Effect of brachial plexus co-activation on phrenic nerve conduction time.
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BACKGROUND: Diaphragm function can be assessed by electromyography of the diaphragm during electrical phrenic nerve stimulation (ES). Whether phrenic nerve conduction time (PNCT) and diaphragm electrical activity can be reliably measured from chest wall electrodes with ES is uncertain. METHODS: The diaphragm compound muscle action potential (CMAP) was recorded using an oesophageal electrode and lower chest wall electrodes during ES in six normal subjects. Two patients with bilateral diaphragm paralysis were also studied. Stimulations were deliberately given in a manner designed to avoid or incur co-activation of the brachial plexus. RESULTS: For the oesophageal electrode the PNCT was similar with both stimulation techniques with mean (SE) values of 7.1 (0.2) and 6.8 (0.2) ms, respectively (pooled left and right values). However, for surface electrodes the PNCT was substantially shorter when the brachial plexus was activated (4.4 (0.1) ms) than when it was not (7.4 (0.2) ms) (mean difference 3.0 ms, 95% CI 2.7 to 3.4, p<0.0001). A small short latency CMAP was recorded from the lower chest wall electrodes during stimulation of the brachial plexus alone. CONCLUSIONS: The results of this study show that lower chest wall electrodes only accurately measure PNCT when care is taken to avoid stimulating the brachial plexus. A false positive CMAP response to phrenic stimulation could be caused by inadvertent stimulation of the brachial plexus. This finding may further explain why the diaphragm CMAP recorded from chest wall electrodes can be unreliable with cervical magnetic stimulation during which brachial plexus activation occurs. (+info)
Role of respiratory motor output in within-breath modulation of muscle sympathetic nerve activity in humans.
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We measured muscle sympathetic nerve activity (MSNA, peroneal microneurography) in 5 healthy humans under conditions of matched tidal volume, breathing frequency, and end-tidal CO(2), but varying respiratory motor output as follows: (1) passive positive pressure mechanical ventilation, (2) voluntary hyperventilation, (3) assisted mechanical ventilation that required the subject to generate -2.5 cm H(2)O to trigger each positive pressure breath, and (4) added inspiratory resistance. Spectral analyses showed marked respiratory periodicities in MSNA; however, the amplitude of the peak power was not changed with changing inspiratory effort. Time domain analyses showed that maximum MSNA always occurred at end expiration (25% to 30% of total activity) and minimum activity at end inspiration (2% to 3% of total activity), and the amplitude of the variation was not different among conditions despite marked changes in respiratory motor output. Furthermore, qualitative changes in intrathoracic pressure were without influence on the respiratory modulation of MSNA. In all conditions, within-breath changes in MSNA were inversely related to small changes in diastolic pressure (1 to 3 mm Hg), suggesting that respiratory rhythmicity in MSNA was secondary to loading/unloading of carotid sinus baroreceptors. Furthermore, at any given diastolic pressure, within-breath MSNA varied inversely with lung volume, demonstrating an additional influence of lung inflation feedback on sympathetic discharge. Our data provide evidence against a significant effect of respiratory motor output on the within-breath modulation of MSNA and suggest that feedback from baroreceptors and pulmonary stretch receptors are the dominant determinants of the respiratory modulation of MSNA in the intact human. (+info)
Synaptic inhibition of cat phrenic motoneurons by internal intercostal nerve stimulation.
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Intracellular recordings from 65 phrenic motoneurons (PMNs) in the C5 segment and recordings of C5 phrenic nerve activity were made in 27 pentobarbitone-anesthetized, paralyzed, and artificially ventilated adult cats. Inhibition of phrenic nerve activity and PMN membrane potential hyperpolarization (48/55 PMNs tested) was seen after stimulation of the internal intercostal nerve (IIN) at a mean latency to onset of 10.3 +/- 2.7 ms. Reversal of IIN-evoked hyperpolarization (n = 14) by injection of negative current or diffusion of chloride ions occurred in six cases, and the hyperpolarization was reduced in seven others. Stimulation of the IIN thus activates chloride-dependent inhibitory synaptic inputs to most PMNs. The inhibitory phrenic nerve response to IIN stimulation was reduced by ipsilateral transection of the lateral white matter at the C3 level and was converted to an excitatory response by complete ipsilateral cord hemisection at the same level. After complete ipsilateral hemisection of the spinal cord at C3 level, stimulation of the IIN evoked both excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) in PMNs (n = 10). It was concluded that IIN stimulation can evoke both excitatory and inhibitory responses in PMNs using purely spinal circuitry, but that excitatory responses are normally suppressed by a descending pathway in intact animals. Fifteen PMNs were tested for possible presynaptic convergence of inputs in these reflex pathways, using test and conditioning stimuli. Significant enhancement (>20%) of IPSPs were seen in seven of eight IIN-evoked responses using pericruciate sensorimotor cortex (SMC) conditioning stimuli, but only one of five IIN-evoked responses were enhanced by superior laryngeal nerve (SLN) conditioning stimuli. The IIN-evoked IPSP was enhanced in one of two motoneurons by stimulation of the contralateral phrenic nerve. It was concluded that presynaptic interneurons were shared by the IIN and SMC pathways, but uncommonly by other pathways. These results indicate that PMNs receive inhibitory synaptic inputs from ascending thoracocervical pathways and from spinal interneurons. These inhibitory reflex pathways activated by afferent inputs from the chest wall may play a significant role in the control of PMN discharge, in parallel with disfacilitation following reduced activity in bulbospinal neurons projecting to PMNs. (+info)
Inhibition of quantal release from motor nerve by wortmannin.
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1. The effects of wortmannin, an inhibitor of phosphatidylinositol (PI) kinases and myosin light chain kinase, on the quantal release of neurotransmitter from mouse phrenic nerve were investigated. 2. Wortmannin (10 - 100 microM) initially enhanced, thereafter progressively depressed spontaneous quantal discharge (miniature endplate potential, mepp). The mean amplitude and the amplitude distribution of mepp were not altered. 3. The compound inhibited and prevented the intensive quantal release evoked by high KC1 solution as well as the mepp burst induced by alpha-latrotoxin, a polypeptide toxin that possesses Ca2+-independent synaptic action to trigger quantal release. The inhibitory actions of wortmannin were partially reversible. 4. Wortmannin depressed the amplitude of endplate potentials (epps) and increased the coefficient of variance of epps. The profile of epps in response to high frequency nerve stimulation exhibited fluctuations between run-down and run-up. The phenomenon is thus different from the consistency of run-up characteristic as the motor nerve Ca2+ channel is blocked by omega-agatoxin IVA. 5. LY294002, another inhibitor of PI 3-kinase, raised mepp frequency without causing late phase suppressions. The compound did not inhibit KC1-, alpha-latrotoxin- or nerve stimulation-evoked quantal release. 6. The results suggest that wortmannin could depress quantal release beyond the step of Ca2+ channel blockade, probably by interfering with the exocytotic cascade. (+info)
Effects of propofol and remifentanil on phrenic nerve activity and nociceptive cardiovascular responses in rabbits.
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BACKGROUND: The effects of propofol, remifentanil, and their combination on phrenic nerve activity (PNA), resting heart rate (HR), mean arterial pressure (MAP), and nociceptive cardiovascular responses were studied in rabbits. METHODS: Basal anesthesia and constant blood gas tensions were maintained with alpha-chloralose and mechanical ventilation. PNA, HR, MAP, and maximum changes in HR and MAP (deltaHR, deltaMAP) evoked by electrical nerve stimulation of tibial nerves were recorded. The comparative effects were observed for propofol at infusion rates from 0.05 to 3.2 mg x kg(-1) x min(-1) (group I) and remifentanil from 0.0125 to 12.8 microg x kg(-1) x min(-1) alone (group II), and during constant infusions of propofol at rates of 0.1 and 0.8 mg x kg(-1) x min(-1) (groups III and IV, respectively). Finally, the effect of remifentanil on propofol blood levels was observed (group V). RESULTS: The infusion rates for 50% depression (ED50) of PNA, deltaHR, and deltaMAP were 0.41, 1.32, and 1.58 mg x kg-(1) x min(-1) for propofol, and 0.115, 0.125, and 1.090 microg x kg(-1) x min(-1) for remifentanil, respectively. The ratios for the ED50 values of deltaHR and deltaMAP to PNA were 3.2 and 3.9 for propofol, and 1.1 and 9.5 for remifentanil, respectively. Analysis of the expected and observed responses and isobologrms showed that although their combined effects on PNA, resting HR, and MAP, and deltaMAP were synergistic for deltaHR, they were merely additive. Remifentanil had no effect on propofol blood levels. CONCLUSION: PNA was abolished by propofol and remifentanil, alone and in combination, before significant depression of nociceptive pressor responses occurred. Their combined effects on PNA, HR, MAP, and deltaMAP are greater than additive, ie., synergistic. Unlike propofol, remifentanil obtunded pressor responses more than the resting circulation. (+info)
Differential effects of angiotensin II on cardiorespiratory reflexes mediated by nucleus tractus solitarii - a microinjection study in the rat.
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1. The effect of microinjecting angiotensin II (ANGII) into the nucleus of the solitary tract (NTS) on both baroreceptor and peripheral chemoreceptor reflexes was compared. 2. Experiments were performed in a working heart-brainstem preparation of rat. Baroreceptors were stimulated by raising perfusion pressure and chemoreceptors were activated with aortic injections of sodium cyanide (0.025 %, 25-75 microl). Reflex changes in phrenic nerve activity and heart rate were measured after bilateral NTS microinjection (50 nl) of ANGII (0.5-5000 fmol). 3. NTS microinjection of 5 fmol ANGII elicited a transient (28.2 +/- 6 s; mean +/- s.e.m.) bradycardia (-18 +/- 3 beats min-1), and decreased phrenic nerve activity cycle length and amplitude (P < 0.05). At higher doses of ANGII a similar respiratory response was seen but heart rate changes were inconsistent. 4. The baroreceptor reflex bradycardia was depressed significantly by NTS microinjections of ANGII (5-5000 fmol) in a dose-dependent manner with the reflex gain decreasing from 1.7 +/- 0.16 to 0.66 +/- 0.1 beats min-1 mmHg-1 (P < 0.01) at 5000 fmol. Although the chemoreceptor reflex bradycardia was depressed at a low dose of ANGII (5 fmol), all higher doses (50-5000 fmol) produced a dose-dependent potentiation of the reflex bradycardia (maximally +64 +/- 8 %). The respiratory component was unaffected. The effects of ANGII on both reflexes were blocked by an ANGII type 1 (AT1) receptor antagonist, losartan (20 microM). 5. The potentiating action of ANGII on the chemoreceptor reflex cardiac response was abolished by a neurokinin type 1 (NK1) receptor blocker (CP-99,994, 5 microM) but this had no effect on the baroreceptor reflex. 6. AT1 receptors in the NTS can depress the baroreceptor reflex bradycardia which is independent of NK1 receptors. The ANGII effect on the cardiac component of the chemoreceptor reflex is bi-directional being inhibited at low concentrations and potentiated at higher concentrations; the latter involves NK1 receptors and presumably results from release of substance P. (+info)
Location of the phrenic nucleus in the human spinal cord.
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Eight normal human spinal cords were studied. Spinal segments were identified and embedded in paraffin wax. Serial cross sections were cut at 25 microm and stained by cresyl violet. Motor columns were reconstructed adapting Elliott's (1942) methods. Motor columns were classified into the medial and lateral divisions and were numbered sequentially from medial to lateral at the level of C1. In the cervical cord, 8 motor columns were traced. Column 1, corresponding to the medial column, presented 3 subdivisions designated as 1a, 1b and 1c with ventral, dorsal and lateral positions respectively. Columns 1a and 1b extended throughout the cervical region while 1c was confined to 3rd, 4th and 5th cervical segments. At the level of C3, 1c was a discrete column situated lateral to 1a and 1b but at C4 and C5 it became displaced medially close to the medial margin of the ventral horn. In cross section, it presented smaller medial and large lateral part. With the help of clinical and developmental evidence an attempt was made to correlate column 1c with the phrenic nucleus. (+info)
Twitch transdiaphragmatic pressure depends critically on thoracoabdominal configuration.
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We measured the effect of thoracoabdominal configuration on twitch transdiaphragmatic pressure (Pdi, t) in response to supramaximal, transcutaneous, bilateral phrenic nerve shocks in three thin normal men. Pdi, t was measured as a function of lung volume (VL) in the relaxation configuration, at functional residual capacity (FRC), and at the same end-tidal VL 1) during relaxation; 2) with the abdomen (Ab) expanded and the rib cage (RC) in its relaxed FRC configuration; 3) with RC expanded and Ab in its relaxed FRC configuration; and 4) in configuration 3 with an active transdiaphragmatic pressure similar to that required to produce configuration 2. In increasing VL from FRC to configuration 1, Pdi, t decreased by 3.6 cmH(2)O; to configuration 2 by 14.8 cmH(2)O; to configuration 3 by 3.7 cmH(2)O; and to configuration 4 by 2.7 cmH(2)O. We argue that changes in velocity of shortening and radius of curvature are unlikely to account for these effects and suggest that changes in diaphragmatic fiber length (L(di)) are primarily responsible. If so, equivolume displacements of Ab and RC change L(di) in a ratio of approximately 4:1. We conclude that Pdi, t is exquisitely sensitive to abdominal displacements that must be rigorously controlled if Pdi, t is to be used to assess diaphragmatic contractility. (+info)