Transvenous phrenic nerve stimulation in anesthetized dogs.

We examined the effect of digitalis on diaphragmatic contractility and fatigability in 19 anesthetized mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. In a first group of five dogs, Pdi-stimulus frequency relationships were compared before and after administration of ouabain in doses of 0.01, 0.02, and 0.04 mg/kg. In a second group, diaphragmatic fatigue was produced by bilateral phrenic nerve stimulation at 30 Hz. Ten seconds of stimulation and 15 s of mechanical ventilation were repeated for 30 min. The rates of decrease in Pdi were compared between two groups, one of 0.05 mg/kg deslanoside-treated dogs (n = 7) and one of nontreated dogs (n = 7). After ouabain administration Pdi was significantly greater at each frequency in a dose-dependent manner. On the other hand, the rate of decrease in Pdi in the deslanoside group was significantly smaller than that in the nontreated group, whereas deslanoside did not greatly change the Pdi-frequency curves in fresh diaphragm. We conclude that ouabain improves contractility of the fresh diaphragm and that deslanoside has a protective effect against fatigability.

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Determinants of diaphragm motion in unilateral diaphragmatic paralysis

Journal of Applied Physiology ◽

10.1152/japplphysiol.00761.2003 ◽

2004 ◽

Vol 96 (1) ◽

pp. 96-100 ◽

Cited By ~ 22

Author(s):

Pierre Scillia ◽

Matteo Cappello ◽

André De Troyer

Keyword(s):

Clinical Practice ◽

Muscle Contraction ◽

Nerve Stimulation ◽

Phrenic Nerve ◽

Diaphragmatic Paralysis ◽

Phrenic Nerve Stimulation ◽

Anesthetized Dogs ◽

Diaphragm Motion ◽

Cardinal Sign ◽

Stimulation Of

Cranial displacement of a hemidiaphragm during sniffs is a cardinal sign of unilateral diaphragmatic paralysis in clinical practice. However, we have recently observed that isolated stimulation of one phrenic nerve in dogs causes the contralateral (inactive) hemidiaphragm to move caudally. In the present study, therefore, we tested the idea that, in unilateral diaphragmatic paralysis, the pattern of inspiratory muscle contraction plays a major role in determining the motion of the inactive hemidiaphragm. We induced a hemidiaphragmatic paralysis in six anesthetized dogs and assessed the contour of the diaphragm during isolated unilateral phrenic nerve stimulation and during spontaneous inspiratory efforts. Whereas the inactive hemidiaphragm moved caudally in the first instance, it moved cranially in the second. The parasternal intercostal muscles were then severed to reduce the contribution of the rib cage muscles to inspiratory efforts and to enhance the force generated by the intact hemidiaphragm. Although the change in pleural pressure (ΔPpl) was unaltered, the cranial displacement of the paralyzed hemidiaphragm was consistently reduced. A pneumothorax was finally induced to eliminate ΔPpl during unilateral phrenic nerve stimulation, and this enhanced the caudal displacement of the inactive hemidiaphragm. These observations indicate that, in unilateral diaphragmatic paralysis, the motion of the inactive hemidiaphragm is largely determined by the balance between the force related to ΔPpl and the force generated by the intact hemidiaphragm.

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Diaphragmatic pressures: transvenous vs. direct phrenic nerve stimulation

Journal of Applied Physiology ◽

10.1152/jappl.1985.59.1.269 ◽

1985 ◽

Vol 59 (1) ◽

pp. 269-273 ◽

Cited By ~ 4

Author(s):

R. F. Planas ◽

R. H. McBrayer ◽

P. A. Koen

Keyword(s):

Analysis Of Variance ◽

Respiratory System ◽

Functional Residual Capacity ◽

Nerve Stimulation ◽

Phrenic Nerve ◽

Phrenic Nerve Stimulation ◽

Transdiaphragmatic Pressure ◽

Residual Capacity ◽

Anesthetized Dogs

Diaphragmatic force, determined by stimulating the phrenic nerve while simultaneously measuring the pressures in a closed respiratory system, was assessed in five anesthetized dogs over a 5-h period to evaluate the inherent variability of this technique. Transdiaphragmatic pressure (Pdi) was measured at functional residual capacity during stimulation (120 Hz, 0.2-ms duration) of one phrenic nerve by either direct phrenic nerve stimulation (DPNS) or transvenous phrenic nerve stimulation (TPNS). An analysis of variance showed no significant (P greater than 0.50) change during the 5-h period. There was a significant correlation (r = 0.94, P less than 0.001) between Pdi obtained by TPNS and that obtained by DPNS. It is concluded that either DPNS or TPNS can be used to evaluate diaphragmatic strength over a 5-h period and that TPNS can be used in lieu of DPNS.

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Botzinger complex region role in phrenic-to-phrenic inhibitory reflex of cat

Journal of Applied Physiology ◽

10.1152/jappl.1989.67.4.1364 ◽

1989 ◽

Vol 67 (4) ◽

pp. 1364-1370 ◽

Cited By ~ 12

Author(s):

D. F. Speck

Keyword(s):

Nerve Stimulation ◽

Phrenic Nerve ◽

Inhibitory Response ◽

Phrenic Nerve Stimulation ◽

Bötzinger Complex ◽

Before And After ◽

Pass Through ◽

Bilateral Lesions ◽

Decerebrate Cats ◽

Inhibitory Reflex

Neuronal recordings, microstimulation, and electrolytic and chemical lesions were used to examine the involvement of the Botzinger Complex (BotC) in the bilateral phrenic-to-phrenic inhibitory reflex. Experiments were conducted in decerebrate cats that were paralyzed, ventilated, thoracotomized, and vagotomized. Microelectrode recordings within the BotC region revealed that some neurons were activated by phrenic nerve stimulation (15 of 69 expiratory units, 9 of 67 inspiratory units, and 19 nonrespiratory-modulated units) at average latencies similar to the onset latency of the phrenic-to-phrenic inhibition. In addition, microstimulation within the BotC caused a short latency transient inhibition of phrenic motor activity. In 17 cats phrenic neurogram responses to threshold and supramaximal (15 mA) stimulation of phrenic nerve afferents were recorded before and after electrolytic BotC lesions. In 15 animals the inhibitory reflex was attenuated by bilateral lesions. Because lesion of either BotC neurons or axons of passage could account for this attenuation, in eight experiments the phrenic-to-phrenic inhibitory responses were recorded before and after bilateral injections of 5 microM kainic acid (30–150 nl) into the BotC. After chemical lesions, the inhibitory response to phrenic nerve stimulation remained; however, neuronal activity typical of the BotC could not be located. These results suggest that axons important in producing the phrenic-to-phrenic reflex pass through the region of the BotC, but that BotC neurons themselves are not necessary for this reflex.

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Management of phrenic nerve stimulation caused by epicardial pacemaker leads in children

The Annals of Thoracic Surgery ◽

10.1016/s0003-4975(03)00557-5 ◽

2003 ◽

Vol 76 (5) ◽

pp. 1757-1758 ◽

Cited By ~ 5

Author(s):

Winfield J Wells ◽

Anjan S Batra

Keyword(s):

Nerve Stimulation ◽

Phrenic Nerve ◽

Phrenic Nerve Stimulation ◽

Pacemaker Leads

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Mapping for Acute Transvenous Phrenic Nerve Stimulation Study (MAPS Study)

Pacing and Clinical Electrophysiology ◽

10.1111/pace.13016 ◽

2017 ◽

Vol 40 (3) ◽

pp. 294-300

Author(s):

LUKAS R.C. DEKKER ◽

BART GERRITSE ◽

AVRAM SCHEINER ◽

LILIAN KORNET

Keyword(s):

Nerve Stimulation ◽

Phrenic Nerve ◽

Phrenic Nerve Stimulation

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Preventing Ventilator–Induced Diaphragmatic Dysfunction With Phrenic Nerve Stimulation*

Critical Care Medicine ◽

10.1097/ccm.0000000000000003 ◽

2014 ◽

Vol 42 (2) ◽

pp. 492-494 ◽

Cited By ~ 8

Author(s):

Franco Laghi ◽

Hameeda Shaikh

Keyword(s):

Nerve Stimulation ◽

Phrenic Nerve ◽

Phrenic Nerve Stimulation ◽

Diaphragmatic Dysfunction

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Excitation of dorsal and ventral respiratory group neurons by phrenic nerve afferents

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.3.946 ◽

1987 ◽

Vol 62 (3) ◽

pp. 946-951 ◽

Cited By ~ 23

Author(s):

D. F. Speck ◽

W. R. Revelette

Keyword(s):

Nerve Stimulation ◽

Phrenic Nerve ◽

Afferent Input ◽

Neuronal Responses ◽

Onset Latency ◽

Phrenic Nerve Stimulation ◽

Group Iii ◽

Neuronal Excitation ◽

Dorsal Columns ◽

The Difference

The projections of phrenic nerve afferents to neurons in the dorsal (DRG) and ventral (VRG) respiratory group were studied in anesthetized, paralyzed, and vagotomized cats. Extracellular recordings of neuronal responses to vagal nerve and cervical phrenic nerve stimulation (CPNS) indicated that about one-fourth of the DRG respiratory-modulated neurons were excited by phrenic nerve afferents with an onset latency of approximately 20 ms. In addition, non-respiratory-modulated neurons within the DRG were recruited by CPNS. Although some convergence of vagal and phrenic afferent input was observed, most neurons were affected by only one type of afferent. In contrast to the DRG, only 3 out of 28 VRG respiratory-modulated neurons responded to CPNS. A second study determined that most of these neuronal responses were due to activation of diaphragmatic afferents since 90% of the DRG units activated by CPNS were also excited at a longer latency by thoracic phrenic nerve stimulation. The difference in onset latency of neuronal excitation indicates an afferent peripheral conduction velocity of about 10 m/s, which suggests that they are predominately small myelinated fibers (group III) making paucisynaptic connections with DRG neurons. Decerebration, decerebellation, and bilateral transection of the dorsal columns at C2 do not abolish the neuronal responses to cervical PNS.

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