Pattern of expiratory muscle activation during lower thoracic spinal cord stimulation. (57/2868)

Large positive airway pressures (Paws) can be generated by lower thoracic spinal cord stimulation (SCS), which may be a useful method of restoring cough in spinal cord-injured patients. Optimal electrode placement, however, requires an assessment of the pattern of current spread during SCS. Studies were performed in anesthetized dogs to assess the pattern of expiratory muscle recruitment during SCS applied at different spinal cord levels. A multicontact stimulating electrode was positioned over the surface of the lower thoracic and upper lumbar spinal cord. Recording electromyographic electrodes were placed at several locations in the abdominal and internal intercostal muscles. SCS was applied at each lead, in separate trials, with single shocks of 0.2-ms duration. The intensity of stimulation was adjusted to determine the threshold for development of the compound action potential at each electrode lead. The values of current threshold for activation of each muscle formed parabolas with minimum values at specific spinal root levels. The slopes of the parabolas were relatively steep, indicating that the threshold for muscle activation increases rapidly at more cephalad and caudal sites. These results were compared with the effectiveness of SCS (50 Hz; train duration, 1-2 s) at different spinal cord levels to produce changes in Paw. Stimulation at the T9 and T10 spinal cord level resulted in the largest positive Paws with a single lead. At these sites, threshold values for activation of the internal intercostal (7-11th interspaces) upper portions of external oblique, rectus abdominis, and transversus abdominis were near their minimum. Threshold values for activation of the caudal portions of the abdominal muscles were high (>50 mA). Our results indicate that 1) activation of the more cephalad portions of the abdominal muscles is more important than activation of caudal regions in the generation of positive Paws and 2) it is not possible to achieve complete activation of the expiratory muscles with a single electrode lead by using modest current levels. In support of this latter conclusion, a two-electrode lead system results in more uniform expiratory muscle activation and significantly greater changes in Paw.  (+info)

Ventilatory effects of 8 h of isocapnic hypoxia with and without beta-blockade in humans. (58/2868)

This study investigated whether changing sympathetic activity, acting via beta-receptors, might induce the progressive ventilatory changes observed in response to prolonged hypoxia. The responses of 10 human subjects to four 8-h protocols were compared: 1) isocapnic hypoxia (end-tidal PO2 = 50 Torr) plus 80-mg doses of oral propranolol; 2) isocapnic hypoxia, as in protocol 1, with oral placebo; 3) air breathing with propranolol; and 4) air breathing with placebo. Exposures were conducted in a chamber designed to maintain end-tidal gases constant by computer control. Ventilation (VE) was measured at regular intervals throughout. Additionally, the subjects' ventilatory hypoxic sensitivity and their residual VE during hyperoxia (5 min) were assessed at 0, 4, and 8 h by using a dynamic end-tidal forcing technique. beta-Blockade did not significantly alter either the rise in VE seen during 8 h of isocapnic hypoxia or the changes observed in the acute hypoxic ventilatory response and residual VE in hyperoxia over that period. The results do not provide evidence that changes in sympathetic activity acting via beta-receptors play a role in the mediation of ventilatory changes observed during 8 h of isocapnic hypoxia.  (+info)

Acute hypoxic pulmonary vasoconstriction in conscious dogs decreases renin and is unaffected by losartan. (59/2868)

Acute hypoxic pulmonary vasoconstriction (HPV) may be mediated by vasoactive peptides. We studied eight conscious, chronically tracheostomized dogs kept on a standardized dietary sodium intake. Normoxia (40 min) was followed by hypoxia (40 min, breathing 10% oxygen, arterial oxygen pressures 36 +/- 1 Torr) during both control (Con) and losartan experiments (Los; iv infusion of 100 microg. min-1. kg-1 losartan). During hypoxia, minute ventilation (by 0.9 l/min in Con, by 1.3 l/min in Los), cardiac output (by 0.36 l/min in Con, by 0.30 l/min in Los), heart rate (by 11 beats/min in Con, by 30 beats/min in Los), pulmonary artery pressure (by 9 mmHg in both protocols), and pulmonary vascular resistance (by 280 and 254 dyn. s. cm-5 in Con and Los, respectively) increased. Mean arterial pressure and systemic vascular resistance did not change. In Con, PRA decreased from 4.2 +/- 0.7 to 2.5 +/- 0.5 ng ANG I. ml-1. h-1, and plasma ANG II decreased from 11.9 +/- 3.0 to 8.2 +/- 2.1 pg/ml. The renin-angiotensin system is inhibited during acute hypoxia despite sympathetic activation. Under these conditions, ANG II AT1-receptor antagonism does not attenuate HPV.  (+info)

Posture effects on timing of abdominal muscle activity during stimulated ventilation. (60/2868)

In humans during stimulated ventilation, substantial abdominal muscle activity extends into the following inspiration as postexpiratory expiratory activity (PEEA) and commences again during late inspiration as preexpiratory expiratory activity (PREA). We hypothesized that the timing of PEEA and PREA would be changed systematically by posture. Fine-wire electrodes were inserted into the rectus abdominis, external oblique, internal oblique, and transversus abdominis in nine awake subjects. Airflow, end-tidal CO2, and moving average electromyogram (EMG) signals were recorded during resting and CO2-stimulated ventilation in both supine and standing postures. Phasic expiratory EMG activity (tidal EMG) of the four abdominal muscles at any level of CO2 stimulation was greater while standing. Abdominal muscle activities during inspiration, PEEA, and PREA, were observed with CO2 stimulation, both supine and standing. Change in posture had a significant effect on intrabreath timing of expiratory muscle activation at any level of CO2 stimulation. The transversus abdominis showed a significant increase in PEEA and a significant decrease in PREA while subjects were standing; similar changes were seen in the internal oblique. We conclude that changes in posture are associated with significant changes in phasic expiratory activity of the four abdominal muscles, with systematic changes in the timing of abdominal muscle activity during early and late inspiration.  (+info)

Effects of experimental cortical seizures on respiratory motor nerve activities in piglets. (61/2868)

Airway obstruction at the level of the larynx causes respiratory insufficiency during experimental seizures in spontaneously breathing, anesthetized piglets (T. E. Terndrup and W. E. Fordyce, Pediatr. Res., 38: 61-66, 1995). To investigate further the neural mechanisms of this obstruction, the activities of the phrenic nerve (PH) and the recurrent laryngeal motor branches to the thyroarytenoid (TA) and posterior cricoarytenoid (PCA) muscles were analyzed in 11 anesthetized, vagotomized, paralyzed, and ventilated piglets. After a control recording period, seizures were induced by subcortical penicillin G injections. Compared with baseline conditions, nerve activities became irregular during seizures. Extraneous TA bursts during PH activation were evident in all piglets during seizures. During ictal phases of seizures, the peak integrated activities of the PH and the expiratory component of the PCA, but not TA or inspiratory PCA activities, were significantly decreased compared with interictal phases. During seizures, a significant delay in the onset of the inspiratory component of PCA activation with respect to the onset of the PH was observed. This study helps to explain respiratory impairment during cortical seizures by providing evidence of impaired timing of activation of laryngeal dilator mechanisms and coordination with those activating the diaphragm. Cyclical PH inhibition during high-intensity cortical discharges may provide a secondary mechanism producing respiratory insufficiency during seizures.  (+info)

Effect of formoterol on clinical parameters and lung functions in patients with bronchial asthma: a randomised controlled trial. (62/2868)

AIMS: To determine the role of formoterol in the treatment of children with bronchial asthma who are symptomatic despite regular use of inhaled corticosteroids. METHODS: A randomised, double blind, parallel group, placebo controlled study to investigate the effects of inhaled formoterol (12 microg twice a day) in 32 children with moderate to severe bronchial asthma. The study consisted of two week run in periods and six week treatment periods, during both of which the patients continued their regular anti-inflammatory drugs. The efficacy parameters were symptom scores, bronchodilator use, daily peak expiratory flow rates (PEFR), methacholine hyper-reactivity, forced expiratory volume in one second (FEV1), lung volumes, and airway conductance. RESULTS: Formoterol treatment for six weeks decreased symptom scores, PEFR variability, and the number of rescue salbutamol doses, and increased morning and evening PEFR significantly. No adverse reactions were seen. CONCLUSION: These findings suggest that inhaled formoterol is effective in controlling chronic asthma symptoms in children who are symptomatic despite regular use of inhaled corticosteroids.  (+info)

Adenosinergic modulation of respiratory neurones in the neonatal rat brainstem in vitro. (63/2868)

1. The mechanism underlying adenosinergic modulation of respiration was examined in vitro by applying the whole-cell patch-clamp technique to different types of respiration-related neurones located in the rostral ventrolateral medulla of neonatal rats (0-4 days old). 2. The adenosine A1-receptor agonist (R)-N6-(2-phenylisopropyl)-adenosine (R-PIA, 10 microM; n = 31) increased the burst distance of rhythmic C4 inspiratory discharges and decreased the duration of inspiratory discharges (control: 8.00 +/- 2.49 s and 918 +/- 273 ms; R-PIA: 12.10 +/- 5.60 s and 726 +/- 215 ms). 3. Expiratory neurones demonstrated a reversible decrease in input resistance (Rin), a depression of action potential discharges and a hyperpolarization of the membrane potential (Vm) during application of R-PIA (1-10 microM). Similar responses of Rin and Vm to R-PIA were evident after synaptic activity had been blocked by 0.5 microM tetrodotoxin (TTX). 4. Some of the biphasic expiratory (biphasic E) neurones, but none of the inspiratory neurones, demonstrated changes in Rin or Vm during R-PIA application. With TTX present, R-PIA did not alter Vm or Rin in biphasic expiratory or inspiratory neurones. 5. Furthermore, R-PIA decreased the spontaneous postsynaptic activities of all neurones examined. The effects of R-PIA on respiratory activity, Rin and Vm could be reversed by the A1-receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthine (DPCPX; 200 nM). 6. Our data suggest that the modulation of respiratory output induced by adenosinergic agents can be explained by (1) a general decrease in synaptic transmission between medullary respiration-related neurones mediated by presynaptic A1-receptors, and (2) an inactivation, via membrane hyperpolarization, of medullary expiratory neurones mediated by postsynaptic A1-receptors. Furthermore, our data demonstrate that inactivation of expiratory neurones does not abolish the respiratory rhythmic activity, but only modulates respiratory rhythm in vitro.  (+info)

Respiratory mechanical advantage of the canine external and internal intercostal muscles. (64/2868)

1. The current conventional view of intercostal muscle actions is based on the theory of Hamberger (1749) and maintains that as a result of the orientation of the muscle fibres, the external intercostals have an inspiratory action on the lung and the internal interosseous intercostals have an expiratory action. This notion, however, remains unproved. 2. In the present studies, the respiratory actions of the canine external and internal intercostal muscles were evaluated by applying the Maxwell reciprocity theorem. Thus the effects of passive inflation on the changes in length of the muscles throughout the rib cage were assessed, and the distributions of muscle mass were determined. The fractional changes in muscle length during inflation were then multiplied by muscle mass and maximum active stress (3.0 kg cm-2) to evaluate the potential effects of the muscles on the lung. 3. The external intercostals in the dorsal third of the rostral interspaces were found to have a large inspiratory effect. However, this effect decreases rapidly both toward the costochondral junctions and toward the base of the rib cage. As a result, it is reversed to an expiratory effect in the most caudal interspaces. The internal intercostals in the caudal interspaces have a large expiratory effect, but this effect decreases ventrally and rostrally, such that it is reversed to an inspiratory effect in the most rostral interspaces. 4. These observations indicate that the canine external and internal intercostal muscles do not have distinct inspiratory and expiratory actions as conventionally thought. Therefore, their effects on the lung during breathing will be determined by the topographic distribution of neural drive.  (+info)