Respiratory activities of intralaryngeal branches of the recurrent laryngeal nerve

To distinguish experimentally between motor nerve activity destined for vocal cord abductor muscles and that bound for muscles that adduct the cords, we recorded efferent activities of intralaryngeal branches of the recurrent laryngeal nerve (RLN) in decerebrate, vagotomized, paralyzed, ventilated cats. Activities of the whole RLN and phrenic nerve were also recorded. Nerve activities were assessed at several steady-state end-tidal O2 and CO2 concentrations. The nerve to the thyroarytenoid (TA) muscle, a vocal cord adductor, was only slightly active under base-line (normocapnic, hyperoxic) conditions but in most cats developed strong activity during expiration in hypocapnia or hypoxia. In severe hypocapnia, phasic expiratory TA activity persisted even during phrenic apnea, indicating continuing activity of the respiratory rhythm generator. The nerve to the posterior cricoarytenoid (PCA) muscle, the vocal cord abductor, was always active in inspiration but often showed expiratory activity as well. This expiratory activity was usually enhanced by hypercapnia and often inhibited by hypoxia. The results are consistent with previous electromyographic findings and emphasize the importance of distinguishing abductor from adductor activity in studies of laryngeal control.     

Course and branches of the recurrent laryngeal nerve, inferior thyroid artery and inferior laryngeal artery

Length, width, and thickness of the recurrent laryngeal nerve and its extra-laryngeal twigs were estimated. Included is the course of the nerve to the suspensory ligament of the thyroid gland, to the inferior horn of the thyroid cartilage and to trachea and esophagus. The origin of the inferior thyroid artery, its width and course to the twigs of the recurrent laryngeal nerve were studied. The origin zone of the inferior laryngeal artery is also described. The different terms and opinions about the twigs of the truncus thyreocervicalis and the thyroid axis are discussed.     

Pulmonary C-fiber activation enhances respiratory-related activities of the recurrent laryngeal nerve in rats

The purpose of the current study was to characterize the response of the recurrent laryngeal nerve (RLN) to pulmonary C-fiber activation. Male rats of Wistar strain were anesthetized by urethane (1.2 g/kg, i.p.). Tracheostomy was performed. Catheter was inserted into the femoral artery and vein. Additional catheter was placed near the entrance of the right atrium via the right jugular vein. The animal was then paralyzed with gallamine triethiodide, ventilated and maintained at normocapnia in hyperoxia. Activities of the phrenic (PNA) and recurrent laryngeal nerves (RLNA) were monitored simultaneously. Two experimental protocols were completed. In the first experiment, various doses of capsaicin were delivered into the right atrium to activate pulmonary C-fibers with vagal intact. Low dose of capsaicin (1.25 microg/kg) produced apnea, a decrease in amplitude of PNA, an enhancement of RLNA during apnea and recovery from apnea, hypotension, and bradycardia. High dose of capsaicin (5 and 20 microg/kg) evoked the same tendency of response for both nerves and biphasic changes in blood pressure. Dose dependency was only seen in the period of apnea but not observable in nerve amplitudes. After bilateral vagotomy, low dose of capsaicin produced an increase in PNA without apnea, no significant change in RLNA, and hypertension. These results suggest that activation of vagal and nonvagal C-fibers could produce different reflex effects on cardiopulmonary functions. The reflex responses evoked by these two types of afferents might play defensive and protective roles in the airways and lungs.     

Anatomy of the recurrent laryngeal nerve in normal Iraqis

A study of the anatomy of the recurrent laryngeal nerve was made on 106 post-mortem cases and fixed dissecting-room cadavers. The usual position of the nerve was in the tracheo-oesophageal groove. The nerve lay posterior to the inferior thyroid artery on the left side in most cases, while its relation was very variable on the right side. The inferior cornu of the thyroid cartilage was the best guide to the site of entry of the nerve into the larynx.     

Motor innervation of the cricopharyngeus muscle by the recurrent laryngeal nerve

Hammond, Carol Smith, Paul W. Davenport, Alastair Hutchison,and Randall A. Otto. Motor innervation of thecricopharyngeus muscle by the recurrent laryngeal nerve.J. Appl. Physiol. 83(1): 89-94, 1997.Patients with recurrent laryngeal nerve (RLN) paresis demonstrate impaired function of laryngeal muscles and swallowing. Thecricopharyngeus muscle (CPM) is a major component of the upper esophageal sphincter. It was hypothesized that the RLN innervates thismuscle. A nerve branch leading from the RLN to the CPM was found in adult sheep by anatomic dissection. Electrical stimulation ofthe RLN elicited a muscle action potential recorded by electrodes placed in the ipsilateral CPM. Swallowing was investigated by mechanical stimulation of oropharynx pre- and postsectioning of theRLN. Severing of the RLN resulted in a loss of the early phases ofswallow-related CPM electromyographic activity; however,late-phase CPM electromyographic activity persisted. The RLN providesmotor innervation of the CPM, which also has innervation from thepharyngeal plexus.

     

Ultrastructural studies on the barrier properties of the paraganglia in the rat recurrent laryngeal nerve.

The permeability of blood capillaries in the paraganglia of the rat recurrent laryngeal nerve (RLN) was investigated by employing the ionic lanthanum tracer at ultrastructural level. Two types of blood capillaries, namely, fenestrated and nonfenestrated types, were observed in the rat RLN and its associated paraganglia (RLN paraganglia). A preferential distribution of fenestrated capillaries in the RLN paraganglia was noted. Nonfenestrated capillaries were distributed in the area of RLN devoid of paraganglia. Minute aberrant ganglia consisting of 4-8 neurons were frequently encountered in the rat RLN near the paraganglia. The capillaries in these neuronal areas were also nonfenestrated. The lanthanum tracer was limited within the vascular lumen, but not in the extravascular space, in the RLN proper and in the area of RLN paraganglia where the neurons were identified. In the RLN paraganglia, the tracer was located in the vascular lumen, extravascular space, periaxonal space of nerve fibers, and the intercellular space of the RLN paraganglionic cells. We concluded that (1) a blood-nerve barrier and a blood-ganglion (or blood-neuron) barrier exist in the area of RLN devoid of paraganglia, and (2) blood-paraganglion barrier and blood-nerve barrier were lacking in the rat RLN paraganglia.     

Central projection of the sensory fibres of the recurrent laryngeal nerve of the cat.

There have been few studies of the central projection of the sensory fibres of the recurrent laryngeal nerve into the medulla oblongata. In the present study terminal degeneration was observed in both the nucleus of the tractus solitarius and the nucleus of the spinal tract of the trigeminal nerve after transection of the nerve and after injection of a lectin, Ricinus communis agglutinin (RCA). Degeneration was observed to be more extensive after RCA injection than after nerve transection. In both instances, however, degeneration was observed bilaterally.     

Influence of lung volume on oxygen cost of resistive breathing

We examined the relationship between the O2 cost of breathing (VO2 resp) and lung volume at constant load, ventilation, work rate, and pressure-time product in five trained normal subjects breathing through an inspiratory resistance at functional residual capacity (FRC) and when lung volume (VL) was increased to 37 +/- 2% (mean +/- SE) of inspiratory capacity (high VL). High VL was maintained using continuous positive airway pressure of 9 +/- 2 cmH2O and with the subjects coached to relax during expiration to minimize respiratory muscle activity. Six paired runs were performed in each subject at constant tidal volume (0.62 +/- 0.2 liters), frequency (23 +/- 1 breaths/min), inspiratory flow rate (0.45 +/- 0.1 l/s), and inspiratory muscle pressure (45 +/- 2% of maximum static pressure at FRC). VO2 resp increased from 109 +/- 15 ml/min at FRC by 41 +/- 11% at high VL (P less than 0.05). Thus the efficiency of breathing at high VL (3.9 +/- 0.2%) was less than that at FRC (5.2 +/- 0.3%, P less than 0.01). The decrease in inspiratory muscle efficiency at high VL may be due to changes in mechanical coupling, in the pattern of recruitment of the respiratory muscles, or in the intrinsic properties of the inspiratory muscles at shorter length. When the work of breathing at high VL was normalized for the decrease in maximum inspiratory muscle pressure with VL, efficiency at high VL (5.2 +/- 0.3%) did not differ from that at FRC (P less than 0.7), suggesting that the fall in efficiency may have been related to the fall in inspiratory muscle strength. During acute hyperinflation the decreased efficiency contributes to the increased O2 cost of breathing and may contribute to the diminished inspiratory muscle endurance.     

Influence of endothelial volume on kinetics of reacting indicators in the lung

The purpose of this work is to show mathematically the relationship between the classical maximum velocity of reaction, Vmax, for enzyme kinetics and an analogous parameter, Vmax, derived by Linehan and Dawson (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47:404-411, 1979) for the analysis of tracers which disappear by saturation kinetics from the lung circulation during the passage of indicators after bolus injection. Rederivation of the original equation for the combination of flow and reaction in a capillary showed that Vmax is equal to the product of enzyme Vmax and the volume of endothelium, Ve, in which the enzyme resides. This implies that Vmax interpreted from multiple-indicator curves in the lung by the Linehan-Dawson method is a combination of an enzyme characteristic Vmax and a measure of functioning capillary surface during passage, Ve. Lung injury could change Vmax, functioning surface (Ve), or both.     

Influence of passive changes of lung volume on upper airways

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.     

Influence of lung volume on pulmonary microvascular pressure-volume characteristics.

The pressure-volume (P-V) characteristics of the lung microcirculation are important determinants of the pattern of pulmonary perfusion and of red and white cell transit times. Using diffuse light scattering, we measured capillary P-V loops in seven excised perfused dog lobes at four lung volumes, from functional residual capacity (FRC) to total lung capacity (TLC), over a wide range of vascular transmural pressures (Ptm). At Ptm 5 cmH(2)O, specific compliance of the microvasculature was 8.6%/cmH(2)O near FRC, decreasing to 2.7%/cmH(2)O as lung volume increased to TLC. At low lung volumes, the vasculature showed signs of strain stiffening (specific compliance fell as Ptm rose), but stiffening decreased as lung volume increased and was essentially absent at TLC. The P-V loops were smooth without sharp transitions, consistent with vascular distension as the primary mode of changes in vascular volume with changes in Ptm. Hysteresis was small (0.013) at all lung volumes, suggesting that, although surface tension may set basal capillary shape, it does not strongly affect capillary compliance.