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British Journal of Anaesthesia Mar 2011During subclavian vein catheterization, a potential, but rare, hazard is the phrenic nerve injury, which compromises respiratory function. We conducted a cadaver study...
BACKGROUND
During subclavian vein catheterization, a potential, but rare, hazard is the phrenic nerve injury, which compromises respiratory function. We conducted a cadaver study focused on the possible anatomical relationships between the subclavian vein and the phrenic nerve.
METHODS
Forty-two adult cadavers (84 heminecks) were dissected. Special attention was given to the topography of the phrenic nerve and subclavian vein.
RESULTS
In all but three cases (81 of 84), normal topography was present, that is, the nerve was posterior to the vein. In two cases, the phrenic nerve crossed anterior to the subclavian vein and in one case traversed the anterior wall of the subclavian vein.
CONCLUSIONS
Variants of the relationship of the subclavian vein and the phrenic nerve should be familiar to anaesthesiologists during subclavian vein cannulation in order to achieve successful vein approach without causing phrenic nerve palsy.
Topics: Aged; Aged, 80 and over; Catheterization, Central Venous; Female; Humans; Male; Phrenic Nerve; Subclavian Vein
PubMed: 21233111
DOI: 10.1093/bja/aeq373 -
Neuropharmacology Feb 2021Sudden unexpected death in epilepsy (SUDEP) is a leading cause of death in patients with refractory epilepsy. Centrally-mediated respiratory dysfunction has been...
Sudden unexpected death in epilepsy (SUDEP) is a leading cause of death in patients with refractory epilepsy. Centrally-mediated respiratory dysfunction has been identified as one of the principal mechanisms responsible for SUDEP. Seizures generate a surge in adenosine release. Elevated adenosine levels suppress breathing. Insufficient metabolic clearance of a seizure-induced adenosine surge might be a precipitating factor in SUDEP. In order to deliver targeted therapies to prevent SUDEP, reliable biomarkers must be identified to enable prompt intervention. Because of the integral role of the phrenic nerve in breathing, we hypothesized that suppression of phrenic nerve activity could be utilized as predictive biomarker for imminent SUDEP. We used a rat model of kainic acid-induced seizures in combination with pharmacological suppression of metabolic adenosine clearance to trigger seizure-induced death in tracheostomized rats. Recordings of EEG, blood pressure, and phrenic nerve activity were made concomitant to the seizure. We found suppression of phrenic nerve burst frequency to 58.9% of baseline (p < 0.001, one-way ANOVA) which preceded seizure-induced death; importantly, irregularities of phrenic nerve activity were partly reversible by the adenosine receptor antagonist caffeine. Suppression of phrenic nerve activity may be a useful biomarker for imminent SUDEP. The ability to reliably detect the onset of SUDEP may be instrumental in the timely administration of potentially lifesaving interventions.
Topics: Adenosine Kinase; Animals; Kainic Acid; Male; Phrenic Nerve; Predictive Value of Tests; Rats; Rats, Wistar; Seizures; Sudden Unexpected Death in Epilepsy; Tubercidin
PubMed: 33212114
DOI: 10.1016/j.neuropharm.2020.108405 -
The Journal of International Medical... Dec 2023Persistent hiccups that occur after abdominal surgery seriously affect postoperative rehabilitation. Phrenic nerve block therapy has been recommended after failure of... (Review)
Review
Persistent hiccups that occur after abdominal surgery seriously affect postoperative rehabilitation. Phrenic nerve block therapy has been recommended after failure of medication or physical maneuvers. However, the phrenic nerve is often difficult to accurately identify because of its small diameter and anatomic variations. We combined ultrasound with the use of a nerve stimulator to quickly and accurately identify and block the phrenic nerve in a patient with postoperative persistent hiccups. The ongoing hiccups were immediately terminated with no adverse effects. The patient reported no recurrence during the 2-week follow-up period. We conclude that the combined use of real-time ultrasound guidance and a nerve stimulator for singular phrenic nerve block might be an effective intervention for terminating postoperative persistent hiccups, although further studies are needed to evaluate the safety and efficacy of this technique. The findings in this case suggest a potential clinical application for this technique in managing persistent hiccups, thereby contributing to improved patient care and outcomes.
Topics: Humans; Hiccup; Phrenic Nerve; Ultrasonography; Nerve Block
PubMed: 38041831
DOI: 10.1177/03000605231216616 -
Physiological Research 2016This study was undertaken to determine pattern sensitivity of phrenic nerve plasticity in respect to different respiratory challenges. We compared long-term effects of...
This study was undertaken to determine pattern sensitivity of phrenic nerve plasticity in respect to different respiratory challenges. We compared long-term effects of intermittent and continuous hypercapnic and hypoxic stimuli, and combined intermittent hypercapnia and hypoxia on phrenic nerve plasticity. Adult, male, urethane-anesthetized, vagotomized, paralyzed, mechanically ventilated Sprague-Dawley rats were exposed to: acute intermittent hypercapnia (AIHc or AIHc(O2)), acute intermittent hypoxia (AIH), combined intermittent hypercapnia and hypoxia (AIHcH), continuous hypercapnia (CHc), or continuous hypoxia (CH). Peak phrenic nerve activity (pPNA) and burst frequency were analyzed during baseline (T0), hypercapnia or hypoxia exposures, at 15, 30, and 60 min (T60) after the end of the stimulus. Exposure to acute intermittent hypercapnia elicited decrease of phrenic nerve frequency from 44.25+/-4.06 at T0 to 35.29+/-5.21 at T60, (P=0.038, AIHc) and from 45.5+/-2.62 to 37.17+/-3.68 breaths/min (P=0.049, AIHc(O2)), i.e. frequency phrenic long term depression was induced. Exposure to AIH elicited increase of pPNA at T60 by 141.0+/-28.2 % compared to baseline (P=0.015), i.e. phrenic long-term facilitation was induced. Exposure to AIHcH, CHc, or CH protocols failed to induce long-term plasticity of the phrenic nerve. Thus, we conclude that intermittency of the hypercapnic or hypoxic stimuli is needed to evoke phrenic nerve plasticity.
Topics: Animals; Hypercapnia; Hypoxia; Long-Term Potentiation; Male; Neuronal Plasticity; Periodicity; Phrenic Nerve; Rats; Rats, Sprague-Dawley
PubMed: 26596313
DOI: 10.33549/physiolres.933012 -
The Journal of Comparative Neurology Dec 2018Structural plasticity in motoneurons may be influenced by activation history and motoneuron-muscle fiber interactions. The goal of this study was to examine the...
Structural plasticity in motoneurons may be influenced by activation history and motoneuron-muscle fiber interactions. The goal of this study was to examine the morphological adaptations of phrenic motoneurons following imposed motoneuron inactivity while controlling for diaphragm muscle inactivity. Well-characterized rat models were used including unilateral C2 spinal hemisection (SH; ipsilateral phrenic motoneurons and diaphragm muscle are inactive) and tetrodotoxin phrenic nerve blockade (TTX; ipsilateral diaphragm muscle is paralyzed while phrenic motoneuron activity is preserved). We hypothesized that inactivity of phrenic motoneurons would result in a decrease in motoneuron size, consistent with a homeostatic increase in excitability. Phrenic motoneurons were retrogradely labeled by ipsilateral diaphragm muscle injection of fluorescent dextrans or cholera toxin subunit B. Following 2 weeks of diaphragm muscle paralysis, morphological parameters of labeled ipsilateral phrenic motoneurons were assessed quantitatively using fluorescence confocal microscopy. Compared to controls, phrenic motoneuron somal volumes and surface areas decreased with SH, but increased with TTX. Total phrenic motoneuron surface area was unchanged by SH, but increased with TTX. Dendritic surface area was estimated from primary dendrite diameter using a power equation obtained from three-dimensional reconstructed phrenic motoneurons. Estimated dendritic surface area was not significantly different between control and SH, but increased with TTX. Similarly, TTX significantly increased total phrenic motoneuron surface area. These results suggest that ipsilateral phrenic motoneuron morphological adaptations are consistent with a normalization of motoneuron excitability following prolonged alterations in motoneuron activity. Phrenic motoneuron structural plasticity is likely more dependent on motoneuron activity (or descending input) than muscle fiber activity.
Topics: Animals; Diaphragm; Disease Models, Animal; Motor Neurons; Neuronal Plasticity; Phrenic Nerve; Rats; Rats, Sprague-Dawley; Respiratory Paralysis
PubMed: 30411341
DOI: 10.1002/cne.24503 -
Pharmacology Research & Perspectives Aug 2021Sevoflurane affects on the A1 receptor in the central nervous system and potentiates the action of neuromuscular blocking agents. In the present study, we investigated...
Effects of sevoflurane and adenosine receptor antagonist on the sugammadex-induced recovery from rocuronium-induced neuromuscular blockade in rodent phrenic nerve-hemidiaphragm tissue specimens.
Sevoflurane affects on the A1 receptor in the central nervous system and potentiates the action of neuromuscular blocking agents. In the present study, we investigated whether sevoflurane (SEVO) has the ability to potentiate the neuromuscular blocking effect of rocuronium and if the specific antagonist of adenosine receptor (SLV320) can reverse this effect. In this study, phrenic nerve-hemidiaphragm tissue specimens were obtained from 40 Sprague-Dawley (SD) rats. The specimens were immersed in an organ bath filled with Krebs buffer and stimulated by a train-of-four (TOF) pattern using indirect supramaximal stimulation at 20 s intervals. The specimens were randomly allocated to control, 2-chloroadenosine (CADO), SEVO, or SLV320 + SEVO groups. In the CADO and SLV320 + SEVO groups, CADO and SLV320 were added to the organ bath from the start to a concentration of 10 μM and 10 nM, respectively. We then proceeded with rocuronium-induced blockade of >95% depression of the first twitch tension of TOF (T1) and TOF ratio (TOFR). In the SEVO and SLV320 + SEVO groups, SEVO was added to the Krebs buffer solution to concentration of 400-500 μM for 10 min. Sugammadex-induced T1 and TOFR recovery was monitored for 30 min until >95% of T1 and >0.9 of TOFR were confirmed, and the recovery pattern was compared by plotting these data. T1 recovery in the SEVO and CADO groups was significantly delayed compared with the control and SLV320 + SEVO groups (p < .05). In conclusion, sevoflurane affects on the A1 receptor at the neuromuscular junction and delays sugammadex-induced recovery from neuromuscular blockade.
Topics: 2-Chloroadenosine; Adenosine A1 Receptor Agonists; Animals; Cyclohexanes; Diaphragm; Heterocyclic Compounds, 2-Ring; In Vitro Techniques; Male; Neuromuscular Blockade; Neuromuscular Nondepolarizing Agents; Phrenic Nerve; Purinergic P1 Receptor Antagonists; Rats, Sprague-Dawley; Rocuronium; Sevoflurane; Sugammadex; Rats
PubMed: 34337892
DOI: 10.1002/prp2.827 -
Respiratory Physiology & Neurobiology Apr 2023We hypothesized that activation of phrenic afferents induces diaphragm motor plasticity. In anesthetized and spontaneously breathing rats we delivered 40 Hz, low...
We hypothesized that activation of phrenic afferents induces diaphragm motor plasticity. In anesthetized and spontaneously breathing rats we delivered 40 Hz, low threshold (twitch and 1.5X twitch threshold), inspiratory-triggered stimulation to the left hemidiaphragm for 30 min to activate ipsilateral phrenic afferents. Diaphragm amplitude ipsilateral and contralateral to stimulation were increased for 60 min following both currents compared to time controls not receiving stimulation. Diaphragm stimulation was repeated in laminectomy controls or following a unilateral C3-C6 dorsal rhizotomy to eliminate phrenic afferent volleys. Laminectomy controls expressed neuromuscular plasticity post-stimulation. In contrast, ipsilateral and contralateral diaphragm amplitude following dorsal rhizotomy was lower than laminectomy controls and no different than time controls, suggesting diaphragm motor plasticity was not induced post-rhizotomy. Our results indicate that diaphragm stimulation induces a novel form of plasticity in the phrenic motor system which requires phrenic afferent activation. Respiratory motor plasticity elicited by diaphragm stimulation may have value as a therapeutic strategy to improve diaphragm output in neuromuscular conditions.
Topics: Rats; Animals; Diaphragm; Thorax; Respiration; Phrenic Nerve; Electric Stimulation
PubMed: 36642318
DOI: 10.1016/j.resp.2023.104014 -
Journal of Physiology and Pharmacology... Sep 2009Stimulation of the raphe pallidus nucleus produces facilitatory effects on respiratory activity. Numerous serotonergic projections from the raphe pallidus have been...
Stimulation of the raphe pallidus nucleus produces facilitatory effects on respiratory activity. Numerous serotonergic projections from the raphe pallidus have been shown to terminate in the phrenic nucleus. This study was undertaken to examine the role of 5-hydroxytryptamine 1A (5-HT(1A)) receptors in the phrenic nucleus on the excitatory response of the phrenic nerve activity elicited from the raphe pallidus. We hypothesized that blockade of 5-HT(1A) receptors in the phrenic nucleus will attenuate raphe-induced facilitation of the phrenic nerve. Chemical stimulation of the raphe pallidus by synaptic excitant D,L-homocysteic acid produced increase in the amplitude of the phrenic nerve activity. After microinjection of the specific 5-HT(1A) receptor antagonist WAY, N-(2-(4,2-methoxyphenyl)-1-piperazinyl)ethyl)-N-2-pyridinyl-cyclohexane-carboxamide maleate into the phrenic nucleus, the raphe-induced facilitation of the phrenic nerve was attenuated. These data suggest that excitation of the phrenic nerve activity elicited by activation of the neurons in the raphe pallidus is mediated by 5-HT(1A) receptors in the phrenic nucleus.
Topics: Animals; Brain Mapping; Cell Nucleus; Male; Microinjections; Phrenic Nerve; Piperazines; Pyridines; Raphe Nuclei; Rats; Rats, Sprague-Dawley; Respiration; Serotonin 5-HT1 Receptor Antagonists; Serotonin Antagonists; Stimulation, Chemical
PubMed: 19826196
DOI: No ID Found -
Journal of Cachexia, Sarcopenia and... Feb 2019Cancer cachexia is an insidious process characterized by muscle atrophy with associated motor deficits, including diaphragm weakness and respiratory insufficiency....
BACKGROUND
Cancer cachexia is an insidious process characterized by muscle atrophy with associated motor deficits, including diaphragm weakness and respiratory insufficiency. Although neuropathology contributes to muscle wasting and motor deficits in many clinical disorders, neural involvement in cachexia-linked respiratory insufficiency has not been explored.
METHODS
We first used whole-body plethysmography to assess ventilatory responses to hypoxic and hypercapnic chemoreflex activation in mice inoculated with the C26 colon adenocarcinoma cell line. Mice were exposed to a sequence of inspired gas mixtures consisting of (i) air, (ii) hypoxia (11% O ) with normocapnia, (iii) hypercapnia (7% CO ) with normoxia, and (iv) combined hypercapnia with hypoxia (i.e. maximal chemoreflex response). We also tested the respiratory neural network directly by recording inspiratory burst output from ligated phrenic nerves, thereby bypassing influences from changes in diaphragm muscle strength, respiratory mechanics, or compensation through recruitment of accessory motor pools.
RESULTS
Cachectic mice demonstrated a significant attenuation of the hypoxic tidal volume (0.26mL±0.01mL vs 0.30mL±0.01mL; p<0.05), breathing frequency (317±10bpm vs 344±6bpm; p<0.05) and phrenic nerve (29.5±2.6% vs 78.8±11.8%; p<0.05) responses. On the other hand, the much larger hypercapnic tidal volume (0.46±0.01mL vs 0.46±0.01mL; p>0.05), breathing frequency (392±5bpm vs 408±5bpm; p>0.05) and phrenic nerve (93.1±8.8% vs 111.1±13.2%; p>0.05) responses were not affected. Further, the concurrent hypercapnia/hypoxia tidal volume (0.45±0.01mL vs 0.45±0.01mL; p>0.05), breathing frequency (395±7bpm vs 400±3bpm; p>0.05), and phrenic nerve (106.8±7.1% vs 147.5±38.8%; p>0.05) responses were not different between C26 cachectic and control mice.
CONCLUSIONS
Breathing deficits associated with cancer cachexia are specific to the hypoxic ventilatory response and, thus, reflect disruptions in the hypoxic chemoafferent neural network. Diagnostic techniques that detect decompensation and therapeutic approaches that support the failing hypoxic respiratory response may benefit patients at risk for cancer cachectic-associated respiratory failure.
Topics: Animals; Cachexia; Cell Line, Tumor; Hypercapnia; Hypoxia; Male; Mice; Neoplasms; Phrenic Nerve; Plethysmography; Respiration
PubMed: 30362273
DOI: 10.1002/jcsm.12348 -
Folia Morphologica 2021During educational dissection of cadavers, we encountered anatomical variability of the left phrenic nerve (PN). In this cadaver, nerve fibres from C3 and C4 descended...
During educational dissection of cadavers, we encountered anatomical variability of the left phrenic nerve (PN). In this cadaver, nerve fibres from C3 and C4 descended and crossed behind the transverse cervical artery (TCA), a branch of the thyrocervical trunk, at the level of the anterior scalene muscle. On the other hand, nerve fibres from C5 descended obliquely above the TCA and then joined the fibres from C3-C4 on the medial side of the anterior scalene muscle to form the PN. To our knowledge, the encircling of the TCA by the left PN in the neck has not yet been reported and may pose a potential risk for nerve compression during movement of the neck. We discuss several types of anatomical variants of the PN and the associated risk during thorax and neck dissection procedures.
Topics: Cadaver; Dissection; Humans; Neck; Phrenic Nerve; Subclavian Artery
PubMed: 33124034
DOI: 10.5603/FM.a2020.0131