Different effects of halothane on diaphragm and hindlimb muscle in rats

1987 ◽  
Vol 63 (5) ◽  
pp. 1757-1762 ◽  
Author(s):  
B. Dureuil ◽  
N. Viires ◽  
Y. Nivoche ◽  
M. Fiks ◽  
R. Pariente ◽  
...  

The effects of halothane administration on diaphragm and tibialis anterior (TA) muscle were investigated in 30 anesthetized mechanically ventilated rats. Diaphragmatic strength was assessed in 17 rats by measuring the abdominal pressure (Pab) generated during supramaximal stimulation of the intramuscular phrenic nerve endings at frequencies of 0.5, 30, and 100 Hz. Halothane was administered during 30 min at a constant minimum alveolar concentration (MAC): 0.5, 1, and 1.5 MAC in three groups of five rats. For each MAC, Pab was significantly reduced for all frequencies of stimulation except at 100 Hz during 0.5 MAC halothane exposure. The effects of halothane (0.5, 1, and 1.5 MAC) on diaphragmatic neuromuscular transmission were assessed in five other rats by measuring the integrated electrical activity of the diaphragm (Edi) during electrical stimulation of the phrenic nerve. No change in Edi was observed during halothane exposure. In five other rats TA contraction was studied by measuring the strength of isometric contraction of the muscle during electrical stimulation of its nerve supply at different frequencies (0.5, 30, and 100 Hz). Muscle function was unchanged during administration of halothane in a cumulative fashion from 0.5 to 1.5 MAC. These results demonstrate that halothane does not affect hindlimb muscle function, whereas it had a direct negative inotropic effect on rat diaphragmatic muscle.

2003 ◽  
Vol 94 (1) ◽  
pp. 220-226 ◽  
Author(s):  
Weirong Zhang ◽  
Paul W. Davenport

It has been demonstrated that phrenic nerve afferents project to somatosensory cortex, yet the sensory pathways are still poorly understood. This study investigated the neural responses in the thalamic ventroposteriolateral (VPL) nucleus after phrenic afferent stimulation in cats and rats. Activation of VPL neurons was observed after electrical stimulation of the contralateral phrenic nerve. Direct mechanical stimulation of the diaphragm also elicited increased activity in the same VPL neurons that were activated by electrical stimulation of the phrenic nerve. Some VPL neurons responded to both phrenic afferent stimulation and shoulder probing. In rats, VPL neurons activated by inspiratory occlusion also responded to stimulation on phrenic afferents. These results demonstrate that phrenic afferents can reach the VPL thalamus under physiological conditions and support the hypothesis that the thalamic VPL nucleus functions as a relay for the conduction of proprioceptive information from the diaphragm to the contralateral somatosensory cortex.


2011 ◽  
Vol 36 (6) ◽  
pp. 1001-1008 ◽  
Author(s):  
Dan Adler ◽  
Stewart B. Gottfried ◽  
Nathalie Bautin ◽  
Tomislav Mirkovic ◽  
Matthieu Schmidt ◽  
...  

Electrical stimulation can enhance muscle function. We applied repetitive cervical magnetic phrenic stimulation (rCMS) to induce diaphragm contractions in 7 healthy subjects (800 ms trains; transdiaphragmatic pressure (Pdi) measurements; tolerance ratings). Each rCMS train produced a sustained diaphragm contraction. Sixty-five percent of the maximal available output at 15 Hz proved the best compromise between Pdi and discomfort with nonfatiguing contractions. rCMS appears feasible and should be investigated for diaphragm conditioning in appropriate clinical populations.


2001 ◽  
Vol 90 (4) ◽  
pp. 1570-1576 ◽  
Author(s):  
Jalal M. Abu-Shaweesh ◽  
Ismail A. Dreshaj ◽  
Musa A. Haxhiu ◽  
Richard J. Martin

Stimulation of the superior laryngeal nerve (SLN) results in apnea in animals of different species, the mechanism of which is not known. We studied the effect of the GABAA receptor blocker bicuculline, given intravenously and intracisternally, on apnea induced by SLN stimulation. Eighteen 5- to 10-day-old piglets were studied: bicuculline was administered intravenously to nine animals and intracisternally to nine animals. The animals were anesthetized and then decerebrated, vagotomized, ventilated, and paralyzed. The phrenic nerve responses to four levels of electrical SLN stimulation were measured before and after bicuculline. SLN stimulation caused a significant decrease in phrenic nerve amplitude, phrenic nerve frequency, minute phrenic activity, and inspiratory time ( P < 0.01) that was proportional to the level of electrical stimulation. Increased levels of stimulation were more likely to induce apnea during stimulation that often persisted beyond cessation of the stimulus. Bicuculline, administered intravenously or intracisternally, decreased the SLN stimulation-induced decrease in phrenic nerve amplitude, minute phrenic activity, and phrenic nerve frequency ( P < 0.05). Bicuculline also reduced SLN-induced apnea and duration of poststimulation apnea ( P < 0.05). We conclude that centrally mediated GABAergic pathways are involved in laryngeal stimulation-induced apnea.


Neurosurgery ◽  
1978 ◽  
Vol 2 (1) ◽  
pp. 43-46 ◽  
Author(s):  
Ronald F. Young

Abstract Most neurosurgical patients with permanent partial or complete respiratory insufficiency are managed with a mechanical ventilator and tracheostomy. This method presents many medical, technical, emotional, and social problems. A case report is presented that illustrates the potential usefulness of electrical stimulation of the phrenic nerve (“diaphragm pacing”) as an alternate method of therapy for respiratory insufficiency. This paper outlines the indications for, methods of, and problems with such a system and is intended to make its availability more widely appreciated among neurosurgeons.


2007 ◽  
Vol 293 (2) ◽  
pp. H1190-H1195 ◽  
Author(s):  
Jihong Xing ◽  
Satoshi Koba ◽  
Valerie Kehoe ◽  
Zhaohui Gao ◽  
Kristen Rice ◽  
...  

During exercise, sympathetic nerve responses are accentuated in heart failure (HF), and this enhances norepinephrine (NE) release and evokes vasoconstriction. Two key pathophysiological responses could contribute to the greater NE release: 1) increased sympathetic nerve discharge and 2) increased NE in the neurovascular junction for a given level of sympathetic discharge. In this report, we focus on the second of these two general issues and test the following hypotheses: 1) in HF for a given level of sympathetic nerve stimulation, NE concentration in the interstitium (an index of neurovascular NE) would be greater, and 2) the greater interstitial NE concentration would be linked to reduced NE uptake. Studies were performed in rats 8–10 wk after induction of myocardial infarction (MI). Interstitial NE samples were collected from microdialysis probes inserted into the hindlimb muscle. Dialysate concentration of NE was determined by the HPLC method. First, interstitial NE concentration increased during electrical stimulation of the lumbar sympathetic nerves in eight control rats. An increase in interstitial NE concentration was significantly greater in 10 rats with severe MI. Additionally, an NE uptake-1 inhibitor (desipramine, 1 μM) was injected into the arterial blood supply of the muscle in six control and eight MI rats. Desipramine increased interstitial NE concentration by 24% in control and by only 3% ( P < 0.05 vs. control) in MI rats. In conclusion, given levels of electrical stimulation of the lumbar sympathetic nerve lead to higher interstitial NE concentration in HF. This effect is due, in part, to reduced NE uptake-1 in HF.


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