ambulatory monitoring system. 2. Systolic and diastolic blood pressure fell significantly at night in orthopaedic subjects but not in quadriplegic patients, and night-time blood pressures were similar in both groups. 3. Cumulative summation of differences from a reference value (cusum analysis) confirmed a markedly diminished diurnal blood pressure variation in the quadriplegic patients. 4. These findings could not be accounted for on the basis of blood pressure variations during chronic postural change. 5. Heart rate fell significantly at night in both groups. 6. The findings suggest that the increase in blood pressure during waking hours in neurologically intact subjects is a consequence of a diurnal variation in sympathetic activity (absent in quadriplegic patients with sympathetic decentralization) which is independent of changes in physical activity.

Power spectral analysis of heart rate and blood pressure variability in anaesthetized dogs

1992 ◽  
Vol 146 (2) ◽  
pp. 155-164 ◽  
Author(s):  
A. E. HEDMAN ◽  
J. E. K. HARTIKAINEN ◽  
K. U. O. TAHVANAINEN ◽  
M. O. K. HAKUMÄKI
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Spectral Analysis ◽  
Blood Pressure Variability ◽  
Power Spectral Analysis ◽  
Power Spectral

Spinal stimulation to locate preganglionic neurons controlling the kidney, spleen, or intestine

1992 ◽  
Vol 263 (4) ◽  
pp. H1026-H1033 ◽  
Author(s):  
R. B. Taylor ◽  
L. C. Weaver
Keyword(s):  
Spinal Cord ◽  
Sympathetic Outflow ◽  
Renal Nerve ◽  
Homocysteic Acid ◽  
Sympathetic Control ◽  
The Third ◽  
Preganglionic Neurons ◽  
Spinal Segments ◽  
Vascular Beds ◽  
Nerve Discharge

The organization of sympathetic preganglionic neurons may be a substrate for selective control of sympathetic outflow to different vascular beds. This study was done to determine the spinal segments containing preganglionic neurons controlling discharge of renal, splenic, and mesenteric postganglionic nerves. In urethan-anesthetized rats, preganglionic neurons were stimulated by microinjecting D,L-homocysteic acid (3 nl, 0.17 M) into the lateral gray matter of the third thoracic (T3) to the fourth lumbar (L4) spinal segments. Responses from all three nerves could be elicited from segments T4-T13. The greatest increases in renal nerve discharge were evoked from segments T8-T12, the largest increase of 59 +/- 9% elicited from T10. Increases in splenic and mesenteric nerve discharge were smaller and were evoked more uniformly from T4-L3. The largest increases in discharge of splenic and mesenteric nerves were 19 +/- 5% (from T5) and 26 +/- 4% (from T10), respectively. The widely overlapping spinal cord segments controlling these three organs suggest that location of the preganglionic neurons in different spinal segments is not part of the mechanism for selective sympathetic control. However, the larger renal nerve responses demonstrate that sympathetic output to these organs can be differentiated at the level of the spinal cord.

Renal denervation alters cardiovascular and endocrine responses to hemorrhage in conscious newborn lambs

1998 ◽  
Vol 275 (1) ◽  
pp. H285-H291 ◽  
Author(s):  
Francine G. Smith ◽  
Isam Abu-Amarah
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Renal Denervation ◽  
Plasma Renin ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Elevated Plasma ◽  
Baseline Levels ◽  
Renal Sympathetic

To investigate the role of renal sympathetic nerves in modulating cardiovascular and endocrine responses to hemorrhage early in life, we carried out three experiments in conscious, chronically instrumented lambs with intact renal nerves (intact; n = 8) and with bilateral renal denervation (denervated; n = 5). Measurements were made 1 h before and 1 h after 0, 10, and 20% hemorrhage. Blood pressure decreased transiently after 20% hemorrhage in intact lambs and returned to control levels. In denervated lambs, however, blood pressure remained decreased after 60 min. After 20% hemorrhage, heart rate increased from 170 ± 16 to 207 ± 18 beats/min in intact lambs but not in denervated lambs, in which basal heart rates were already elevated to 202 ± 21 beats/min. Despite an elevated plasma renin activity (PRA) measured in denervated (12.0 ± 6.4 ng ANG I ⋅ ml−1 ⋅ h−1) compared with intact lambs (4.0 ± 1.1 ng ANG I ⋅ ml−1 ⋅ h−1), the increase in PRA in response to 20% hemorrhage was similar in both groups. Plasma levels of arginine vasopressin increased from 11 ± 8 to 197 ± 246 pg/ml after 20% hemorrhage in intact lambs but remained unaltered in denervated lambs from baseline levels of 15 ± 10 pg/ml. These observations provide evidence that in the newborn, renal sympathetic nerves modulate cardiovascular and endocrine responses to hemorrhage.

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