Lumbar Sympathetic Chain Research Articles

Incidence and Risk Factors for Lumbar Sympathetic Chain Injury After Oblique Lumbar Interbody Fusion.

Oblique lumbar interbody fusion (OLIF), performed using a retroperitoneal approach, can lead to complications related to the approach, such as lumbar sympathetic chain injury (LSCI). Although LSCI is a common complication of OLIF, its reported incidence varies across studies due to an absence of specific diagnostic criteria. Moreover, research on the risk factors of postoperative sympathetic chain injuries after OLIF remains limited. Therefore, this study aimed to describe the incidence, and identify independent risk factors for LSCI, in patients with degenerative lumbar spinal diseases who underwent OLIF. Between October 2020 and August 2023, a retrospective review was conducted at our institute on 200 patients who underwent OLIF at 1 to 4 consecutive spinal levels (L1-5) for degenerative spinal diseases including spinal stenosis, spondylolisthesis, degenerative scoliosis. We excluded those with infections, trauma, tumors, and lower extremity edema/warmth due to other causes. The patients were categorized into 2 groups: those with and without LSCI symptoms. Demographic data, operative data, and pre- and postoperative parameters were evaluated for their association with LSCI using a univariate logistic regression model. Variables with a p-value <0.1 in the univariate analysis were included in a multivariate model to identify the independent risk factors. Thirty-five of 200 patients (17.5%) developed LSCI symptoms after OLIF. Multivariate logistic regression analysis indicated that prolonged retraction time, particularly exceeding 31.5 miniutes, remained an independent risk factor (adjusted odds ratio, 12.59; p<0.001). This study demonstrated that prolonged retraction time was an independent risk factor for LSCI following OLIF, particularly when it exceeded 31.5 minutes. Protecting the lumbar sympathetic chain during surgery and minimizing retraction time are crucial to avoiding LSCI following OLIF.

Estrogen, Exercise Training, and Nitric-oxide Mediated Sympatholysis

Our laboratory has previously reported that nitric oxide (NO)-mediated inhibition of sympathetic vasoconstriction in contracting muscle (sympatholysis) was enhanced in female, compared with male rats. Estrogen has been shown to modulate NO synthase (NOS) expression and NO-mediated sympatholysis. Therefore, this study investigated the hypothesis that NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle of female rats would be a function of estrogen bioavailability. Further, exercise training has been shown to enhance sympatholysis. Thus, we also investigated the hypothesis that exercise training would restore sympatholysis in estrogen-deficient rats. Female Sprague-Dawley rats were randomized to sedentary ovary-intact (SOI, n=10), sedentary ovariectomized (SOVX, n=9), exercise-trained (10 weeks, 5 days/week, 600m, 40m·min−1, 5% grade) ovary-intact (TOI, n=13), or exercise-trained ovariectomized (TOVX, n=10) groups. OVX rats had both ovaries surgically removed. Following sedentary behavior or exercise training, rats were anesthetized and instrumented for measurement of blood pressure, femoral vascular conductance (FVC), stimulation of the lumbar sympathetic chain, and contraction of the triceps surae muscle group. The percentage change of FVC (%FVC) in response to sympathetic chain stimulation delivered at 2 and 5 Hz was determined at rest and during muscle contraction (60% maximal contractile force) in control, selective neuronal NOS (nNOS) inhibition (SMTC; 0.6 mg·kg−1 IV), and non-selective NOS inhibition (L-NAME; 10 mg·kg−1 IV) conditions. In the Control condition, sympathetic vasoconstrictor responsiveness (%FVC) in resting and contracting skeletal muscle was not different between groups. Under resting conditions, sympathetic vasoconstrictor responsiveness was not different following selective nNOS inhibition (p&gt;0.05), but was increased (p&lt;0.05, main effect of drug) following non-selective NOS inhibition compared with control and selective nNOS inhibition conditions at both 2 Hz and 5 Hz. During muscle contraction, sympathetic vasoconstrictor responsiveness to 2 Hz sympathetic stimulation was unchanged (p&gt;0.05) in the presence of selective nNOS inhibition, but was increased (p&lt;0.05, main effect of drug) following non-selective NOS inhibition compared with control and selective nNOS inhibition conditions. At 5 Hz, sympathetic vasoconstrictor responsiveness was increased (p&lt;0.05, main effect of drug) by selective nNOS inhibition, and increased further (p&lt;0.05, main effect of drug) by non-selective NOS inhibition. The magnitude of sympatholysis at 2 Hz was not different (p&gt;0.05) between groups or drug conditions. At 5 Hz, sympatholysis was blunted (p&lt;0.05, main effect of drug) in the selective nNOS inhibition condition, and further reduced (p&lt;0.05, main effect of drug condition) following non-selective NOS inhibition in all groups. Sympatholysis was not different (p&gt;0.05) between sedentary and exercise trained groups. In conclusion: 1) sympathetic vasoconstrictor responsiveness in resting and contracting skeletal muscle was not dependent on estrogen bioavailability; 2) NO blunted vasoconstriction in all groups, however, NO-mediated sympatholysis was not altered by estrogen status, and; 3) exercise training did not alter sympathetic vasoconstrictor responsiveness or sympatholysis regardless of estrogen bioavailability. NSERC, Canada, Canadian Foundation for Innovation. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Risk factors for postoperative sympathetic chain dysfunction following oblique lateral lumbar interbody fusion: a multivariate analysis.

Postoperative sympathetic chain dysfunction (PSCD) was a relatively common complication after anterior lumbar interbody fusion due to the manipulation adjacent to the lumbar sympathetic chain (LSC). This study aimed to investigate the incidence of PSCD and identify its related independent risk factors after oblique lateral lumbar interbody fusion (OLIF) surgery. PSCD was defined as either of the following in the affected lower limb compared to the contralateral: (1) increase in skin temperature by 1 ºC or more, (2) reduced skin perspiration, (3) limb swelling or skin discoloration. Consecutive patients who underwent OLIF at L4/5 level from February 2018 and May 2022 at a single institution were retrospectively reviewed and divided into two groups: patients with PSCD and patients without PSCD. Binary logistic regression analyses were performed on patients' demographic, comorbidities, radiological datum and perioperative factors to identify independent risk factors for PSCD. Twelve (5.7%) of 210 patients experienced PSCD following OLIF surgery. Multivariate logistic regression analysis identified the identification of lumbar dextroscoliosis (OR = 7.907, P = 0.012) and the presence of "tear-drop" psoas (OR = 7.216, P = 0.011) as independent risk factors for the PSCD following OLIF. This study identified the lumbar dextroscoliosis and the "tear-drop" psoas as independent risk factors for the development of PSCD after OLIF. Spine alignment examination and the morphological identification of psoas major muscle should be highly noticed for the PSCD prevention following OLIF.

Lumbar Sympathetic Chain Tract and Mobility of Oblique Lumbar Interbody Fusion Approach: A Cadaveric Study

To assess lumbar sympathetic chain (LSC) relation to the surgical corridor for oblique lumbar approach and the ability to mobilize the LSC. Forty-three cadavers were included. Left-sided anterior retroperitoneal approach was performed in a supine position. Distance between the great vessels and psoas muscle (oblique corridor) and distance between great vessels and LSC at L2/3, L3/4, and L4/5 disc levels were measured. Mobilization of LSC at each disc level was done either close to or away from the psoas muscle and each mobilization distance was measured. The presence rates of LSC in oblique corridor were 19.5%, 43%, and 75.7% at L2/3, L3/4, and L4/5 levels, respectively. At L2/3 disc level, mean distance between psoas muscle and LSC and its mobility were 0.61±1.31 mm, and 2.72±1.24 mm, respectively. At L3/4 disc level, mean distance between psoas muscle and LSC and its mobility were 1.72±2.53 mm, and 3.11±1.02 mm, respectively. At L4/5 disc level, mean distance between psoas muscle and LSC and its mobility were 2.94±3.52 mm, and 2.53±1.03 mm, respectively. The mean width of corridor of L2/3, L3/4, and L4/5 were 10.73±5.82, 12.63±5.02, and 15.43±6.31 mm, respectively. The LSC tract usually lies in the oblique corridor in L4/5 but keeps decreasing in prevalence when approaching L3/4 and L2/3 levels. It can be mobilized a few millimeters close to or away from the psoas muscle. Care should be taken to prevent LSC injury, particularly when the LSC needs to be retracted along with the psoas muscle.

A comprehensive study of the abdominal ganglia part 3: An overview of the most commonly observed ganglion patterns.

Chronic pain from untreatable abdominal cancers or pancreatitis can severely decrease an individual's quality of life due to accompanying neuropathic pain, the most difficult pain mechanism to treat. Current treatment modalities focus on peripheral block or neurolysis procedures of the sympathetic ganglia in an attempt to curb the pain and improve quality of life. Reports indicated that these treatments are ineffective with patients either experiencing no relief or return the pain in a few weeks. The aim of this study was to investigate the location, macro- and microscopic morphology, and interconnections of the abdominal ganglia. The abdominal sympathetic ganglia of nine adult cadavers were investigated. The locations, morphology, interconnections, and microscopic structure were studied in 108 potential abdominal ganglia. Particular emphasis was placed on direct interconnectivity between the ganglia and histological morphology. A total of 100 ganglia were confirmed histologically to contain ganglion cells. The number and locations of most of the ganglia identified in our study does not correspond to that described by previous reports. Numerous interconnections between the different ganglia, as well as direct communications with the lumbar sympathetic chain ganglia were observed. The interconnections and presence of ganglion cells the nerves connecting the ganglia lead to the belief that the system should be considered as a unit and that pain fibers may be transmitted via alternative previously undiscovered pathways. If the pain treatments are to be reassessed with this information in mind, we believe that greater success could be achieved.

Evaluation of blood perfusion using laser doppler flowmetry during endoscopic lumbar sympathectomy in patients with plantar hyperhidrosis: a retrospective observational study

The purpose of this study is to evaluate whether monitoring the changes of skin blood flow may be effective in assessing blood perfusion during endoscopic lumbar sympathectomy (ELS) in patients with plantar hyperhidrosis. In this study, a total of 30 patients who underwent surgical treatment for plantar hyperhidrosis at the Department of Thoracic and Cardiovascular Surgery in Yonsei University Gangnam Severance Hospital, Seoul, Korea, between July 2020 and December 2020, were retrospectively analyzed. Sympathetic denervation was performed on the third lumbar ganglion, and intraoperative laser doppler flowmetry (LDF) was used to detect the lumbar sympathetic chain accurately. We observed an abrupt increase of peripheral blood flow after sympathetic denervation, and the median percent changes of perfusion unit were 173.27 (inter-quartile range, IQR 195.48) and 392.98 (IQR 597.27) for the left and right sympathectomies, respectively. This study demonstrated the efficacy of monitoring skin blood flow via LDF during ELS. This result suggests that exact detection of blood flow using LDF is essential for improving the accuracy of ELS by checking the perfusion site on the sole in patients with plantar hyperhidrosis.

Electrical Stimulation of Afferent Lumbar Sympathetic Nerve Impacts Cardio‐Respiratory Functions in Anesthetized Rats

The lumbar sympathetic chains (LSC) contain post-ganglionic vasodilator and vasoconstrictor fibers that control hindlimb vascular tone. The LSC also contain dorsal root ganglion afferent fibers whose roles in cardiorespiratory status remain poorly understood. The objective of the present study was to characterize the cardiorespiratory responses elicited by electrical stimulation (ES) of a LSC in urethane-anaesthetized male Sprague-Dawley rats (n=6) instrumented to measure/calculate mean arterial blood pressure (MAP), femoral artery blood flow (FBF) and femoral vascular resistance (FVR), brachial artery blood flow (BBF), and brachial vascular resistances (BVR), upper airway pressure (UAP), diaphragmatic EMG, respiratory frequency, inspiratory (iTV) and expiratory (eTV) tidal volumes. The right LSC was identified at the level of L4-L6 and a bipolar electrode was placed for ES (5 Hz, 0.5 msec duration, 0.5 mA amplitude for 10 sec). LSC stimulation caused a distinct pattern of cardiorespiratory responses including (a) a 12% decrease in MAP, (b) 15% decrease in ipsilateral FVR, (c) a 10% decrease in BVR (all measured at the peak decrease in MAP), (d) a 15% increase in iVT, (e) a 10% increase in eVT, (f) a15% increase in respiratory frequency, and (g) a 9% increase in diaphragmatic EMG activity. The result of this study demonstrates that ES of afferent fibers within the LSC elicits an array of cardiorespiratory changes in anesthetized rats that would be consistent with preparing the rats for exercise and for flight.

Microdissection of the Human Renal Nervous System: Implications for Performing Renal Denervation Procedures.

Despite the use of renal denervation to treat hypertension, the anatomy of the renal nervous system remains poorly understood. We performed a detailed quantitative analysis of the human renal nervous system anatomy with the goal of optimizing renal denervation procedural safety and efficacy. Sixty kidneys from 30 human cadavers were systematically microdissected to quantify anatomic variations in renal nerve patterns. Contrary to current clinical perception, not all renal innervation followed the main renal artery. A significant portion of the renal nerves (late arriving nerves) frequently reached the kidney (73% of the right kidney and 53% of the left kidney) bypassing the main renal artery. The ratio of the main renal artery length/aorta-renal hilar distance proved to be a useful variable to identify the presence/absence of these late arriving nerves (odds ratio, 0.001 (95% CI, 0.00002-0.0692; P: 0.001) with a cutoff of 0.75 (sensitivity: 0.68, specificity: 0.83, area under ROC curve at threshold: 0.76). When present, polar arteries were also highly associated with the presence of late arriving nerve. Finally, the perivascular space around the proximal main renal artery was frequently occupied by fused ganglia from the solar plexus (right kidney: 53%, left kidney: 83%) and/or by the lumbar sympathetic chain (right kidney: 63%, left kidney: 60%). Both carried innervation to the kidneys but importantly also to other abdominal and pelvic organs, which can be accidentally denervated if the proximal renal artery is targeted for ablation. These novel anatomic insights may help guide future procedural treatment recommendations to increase the likelihood of safely reaching and destroying targeted nerves during renal denervation procedures.

Neuroanatomical interconnection of the complementary acupoints in the rat hindlimb

ObjectiveThe innervations in Yīnlíngquán (阴陵泉 SP9) and Yánglíngquán (阳陵泉 GB34) were investigated to explore the neuroanatomical interconnection of the complementary acupoints in the rat hindlimb. MethodsA dual neural tracing technique was used, six male Sprague-Dawley rats were included in experiment. Under anesthesia with isoflurane, cholera toxin subunit B conjugated with Alexa Fluor 488 and 594 (CTB-AF488/594) were separately injected into SP9 and GB34 in the same rat. Three days later, the neural labeling was examined in the dorsal root ganglion (DRG), spinal cord, and sympathetic chain at lumbar (L) spinal segments under a laser scanning confocal microscope. ResultsAll neural labeling were present on the ipsilateral side of tracer injection, including sensory, motor and sympathetic postganglionic neurons. The sensory neurons associated with SP9 and GB34 were distributed in the DRG from L2 to L6 and concentrated in L3-L4 and L4-L5 respectively, while most of the double labeled sensory neurons were presented in L4. On the other hand, the labeled motor neurons for SP9 and GB34 were observed in the dorsolateral part of spinal ventral horn at L2-L4 and L3-L5 respectively, and some of them were double labeled at L4. In addition, the sympathetic postganglionic neurons related to SP9 and GB34 were found in the lumbar sympathetic chain respectively. ConclusionThe similarities of the sensory, motor, and sympathetic innervation of SP9 and GB34 in the rat provide the neuroanatomical evidence to understand the synergetic effect that arise from the stimulation at the complementary acupoints.

β-Adrenoreceptors do not oppose sympathetic vasoconstriction in resting and contracting skeletal muscle of male rats.

Sympathetic nervous system (SNS) vasoconstriction is primarily achieved through the binding of norepinephrine (NE) to α-adrenoreceptors. However, NE may also bind to β-adrenoreceptors and cause vasodilation that may oppose/blunt SNS-mediated vasoconstriction. Therefore, this study investigated the hypothesis that β-adrenoreceptor-mediated vasodilation opposes evoked vasoconstriction in resting and contracting skeletal muscle. Male (n = 9) Sprague-Dawley rats were anesthetized and surgically instrumented for stimulation of the lumbar sympathetic chain and measurement of arterial blood pressure and femoral artery blood flow. The percentage change of femoral vascular conductance in response to sympathetic chain stimulation delivered at 2 and 5 Hz was determined at rest and during triceps surae skeletal muscle contraction before (control) and after β-adrenoreceptor blockade (propranolol; 0.075 mg·kg-1, intravenously). β-Adrenoreceptor blockade did not alter (P > 0.05) baseline hemodynamics or the hyperemic response to exercise. At the 2 Hz stimulation frequency, sympathetic vasoconstriction was similar (P > 0.05) in control and β-blockade conditions in resting (control, -34% ± 6%; β-blockade, -33% ± 8%) and contracting (control, -16% ± 6%; β-blockade, -14% ± 7%) muscle. At the 5 Hz stimulation frequency, sympathetic vasoconstrictor responsiveness was reduced (main effect of drug, P < 0.05) following β-blockade (rest: control, -52% ± 7%; β-blockade, -51% ± 9%; contraction: control, -32% ± 11%; β-blockade, -29% ± 13%). Novelty These data indicate that β-adrenoreceptor blockade did not augment sympathetic vasoconstriction at rest or during exercise. The study demonstrates that β-adrenoreceptors do not oppose evoked sympathetic vasoconstriction in resting or contracting skeletal muscle or contribute to functional sympatholysis.

Lumbar Sympathectomy in an Ankylosing Spondylitis Patient with Vasculitis: A Case Report

In ankylosing spondylitis (AS), the axial skeleton, peripheral joints, and extra-articular structures are also frequently involved. Cutaneous lesions and vasculitis is extremely rare. Lumbar sympathectomy has a definite role in patients with painful cutaneous vasculitis and ischemic leg ulcer, especially those refractory to medical management. Despite the relatively small percentage of patients suffering from chronic leg ulcer, it has a significant impact on the patient's quality of life. A 44-year-old male AS patient with low backache (LBA) of 15 years and bilateral leg pain came to us. But in the past 2 years, severity of pain worsened resulting in infection and ulcer of dorsum of both feet. Examination confirmed multiple ulcers along with sensory loss on the dorsum of foot bilaterally. Not only he was refractory to conventional medical management, but he also had developed various side effects. Our results of diagnostic left lumbar sympathetic block (LSB) turned out to be positive. Next day, radiofrequency ablation (RFA) of lumbar sympathetic chain bilaterally at L2, L3, and L5 was done, and the patient was discharged pain free. At the 3-month review, the leg ulcers had healed, and the patient was pain free. So here, we discuss about the possible mechanisms and the role of LSB in vasculitic leg ulcers.

Ad libidum exercise improves functional sympatholysis in rats with spontaneous hypertension via the nitric oxide signal pathway

Objective To explore the effect of exercise on functional sympatholysis in rats modeling spontaneous hypertension and the role of the nitric oxide signal pathway. Methods Thirty Wistar rats with spontaneous hypertension were randomly divided into a sedentary group and an exercise group, each of 15, while another fifteen healthy rats acted as controls. The exercise group performed eight weeks of voluntary wheel running exercise while the other two groups did not. The rats were instrumented to stimulate the lumbar sympathetic chain (at 1 Hz, 2.5 Hz or 5 Hz) to induce vasoconstriction and the triceps surae muscle group was forced to contract by stimulating the tibial nerve electrically. The change in the femoral artery vascular conductance (FAVC) in response to sympathetic stimulation was recorded at rest and during contraction. The functional sympatholysis was calculated as the percentage difference in FAVC (△%FAVC) in response to sympathetic stimulation during muscular contraction and at rest (△%FAVC=%FAVC during contraction-%FAVC at rest). After administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), changes in FAVC were repeatedly determined. Results The average △%FAVC of the sedentary group was significantly lower than that of the control group at all stimulation frequencies, while the average △%FAVC in the exercise group was significantly higher than in the sedentary group. There were no significant differences between the exercise and control groups. After the administration of L-NAME, significant decrease was observed in the average △%FAVCs of the control and exercise groups, but there was no significant change in the sedentary group. Conclusion Voluntary exercise may improve functional sympatholysis in rats with spontaneous hypertension through improving NO-dependent signalling. Key words: Exercise; Hypertension; Functional sympatholysis; Nitric oxide

Relation of lumbar sympathetic chain to the open corridor of retroperitoneal oblique approach to lumbar spine: an MRI study.

Retroperitoneal oblique approach to lumbar spine used surgical corridor between psoas muscle and aorta for exposure to anterior part of lumbar spine. Lumbar sympathetic chain (LSC) runs in the corridor to make it a structure at risk of injury. Does LSC relationship with surgical corridor for minimally invasive retroperitoneal anterolateral oblique approach change in different intervertebral disc level? Left LSC was identified in axial magnetic resonance imaging images at L2-3, L3-4 and L4-5 intervertebral disc levels of 144 patients. Distances between LSC and left psoas muscle and aorta were recorded. Mean age of the patients was 62.3years. LSC was identifiable in 90.9% of levels. Distance between LSC and psoas muscle at L2-3, L3-4 and L4-5 was 4.0mm, 4.7mm and 5.2mm. Statistical difference was found between L2-3 and L4-5 level (p = 0.006). Distance between LSC and aorta at each level was 12.4mm, 12.3mm and 10.6mm without statistical difference. In non-scoliosis group distance between LSC and psoas muscle at each level was 3.1mm, 3.3mm and 4.0mm. Statistical difference was found between L2-3 and L4-5 level (p = 0.012) and between L3-4 and L4-5 level (p = 0.041). Distance between LSC and aorta at each level was 11.9mm, 11.4mm and 10.2mm. Statistical difference was found between L2-3 and L4-5 disc level (p = 0.039). LSC moves away from psoas muscle and becomes closer to aorta in L4-5 disc level. These slides can be retrieved under Electronic Supplementary Material.

The Effect of Exercise Training on Sympathetic Vasoconstrictor Responsiveness and Sympatholysis in Female Rats

Our laboratory has previously reported that aerobic exercise training enhances contraction‐mediated inhibition of sympathetic vasoconstriction (sympatholysis) in male rats. Whether aerobic exercise training has a similar effect in female rats has not been established. Therefore, the purpose of the present study was to investigate the hypothesis that aerobic exercise training would blunt sympathetic vasoconstrictor responsiveness and enhance sympatholysis in female rats. Female Sprague‐Dawley rats were randomly assigned to sedentary (n=10) or treadmill exercise training (n=8) groups (15 min at 40 m/min, 5% gradient; 5 d/week) for 10 weeks. Following the completion of the sedentary behavior or exercise training intervention, rats were anaesthetized and instrumented for stimulation of the lumbar sympathetic chain and the measurement of arterial blood pressure and femoral vascular conductance (FVC). The triceps surae muscle group was stimulated to contract rhythmically at 60% of maximal contractile force. The percentage change of FVC (Δ%FVC) in response to sympathetic stimulation delivered at 2 and 5 Hz was determined at rest and during contraction. At rest, sympathetic vasoconstrictor responsiveness (Δ%FVC) was not different (p&gt;0.05) between sedentary and exercise trained rats in response to sympathetic stimulation delivered at 2Hz (Sedentary: −39 ± 12 %; Exercise Trained: −45 ± 9 %) and 5Hz (Sedentary: −57 ± 8 %; Exercise Trained: −61 ± 9 %). Muscle contraction blunted (p&lt;0.05) sympathetic vasoconstrictor responsiveness in both sedentary and exercise trained rats and the magnitude of sympatholysis was not different (p&gt;0.05) between sedentary (2Hz: 24 ± 8 %; 5Hz: 29 ± 10 %) and exercise‐trained (2Hz: 30 ± 10 %; 5Hz: 29 ± 13 %) rats. These data demonstrate that aerobic exercise training does not alter sympathetic vasoconstrictor responsiveness or contraction mediated inhibition of sympathetic vasoconstriction (sympatholysis) in female rats. Further investigation is required to determine why female rats respond differently to exercise training than male rats.Support or Funding InformationNatural Sciences and Engineering Research Council of Canada, Canadian Foundation for Innovation, and Alberta Advanced Education and Technology.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

The Effect of Beta‐Adrenergic Receptor Blockade on Sympathetic Vasoconstrictor Responsiveness in Sedentary and Exercise‐Trained Female Rats

Stimulation of the sympathetic nervous system evokes the release of neurotransmitters and produces vasoconstriction that is primarily mediated by the binding of norepinephrine (NE) to alpha‐adrenergic receptors. However, NE may also bind to beta‐ adrenergic receptors and produce vasodilation that opposes vasoconstriction. Therefore, in the present study, we tested the hypothesis that beta‐adrenergic receptor blockade would augment sympathetic vasoconstrictor responsiveness in resting and contracting skeletal muscle of sedentary and exercise trained female rats, demonstrating beta‐adrenergic receptor mediated opposition of vasoconstriction. We also hypothesized that the increase in sympathetic vasoconstrictor responsiveness in the presence of beta‐adrenergic blockade would be larger in exercise‐trained rats, indicating that exercise training augments beta‐adrenergic receptor mediated opposition of vasoconstriction. Female Sprague‐Dawley rats were randomized to Sedentary (n=8, 265 ± 28 g) and Exercise Trained (n=9, 290 ± 27 g) groups. Exercise Trained rats completed a 4‐week treadmill training regimen (5 d/week, 15 min at 40 m/min, 5% gradient). Subsequently, rats were anaesthetized and instrumented for the measurement of femoral vascular conductance (FVC), stimulation of the lumbar sympathetic chain, and contraction of the triceps surae muscle group. The percentage change of femoral vascular conductance (Δ%FVC) in response to sympathetic chain stimulation delivered at 2 and 5 Hz was determined at rest and during triceps surae muscle contraction (60% maximal contractile force) before (Control) and after beta‐adrenergic blockade (Propranolol; 0.075 mg/kg body mass, I.V.). Sympathetic vasoconstrictor responsiveness (Δ%FVC) was not different (P &gt; 0.05) between Sedentary and Exercise Trained rats at rest or during contraction. At rest, beta‐adrenergic receptor blockade did not increase (P &gt; 0.05) sympathetic vasoconstrictor responsiveness in Sedentary (Control: 2Hz: −34 ± 9 %, 5Hz: −53 ± 8 %; Propranolol: 2Hz: −31 ± 10 %, 5Hz: −49 ± 8 %) or Exercise Trained (Control: 2Hz: −38 ± 9 %, 5Hz: −57 ± 8 %; Propranolol: 2Hz: −34 ± 7 %, 5Hz: −53 ± 8 %) rats. Similarly, beta‐adrenergic receptor blockade did not increase (P &gt; 0.05) sympathetic vasoconstrictor responsiveness during exercise in Sedentary (Control: 2Hz: −7 ± 4 %, 5Hz: −20 ± 11 %; Propranolol: 2Hz: −6 ± 5 %, 5Hz: −18 ± 10 %) or Exercise Trained (Control: 2Hz: −10 ± 8 %, 5Hz: −28 ± 8 %; Propranolol: 2Hz: −6 ± 5 %, 5Hz: −24 ± 12 %) rats. In conclusion, beta‐adrenergic receptor blockade did not augment sympathetic vasoconstrictor responsiveness in resting or contracting skeletal muscle of sedentary or exercise‐trained female rats, suggesting that beta‐adrenergic receptor mediated vasodilation did not oppose vasoconstriction, regardless of training status.Support or Funding InformationNatural Sciences and Engineering Research Council of Canada, Canadian Foundation for Innovation, and Alberta Advanced Education and Technology.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Sex differences in sympathetic vasoconstrictor responsiveness and sympatholysis

Sex differences in the neurovascular control of blood pressure and vascular resistance have been reported. However, the mechanisms underlying the modulatory influence of sex have not been fully elucidated. Nitric oxide (NO) has been shown to inhibit sympathetic vasoconstriction in resting and contracting skeletal muscle, and estrogen modulates NO synthase (NOS) expression and NO bioavailability. Therefore NO-mediated inhibition of sympathetic vasoconstriction may be enhanced in females. Thus the purpose of the present study was to investigate the hypothesis that sympathetic vasoconstrictor responsiveness would be blunted and NO-mediated inhibition of sympathetic vasoconstriction would be enhanced in females compared with males. Male (M; n = 8) and female (F; n = 10) Sprague-Dawley rats were anesthetized and surgically instrumented for measurement of arterial blood pressure and femoral artery blood flow and stimulation of the lumbar sympathetic chain. The percentage change of femoral vascular conductance in response to sympathetic chain stimulation delivered at 2 and 5 Hz was determined at rest and during triceps surae muscle contraction before (control) and after NOS blockade [Nω-nitro-l-arginine methyl ester (l-NAME), 10 mg/kg iv]. At rest, sympathetic vasoconstrictor responsiveness was augmented (P < 0.05) in female compared with male rats at 2 Hz [F: -33 ± 8% (SD); M: -26 ± 6%] but was not different at 5 Hz (F: -55 ± 7%; M: -47 ± 7%). During muscle contraction, evoked vasoconstriction was similar (P > 0.05) in females and males at 2 Hz (F: -12 ± 5%; M: -13 ± 5%) but was blunted (P < 0.05) in females compared with males at 5 Hz (F: -24 ± 5%; M: -34 ± 8%). l-NAME increased (P < 0.05) sympathetic vasoconstrictor responsiveness in both groups at rest and during contraction. Contraction-mediated inhibition of vasoconstriction (sympatholysis) was enhanced (P < 0.05) in females compared with males; however, sympatholysis was not different (P > 0.05) between males and females in the presence of NOS blockade, indicating that NO-mediated sympatholysis was augmented in female rats. These data suggest that sex modulates sympathetic vascular control in resting and contracting skeletal muscle and that a portion of the enhanced sympatholysis in female rats was NO dependent.NEW & NOTEWORTHY Sex differences in the neurovascular regulation of blood pressure and vascular resistance have been documented. However, our understanding of the underlying mechanisms that mediate these differences is incomplete. The present study demonstrates that female rats have an enhanced capacity to inhibit sympathetic vasoconstriction during exercise (sympatholysis) and that NO mediates a portion of the enhanced sympatholysis.

Lumbar sympathetic chain: anatomical variation and clinical perspectives.

The sympathetic and parasympathetic nervous systems constitute the autonomic nervous system which controls the entropy of the body and maintain the equilibrium. The sympathetic chain forms a definitive anatomic entity which is quite variable with respect to its position and the number of ganglia. The sympathetic nervous system causes vasoconstriction and thus forms the basis of Lumbar sympathetic surgeries being performed in patients with peripheral vascular diseases. The anatomic variations in this region hence gains immense importance for the operating surgeons and consulting radiologists. In the present study, the rami communicantes of either side of lumbar sympathetic chain crossed the common iliac arteries from lateral to medial side and united in front of first piece of sacrum. These rami communicantes encircled the right gonadal artery and could be a threat to the gonadal vascularity causing infertility. This was an unusual feature of the lumbar sympathetic chain and its rami communicantes that were noted in this particular case.

Exercise training and α1-adrenoreceptor-mediated sympathetic vasoconstriction in resting and contracting skeletal muscle.

Exercise training (ET) increases sympathetic vasoconstrictor responsiveness and enhances contraction-mediated inhibition of sympathetic vasoconstriction (i.e., sympatholysis) through a nitric oxide (NO)-dependent mechanism. Changes in α2-adrenoreceptor vasoconstriction mediate a portion of these training adaptations, however the contribution of other postsynaptic receptors remains to be determined. Therefore, the purpose of this study was to investigate the effect of ET on α1-adrenoreceptor-mediated vasoconstriction in resting and contracting muscle. It was hypothesized that α1-adrenoreceptor-mediated sympatholysis would be enhanced following ET. Male Sprague Dawley rats were randomized to sedentary (S; n=12) or heavy-intensity treadmill ET (n=11) groups. Subsequently, rats were anesthetized and instrumented for lumbar sympathetic chain stimulation and measurement of femoral vascular conductance (FVC) at rest and during muscle contraction. The percentage change in FVC in response to sympathetic stimulation was measured in control, α1-adrenoreceptor blockade (Prazosin; 20μg, IV), and combined α1 and NO synthase (NOS) blockade (l-NAME; 5mg·kg(-1) IV) conditions. Sympathetic vasoconstrictor responsiveness was increased (P<0.05) in ET compared to S rats at low, but not high (P>0.05) stimulation frequencies at rest (S: 2Hz: -25±4%; 5Hz: -45±5 %; ET: 2Hz: -35±7%, 5Hz: -52±7%), whereas sympathetic vasoconstrictor responsiveness was not different (P>0.05) between groups during contraction (S: 2Hz: -11±8%; 5Hz: -26±11%; ET: 2Hz: -10±7%, 5Hz: -27±12%). Prazosin blunted (P<0.05) vasoconstrictor responsiveness in S and ET rats at rest and during contraction, and abolished group differences in vasoconstrictor responsiveness. Subsequent NOS blockade increased vasoconstrictor responses (P<0.05) in S at rest and during contraction, whereas in ET vasoconstriction was increased (P<0.05) in response to sympathetic stimulation at 2Hz at rest and unchanged (P>0.05) during contraction. ET enhanced (P<0.05) sympatholysis, however the training-mediated improvements in sympatholysis were abolished by α1-adrenoreceptor blockade. Subsequent NOS inhibition did not alter (P>0.05) sympatholysis in S or ET rats. In conclusion, ET augmented α1-adrenoreceptor-mediated vasoconstriction in resting skeletal muscle and enhanced α1-adrenoreceptor-mediated sympatholysis. Furthermore, these data suggest that NO is not required to inhibit α2-adrenoreceptor- and nonadrenoreceptor-mediated vasoconstriction during exercise.

Hindlimb unweighting does not alter vasoconstrictor responsiveness and nitric oxide-mediated inhibition of sympathetic vasoconstriction.

Physical inactivity increases the risk of cardiovascular disease and may alter sympathetic nervous system control of vascular resistance. Hindlimb unweighting (HU), a rodent model of physical inactivity, has been shown to diminish sympathetic vasoconstrictor responsiveness and reduce NO synthase expression in isolated skeletal muscle blood vessels. Our understanding of the effects of HU on sympathetic vascular regulation in vivo is very limited. The present findings demonstrate that HU did not alter sympathetic vasoconstrictor responsiveness and NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. This study suggests that short-term physical inactivity does not alter in vivo sympathetic vascular control in the skeletal muscle vascular bed at rest and during contraction. We tested the hypothesis that physical inactivity would increase sympathetic vasoconstrictor responsiveness and diminish NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. Sprague-Dawley rats (n=33) were randomly assigned to sedentary time control (S) or hindlimb unweighted (HU) groups for 21days. Following the intervention, rats were anaesthetized and instrumented for measurement of arterial blood pressure and femoral artery blood flow and stimulation of the lumbar sympathetic chain. The percentage change of femoral vascular conductance (%FVC) in response to sympathetic chain stimulation delivered at 2 and 5Hz was determined at rest and during triceps surae muscle contraction before (control) and after NO synthase blockade with l-NAME (5mgkgi.v.). Sympathetic vasoconstrictor responsiveness was not different (P>0.05) in S and HU rats at rest (S, 2Hz, -26±8% and 5Hz, -46±12%; and HU, 2Hz, -29±9% and 5Hz, -51±10%) and during contraction (S, 2Hz, -10±7% and 5Hz, -23±11%; and HU, 2Hz, -9±5% and 5Hz, -22±7%). Nitric oxide synthase blockade caused a similar increase (P>0.05) in sympathetic vasoconstrictor responsiveness in HU and S rats at rest (S, 2Hz, -41±7% and 5Hz, -58±8%; and HU, 2Hz, -43±6% and 5Hz, -63±8%) and during muscle contraction (S, 2Hz, -15±6% and 5Hz, -31±11%; and HU, 2Hz, -12±5% and 5Hz, -29±8%). Skeletal muscle NO synthase expression and ACh-mediated vasodilatation were also not different between HU and S rats. These data suggest that HU does not alter sympathetic vasoconstrictor responsiveness and NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.

Exercise training augments neuronal nitric oxide synthase-mediated inhibition of sympathetic vasoconstriction in contracting skeletal muscle of rats.

We tested the hypothesis that exercise training would increase neuronal nitric oxide synthase (nNOS)-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. Sprague-Dawley rats (n=18) were randomized to sedentary or exercise-trained (40mmin(-1), 5° grade; 5daysweek(-1) for 4 weeks) groups. Following completion of sedentary behaviour or exercise training, rats were anaesthetized and instrumented with a brachial artery catheter, femoral artery flow probe and stimulating electrodes on the lumbar sympathetic chain. The percentage change of femoral vascular conductance (%FVC) in response to sympathetic chain stimulations delivered at 2 and 5Hz was determined at rest and during triceps surae muscle contraction before (control) and after selective nNOS blockade with S-methyl-l-thiocitrulline (SMTC, 0.6mgkg(-1), i.v.) and subsequent non-selective NOS blockade with l-NAME (5mgkg(-1), i.v.; SMTC+l-NAME). At rest, sympathetic vasoconstrictor responsiveness was greater (P<0.05) in exercise-trained compared to sedentary rats in control, SMTC and SMTC+l-NAME conditions. During contraction, the constrictor response was not different (P>0.05) between exercise trained (2Hz: -11±4%FVC; 5Hz: -21±5%FVC) and sedentary rats (2Hz: -7±6%FVC; 5Hz: -18±10%FVC) in control conditions. SMTC augmented (P<0.05) sympathetic vasoconstriction in sedentary and exercise-trained rats; however, sympathetic vasoconstrictor responsiveness was greater (P<0.05) in exercise-trained (2Hz: -27±5%FVC; 5Hz: -39±5%FVC) compared to sedentary (2Hz: -17±6%FVC; 5Hz: -27±8%FVC) rats during selective nNOS inhibition. SMTC + l-NAME further augmented (P<0.05) sympathetic vasoconstrictor responsiveness by a similar magnitude (P>0.05) in exercise-trained and sedentary rats. These data demonstrate that exercise training augmented nNOS-mediated inhibition of sympathetic vasoconstriction in contracting muscle.