Effects of thoracic dorsal rhizotomies on the respiratory pattern in anesthetized cats

1977 ◽  
Vol 43 (1) ◽  
pp. 20-26 ◽  
Author(s):  
R. Shannon

Experiments were conducted to determine if thoracic wall proprioceptor afferents are involved in the modulation of respiratory activity during eupnea. The effects of elimination of thoracic wall afferents (thoracic dorsal rhizotomies (TDR) on tidal volume (VT), frequency (f), inspiratory time (ti) and expiratory time (te) were studied in vagotomized cats anesthetized with diallylbarbituric acid (Dial). Dorsal rhizotomies 1–12 resulted primarily in a decreased VT and ti, and an increased f. Further experiments were performed to determine if these changes in respiratory pattern could be correlated with known reflexes from the middle and lower intercostal muscles, or lungs, via thoracic dorsal roots. Afferents from these sources were eliminated by TDR 5–9, 10–13, and 1–4. TDR 1–4 had no significant effect on the respiratory pattern. TDR 5–9 and TDR 10–13 produced changes similar in direction to TDR 1–12. The results indicate that: a) afferents 1–4 from the upper intercostal muscles and lungs (sympathetic afferents) do not contribute significantly to the control of the spontaneous respiratory rhythm, and b) afferents via the middle thoracic roots, 5–9, and the lower thoracic roots, 10–13, contribute significantly to the rhythm. The results do not completely correlate with known intercostal reflexes, but it is suggested that elimination of intercostal muscle proprioceptor afferents is responsible for the observed effects of thoracic dorsal rhizotomies.

1982 ◽  
Vol 52 (3) ◽  
pp. 716-724 ◽  
Author(s):  
J. P. Mortola ◽  
J. T. Fisher ◽  
J. B. Smith ◽  
G. S. Fox ◽  
S. Weeks ◽  
...  

We studied the ventilatory parameters and the pattern of breathing including the onset of respiration in 20 healthy infants immediately after cesarean-section delivery. In eight of the infants further measurements were obtained at 60 min of life. The pattern of breathing immediately after delivery is very irregular with a marked tendency to keep the lung inflated mainly through interruptions of expiration. After the first expiration some air remains in the lung representing the formation of functional residual capacity (FRC). FRC obtained with the first breath is proportional to the previous inspired volume and is the largest contribution towards the full establishment of FRC. Tidal volume and FRC of the first breath are similar to that reported in babies delivered vaginally, which suggests that the forces required for lung inflation are similar in the two groups of infants. The first breath tends to be deeper and slower and has a longer expiratory time than subsequent breaths. At 60 min of life the respiratory pattern becomes more regular, tidal volume is further decreased, and respiratory frequency is increased through a reduction of expiratory time.


1981 ◽  
Vol 51 (5) ◽  
pp. 1150-1156 ◽  
Author(s):  
M. L. Nochomovitz ◽  
M. Goldman ◽  
J. Mitra ◽  
N. S. Cherniack

The effects of diaphragm paralysis on respiratory activity were assessed in 13 anesthetized, spontaneously breathing dogs studied in the supine position. Transient diaphragmatic paralysis was induced by bilateral phrenic nerve cooling. Respiratory activity was assessed from measurements of ventilation and from the moving time averages of electrical activity recorded from the intercostal muscles and the central end of the fifth cervical root of the phrenic nerve. The degree of diaphragm paralysis was evaluated from changes in transdiaphragmatic pressure and reflected in rib cage and abdominal displacements. Animals were studied both before and after vagotomy breathing O2, 3.5% CO2 in O2, or 7% CO2 in O2. In dogs with intact vagi, both peak and rate of rise of phrenic and inspiratory intercostal electrical activity increased progressively as transdiaphragmatic pressure fell. Tidal volume decreased and breathing frequency increased as a result of a shortening in expiratory time. Inspiratory time and ventilation were unchanged by diaphragm paralysis. These findings were the same whether O2 or CO2 in O2 was breathed. After vagotomy, no significant change in phrenic or inspiratory intercostal activity occurred with diaphragm paralysis in spite of increased arterial CO2 partial pressure. Ventilation and tidal volume decreased significantly, and respiratory timing was unchanged. These results suggest that mechanisms mediated by the vagus nerves account for the compensatory increase in respiratory electrical activity during transient diaphragm paralysis. That inspiratory time is unchanged by diaphragm paralysis whereas the rate or rise of phrenic nerve activity increases suggest that reflexes other than the Hering-Breuer reflex contribute to the increased respiratory response.


1985 ◽  
Vol 59 (5) ◽  
pp. 1515-1520 ◽  
Author(s):  
W. Perez ◽  
M. J. Tobin

Employment of mouthpiece and noseclips (MP + NC) has repeatedly been shown to increase tidal volume (VT), but its effect on respiratory frequency (f) and its subsets is controversial. The mechanisms accounting for this alteration in breathing pattern are poorly understood and may include stimulation of oral or nasal sensory receptors or alteration in the route of breathing. In this study we demonstrated that use of a MP + NC, compared with nonobtrusive measurement with a calibrated respiratory inductive plethysmograph, alters the majority of the volume and time indexes of breathing pattern, with increases in minute ventilation (P less than 0.01), VT (P less than 0.001), inspiratory time (TI, P less than 0.05), expiratory time (TE, P less than 0.05), mean inspiratory flow (P less than 0.05), and mean expiratory flow (P less than 0.05) and a decrease in f(P less than 0.05). Separating the potential mechanisms we found that when the respiratory route was not altered, independent oral stimulation (using an occluded MP) or nasal stimulation (by applying paper clips to the alae nasi) did not change the breathing pattern. In contrast, obligatory oral breathing without additional stimulation of the oral or nasal sensory receptors caused increases in VT (P less than 0.05), TI (P less than 0.05), and TE (P less than 0.01) and a fall in f(P less than 0.05). Heating and humidifying the inspired air did not prevent the alteration in breathing pattern with a MP. Thus change in the respiratory route is the major determinant of the alteration in breathing pattern with a MP + NC.


1994 ◽  
Vol 76 (3) ◽  
pp. 1330-1339 ◽  
Author(s):  
H. V. Forster ◽  
T. F. Lowry ◽  
L. G. Pan ◽  
B. K. Erickson ◽  
M. J. Korducki ◽  
...  

We determined the effect of pulmonary vagal (hilar nerve) denervation (HND) and diaphragm deafferentation (DD) on inspiratory load compensation. We studied awake intact (I; n = 10), DD (n = 5), HND (n = 4), and DD+HND (n = 7) ponies at rest and during mild (1.8 mph, 5% grade) and moderate (1.8 mph, 15% grade) treadmill exercise before, during, and after resistance of the inspiratory circuit was increased from approximately 1.5 to approximately 20 cmH2O.l–1.s. During the first loaded breath in I ponies at rest, inspiratory time (TI) increased, expiratory time decreased, and inspiratory drive increased. There were minimal changes after the first breath, and inspiratory minute ventilation (VI) and arterial PCO2 did not change (P > 0.10) from control values. On the first loaded breath during exercise, TI increased but inspiratory drive either did not change or decreased from control values. TI and drive increased after the first breath, but the increases were insufficient to maintain VI and arterial PCO2 at control levels. First-breath load compensation remained after DD, HND, and DD+HND, but after DD+HND tidal volume and VI were compensated 5–10% less (P < 0.05) than in I ponies. In all groups inspiratory drive, tidal volume, and VI were markedly augmented on the first breath after loading was terminated with a gradual return toward control. We conclude that diaphragm and pulmonary afferents contribute to but are not essential for inspiratory load compensation in awake ponies.


1987 ◽  
Vol 63 (1) ◽  
pp. 221-228 ◽  
Author(s):  
E. van Lunteren ◽  
M. A. Haxhiu ◽  
E. C. Deal ◽  
J. S. Arnold ◽  
N. S. Cherniack

The purpose of the present study was to assess the effects of bronchoconstriction on respiratory changes in length of the costal diaphragm and the parasternal intercostal muscles. Ten dogs were anesthetized with pentobarbital sodium and tracheostomized. Respiratory changes in muscle length were measured using sonomicrometry, and electromyograms were recorded with bipolar fine-wire electrodes. Administration of histamine aerosols increased pulmonary resistance from 6.4 to 14.5 cmH2O X l–1 X s, caused reductions in inspiratory and expiratory times, and decreased tidal volume. The peak and rate of rise of respiratory muscle electromyogram (EMG) activity increased significantly after histamine administration. Despite these increases, bronchoconstriction reduced diaphragm inspiratory shortening in 9 of 10 dogs and reduced intercostal muscle inspiratory shortening in 7 of 10 animals. The decreases in respiratory muscle tidal shortening were less than the reductions in tidal volume. The mean velocity of diaphragm and intercostal muscle inspiratory shortening increased after histamine administration but to a smaller extent than the rate of rise of EMG activity. This resulted in significant reductions in the ratio of respiratory muscle velocity of shortening to the rate of rise of EMG activity after bronchoconstriction for both the costal diaphragm and the parasternal intercostal muscles. Bronchoconstriction changed muscle end-expiratory length in most animals, but for the group of animals this was statistically significant only for the diaphragm. These results suggest that impairments of diaphragm and parasternal intercostal inspiratory shortening occur after bronchoconstriction; the mechanisms involved include an increased load, a shortening of inspiratory time, and for the diaphragm possibly a reduction in resting length.


1991 ◽  
Vol 70 (5) ◽  
pp. 2045-2051 ◽  
Author(s):  
S. S. Naqvi ◽  
A. S. Menon ◽  
B. E. Shykoff ◽  
A. S. Rebuck ◽  
A. S. Slutsky

We studied the effects of removing cyclic pulmonary afferent neural information on respiratory pattern generation in anesthetized dogs. Phrenic neural output during spontaneous breathing (SB) was compared with that occurring during constant-flow ventilation (CFV) at several levels of eucapnic hypoxemia. Hypoxia caused an increase in both the frequency and the amplitude of the moving time average (MTA) phrenic neurogram during both SB and CFV. The change in frequency as arterial saturation was reduced from 90 to 60% during SB was significantly higher than that during CFV [SB, 32.3 +/- 10.9 (SD) breaths/min; CFV, 10.3 +/- 5.8 breaths/min; P = 0.001]. By contrast, the increase in the amplitude of the MTA phrenic neurogram was smaller (SB, 0.62 +/- 0.68 units; CFV, 1.35 +/- 0.81 units; P = 0.01). The changes in frequency with hypoxia during both modes of ventilation resulted primarily from a shortening of expiratory time. Both inspiratory time and expiratory time were greater during CFV than during SB, but their change in response to hypoxia was not significantly different. We conclude that the amplitude response of the MTA phrenic neurogram to hypoxia is similar to that seen during hypercapnia; in the presence of phasic afferent feedback the MTA amplitude response is decreased and the frequency response is increased relative to the response observed in the absence of phasic afferents.


1995 ◽  
Vol 78 (5) ◽  
pp. 1910-1920 ◽  
Author(s):  
G. F. Rafferty ◽  
J. Evans ◽  
W. N. Gardner

Combinations of 17 normal awake humans breathed mildly hyperoxic and hypercapnic gas mixtures via a pneumotachograph into an open circuit. Respiratory pattern was measured for each breath in real time by computer. Use of computer-controlled auditory feedback at a constant end-tidal PCO2 (PETCO2) allowed prolonged changes of 1) inspiratory time (TI) at constant inspired tidal volume (VTI), 2) VTI up and down in repeated steps at constant TI, and 3) expiratory time (TE) at constant VTI. The remaining variables were free to be determined by the subjects' automatic respiratory control mechanisms. We showed that TE changed in parallel with the change in TI despite constant VTI, TE did not change in response to step changes in VTI at constant TI, and large changes in TE had no influence on the subsequent TI, but VTI increased slightly as TE lengthened despite clamping. Time for expiratory flow (TE--end-expiratory pause) changed in parallel with TE in all protocols. Thus, in conscious humans, inspiratory timing has a direct influence on expiratory timing, independent of volume change and chemical drive, but expiratory timing has no influence on the inspiratory timing of the subsequent breath but has a small influence on volume.


1992 ◽  
Vol 72 (2) ◽  
pp. 779-786 ◽  
Author(s):  
G. A. Fontana ◽  
T. Pantaleo ◽  
F. Bongianni ◽  
F. Cresci ◽  
L. Viroli ◽  
...  

We studied the influence of mastication on respiratory activity in nine healthy volunteers who were requested to masticate a 5-g chewing gum bolus at a spontaneous rate (SR) for 5 min and “at the maximum possible rate” (MPR) for 1 min. Significant increases in respiratory frequency were induced by SR mastication due to a decrease in both the inspiratory and expiratory time. Tidal volume displayed slight nonsignificant decreases, but minute ventilation and mean inspiratory flow significantly increased. The duty cycle (TI/TT) did not change significantly. Total airway resistance significantly increased. Both peak and rate of rise of the integrated electromyographic activity of inspiratory muscles presented marked increases, accompanied by the appearance of a low level of tonic muscular activity. Similar but more intense effects on respiratory activity were induced by MPR mastication; in addition, a significant decrease in tidal volume and a significant increase in TI/TT were observed. Rhythmic handgrip exercise performed at metabolic rates comparable to those attained during SR or MPR mastication induced similar changes in the drive and time components of the breathing pattern, although accompanied respectively by nonsignificant or significant increases in tidal volume. Furthermore, the frequency of SR mastication significantly entrained the respiratory rhythm. The results suggest that mastication-induced hyperpnea does not merely represent a ventilatory response to exercise but also reflects complex interactions between respiratory and nonrespiratory functions of the upper airway and chest wall muscles.


1983 ◽  
Vol 54 (6) ◽  
pp. 1736-1744 ◽  
Author(s):  
T. Trippenbach ◽  
G. Kelly ◽  
D. Marlot

Effects of intercostal muscle stimulation were studied in 2- to 7-day-old kittens under ketamine-acepromazine anesthesia. Animals were vagotomized, paralyzed, and artificially ventilated. Stimuli applied during inspiration (TI) inhibited this phase. Stimulus strength necessary for TI inhibition decreased with time. However, an all-or-nothing effect was not always observed. Stimulation during expiration (TE) prolonged this phase. The responsiveness increased with increasing stimulus delay. The effects of intercostal muscle stimulation were compared with those recorded during saphenous nerve stimulation. Stimulation during TI prolonged this phase. Phrenic activity increased after a short-lasting decrease in the on-going activity. Stimulation during the first 50% of TE had variable effects, whereas stimulation with longer delay shortened this phase. Our results indicated that the pattern of breathing in newborns can be affected by both intercostal muscle and other somatic efferents. However, the mechanisms controlling respiratory timing may differ in newborns and in adults. Different effects of respiratory muscle and saphenous nerve stimulation suggest different transmitters involved or different sites of interaction of these inputs with the medullary respiratory rhythm generator.


1988 ◽  
Vol 64 (6) ◽  
pp. 2458-2462 ◽  
Author(s):  
D. C. Bolser ◽  
B. G. Lindsey ◽  
R. Shannon

Large-amplitude vibration of the intercostal muscles/ribs has an inhibitory effect on inspiratory motor output. This effect has been attributed, in part, to the stimulation of intercostal muscle tendon organs. Intercostal muscle/rib vibration can also produce a decrease or increase in respiratory frequency. Studies were conducted 1) to determine whether, in addition to intercostal tendon organs, costovertebral joint mechanoreceptors (CVJR's) contribute to the inspiratory inhibitory effect of intercostal muscle/rib vibration (IMV) and 2) to explain the different respiratory frequency responses to IMV previously reported. Phrenic (C5) activity was monitored in paralyzed thoracotomized, artificially ventilated cats. Vibration (125 Hz) at amplitudes greater than 1,200 micron of one T6 intercostal space in decerebrated vagotomized rats reduced phrenic activity. This response was still present but weaker in some animals after denervation of the T6 intercostal muscles. Subsequent denervation of the T6 CVJR's by dorsal root sections eliminated this effect. Respiratory frequency decreased during simultaneous vibration (greater than 1,200 micron) of the T5 and T7 intercostal spaces in vagotomized cats. Respiratory frequency increased during IMV of two intercostal spaces (greater than 1,300 micron) in vagal intact cats. The use of different anesthetics (pentobarbital, allobarbital) did not alter these results. We conclude that CVJR's may contribute to the inhibitory effect of IMV on medullary inspiratory activity. The presence or absence of pulmonary vagal afferents can account for the different respiratory frequency responses to IMV, and different anesthetics did not influence these results.


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