Respiratory muscle control during vomiting

1990 ◽  
Vol 68 (2) ◽  
pp. 237-241 ◽  
Author(s):  
Alan D. Miller

The changes in thoracic and abdominal pressures that generate vomiting are produced by coordinated action of the major respiratory muscles. During vomiting, the diaphragm and external intercostal (inspiratory) muscles co-contract with abdominal (expiratory) muscles in a series of bursts of activity that culminates in expulsion. Internal intercostal (expiratory) muscles contract out of phase with these muscles during retching and are inactive during expulsion. The periesophageal portion of the diaphragm relaxes during expulsion, presumably facilitating rostral movement of gastric contents. Recent studies have begun to examine to what extent medullary respiratory neurons are involved in the control of these muscles during vomiting. Bulbospinal expiratory neurons in the ventral respiratory group caudal to the obex discharge at the appropriate time during (fictive) vomiting to activate either abdominal or internal intercostal motoneurons. The pathways that drive phrenic and external intercostal motoneurons during vomiting have yet to be identified. Most bulbospinal inspiratory neurons in the dorsal and ventral respiratory groups do not have the appropriate response pattern to initiate activation of these motoneurons during (fictive) vomiting. Relaxation of the periesophageal diaphragm during vomiting could be brought about, at least in part, by reduced firing of bulbospinal inspiratory neurons.Key words: brain stem, bulbospinal respiratory neurons, vomiting center critique, diaphragm, abdominal muscles.

1965 ◽  
Vol 20 (4) ◽  
pp. 647-652 ◽  
Author(s):  
Sabbo Woldring

In anesthetized cats with open thorax the activity of the respiratory muscles (diaphragm and abdominal muscles) is studied as a function of lung volume and arterial CO2 tension. It is shown that the sensitivity of the inspiratory muscles to a given change in lung volume (V) (Hering-Breuer reflex) varies with the arterial pCO2 level, and conversely, that the CO2 sensitivity of the inspiratory motor system is dependent upon the volume of the lungs. The relations are fairly linear and can be expressed by the equation: M — M0 = K (pa CO2 — p0) (V0 — V), in which M represents inspiratory motor activity and M0, p0, and V0 and K are constants. The activity of the expiratory muscles is not dependent on CO2. regulation of respiration; Hering-Breuer reflex; electromyography of respiratory muscles Submitted on September 24, 1964


1987 ◽  
Vol 57 (4) ◽  
pp. 1101-1117 ◽  
Author(s):  
B. G. Lindsey ◽  
L. S. Segers ◽  
R. Shannon

Arrays of extracellular electrodes were used to monitor simultaneously several (2-8) respiratory neurons in the lateral medulla of anesthetized, paralyzed, bilaterally vagotomized, artificially ventilated cats. Efferent phrenic nerve activity was also recorded. The average discharge rate as a function of time in the respiratory cycle was determined for each neuron. Most cells were tested for spinal or vagal axonal projections using antidromic stimulation methods. Cross-correlational methods were used to analyze spike trains of 480 cell pairs. Each pair included at least one neuron most active during the expiratory phase. All simultaneously recorded neurons were located in the same side of the brain stem. Twenty-six percent (33/129) of the expiratory (E) neuron pairs exhibited short time scale correlations indicative of paucisynaptic interactions or shared inputs, whereas 8% (27/351) of the pairs consisting of an E neuron and an inspiratory (I) cell were similarly correlated. Evidence for several inhibitory actions of E neurons was found: 1) inhibition of I neurons by E neurons with both decrementing (DEC) and augmenting (AUG) firing patterns; 2) inhibition of E-DEC and E-AUG neurons by E-DEC cells; 3) inhibition of E-DEC and E-AUG neurons by E-AUG neurons; and 4) inhibition of E-DEC neurons by tonic I-E phase-spanning cells. Because several cells were recorded simultaneously, direct evidence for concurrent parallel and serial inhibitory processes was also obtained. The results suggest and support several hypotheses for mechanisms that may help to generate and control the pattern and coordination of respiratory motoneuron activities.


1985 ◽  
Vol 59 (4) ◽  
pp. 1201-1207 ◽  
Author(s):  
W. M. St John ◽  
A. L. Bianchi

The purpose was to evaluate activities of medullary respiratory neurons during equivalent changes in phrenic discharge resulting from hypercapnia and hypoxia. Decerebrate, cerebellectomized, paralyzed, and ventilated cats were used. Vagi were sectioned at left midcervical and right intrathoracic levels caudal to the origin of right recurrent laryngeal nerve. Activities of phrenic nerve and single respiratory neurons were monitored. Neurons exhibiting antidromic action potentials following stimulations of the spinal cord and recurrent laryngeal nerve were designated, respectively, bulbospinal or laryngeal. The remaining neurons were not antidromically activated. Hypercapnia caused significant augmentations of discharge frequencies for all neuronal groups. Many of these neurons had no change or declines of activity in hypoxia. We conclude that central chemoreceptor afferent influences are ubiquitous, but excitatory influences from carotid chemoreceptors are more limited in distribution among medullary respiratory neurons. Hypoxia will increase activities of neurons that receive sufficient excitatory peripheral chemoreceptor afferents to overcome direct depression by brain stem hypoxia. The possibility that responses of respiratory muscles to hypoxia are programmed within the medulla is discussed.


1991 ◽  
Vol 70 (3) ◽  
pp. 1265-1270 ◽  
Author(s):  
D. Zhou ◽  
M. J. Wasicko ◽  
J. M. Hu ◽  
W. M. St John

Our purpose was to compare further eupneic ventilatory activity with that of gasping. Decerebrate, paralyzed, and ventilated cats were used; the vagi were sectioned within the thorax caudal to the laryngeal branches. Activities of the phrenic nerve and medullary respiratory neurons were recorded. Antidromic invasion was used to define bulbospinal, laryngeal, or not antidromically activated units. The ventilatory pattern was reversibly altered to gasping by exposure to 1% carbon monoxide in air. In eupnea, activities of inspiratory neurons commenced at various times during inspiration, and for most the discharge frequency gradually increased. In gasping, the peak discharge frequency of inspiratory neurons was unaltered. However, all commenced activities at the start of the phrenic burst and reached peak discharge almost immediately. The discharge frequencies of all groups of expiratory neurons fell in gasping, with many neurons ceasing activity entirely. These data are consistent with the hypothesis that brain stem mechanisms controlling eupnea and gasping differ fundamentally.


1993 ◽  
Vol 264 (2) ◽  
pp. R331-R336
Author(s):  
J. P. Farber

Changes in breathing pattern between immature and adult animals could be due in part to changing postsynaptic sensitivity to particular neurotransmitters by respiratory neurons and/or to the fate of these neurotransmitters after release. To probe for such effects, gamma-aminobutyric acid (GABA) and the GABAA antagonist, bicuculline, were pressure injected by micropipette in very small volumes (approximately 25 pl) near identified medullary respiratory neurons in Inactin-anesthetized adult and suckling opossums. At a concentration of 10 mM, GABA induced suppression of respiratory neurons firing in animals from about 3 wk of age (the youngest animals tested) onward, with the largest responses occurring in adults. For those age groups tested with 0.5 and 50 mM GABA, shorter and longer responses, respectively, were observed. Bicuculline increased the discharge of respiratory units at all ages tested, but responses normalized to initial firing rates did not systematically differ between sucklings down to 4 wk of age and adults. Bicuculline also influenced the onset and cessation of firing in both inspiratory and expiratory neurons. Discharge of respiratory neurons in immature suckling opossums is characterized by few spikes and low firing rates with each breath. However, recovery of neuronal firing from an exogenous load of GABA and release of neuronal firing after antagonism of GABAA receptors does not show a developmental pattern that would implicate GABA as the crucial mediator of these effects.


1963 ◽  
Vol 18 (3) ◽  
pp. 497-504 ◽  
Author(s):  
J. Milic-Emili ◽  
J. M. Tyler

End-tidal CO2 tension, pulmonary ventilation, and work output of respiratory muscles were determined in six normal subjects breathing various mixtures of carbon dioxide in air, with three graded resistances added to both inspiration and expiration. In two individuals, the resistances were also added separately to inspiration or expiration. A linear relationship was found between work output of inspiratory muscles and end-tidal CO2 tension; this relationship was uninfluenced by added resistance. No consistent relationship was observed between either ventilation or work output of expiratory muscles and end-tidal CO2 tension. These results suggest that carbon dioxide controls directly the activity of inspiratory muscles alone and that the activity of expiratory muscles is only coincidentally involved. The possible role of intrinsic properties of respiratory muscles and of nervous mediation in the control of breathing is discussed. Submitted on October 22, 1962


2009 ◽  
Vol 107 (3) ◽  
pp. 962-970 ◽  
Author(s):  
Martin J. Tobin ◽  
Franco Laghi ◽  
Laurent Brochard

It is problematic to withhold therapy in a patient with chronic obstructive pulmonary disease (COPD) who presents with acute respiratory failure so that detailed physiological measurements can be obtained. Accordingly, most information on respiratory muscle activity in patients experiencing acute respiratory failure has been acquired by studying patients who fail a trial of weaning after a period of mechanical ventilation. Such patients experience marked increases in inspiratory muscle load consequent to increases in resistance, elastance, and intrinsic positive end-expiratory pressure. Inspiratory muscle strength is reduced secondary to hyperinflation and possibly direct muscle damage and the release of inflammatory mediators. Most patients recruit both their sternomastoid and expiratory muscles, even though airflow limitation prevents the expiratory muscles from lowering lung volume. Even when acute hypercapnia is present, patients do not exhibit respiratory center depression; indeed, voluntary activation of the diaphragm, in absolute terms, is greater in hypercapnic patients than in normocapnic patients. Instead, the major mechanism of acute hypercapnia is the development of rapid shallow breathing. Despite the marked increase in mechanical load and decreased force-generating capacity of the inspiratory muscles, patients do not develop long-lasting muscle fatigue, at least over the period of a failed weaning trial. Although the disease originates within the lung parenchyma, much of the distress faced by patients with COPD, especially during acute respiratory failure, is caused by the burdens imposed on the respiratory muscles.


1998 ◽  
Vol 84 (4) ◽  
pp. 1198-1207 ◽  
Author(s):  
Michael S. Hedrick ◽  
Melinda R. Dwinell ◽  
Patrick L. Janssen ◽  
Josue Pizarro ◽  
Gerald E. Bisgard

The purpose of this study was to test the hypothesis that dysrhythmic breathing induced by the α2-agonist clonidine is accompanied by differential recruitment of respiratory muscles. In adult goats ( n = 14) electromyographic (EMG) measurements were made from inspiratory muscles (diaphragm and parasternal intercostal) and expiratory muscles [triangularis sterni (TS) and transversus abdominis (Abd)]. EMG of the thyroarytenoid (TA) muscle was used as an index of upper airway (glottal) patency. Peak EMG activities of all spinal inspiratory and expiratory muscles were augmented by central and peripheral chemoreceptor stimuli. Phasic TA was apparent in the postinspiratory phase of the breathing cycle under normoxic conditions. During dysrhythmic breathing episodes induced by clonidine, TS and Abd activities were attenuated or abolished, whereas diaphragm and parasternal intercostal activities were unchanged. There was no tonic activation of TS or Abd EMG during apneas; however, TA activity became tonic throughout the apnea. We conclude that 1) α2-adrenoceptor stimulation results in differential recruitment of respiratory muscles during respiratory dysrhythmias and 2) apneas are accompanied by active glottic closure in the awake goat.


1964 ◽  
Vol 19 (2) ◽  
pp. 217-223 ◽  
Author(s):  
Joseph Milic-Emili ◽  
Marcello M. Orzalesi ◽  
Charles D. Cook ◽  
James M. Turner

The behavior of the diaphragm and the thoracic and abdominal muscles during various static and dynamic respiratory maneuvers was studied in six trained men by measuring intrathoracic (esophageal) and intra-abdominal (gastric) pressures together with lung volumes. The static maneuvers included voluntary relaxation of respiratory muscles, maximal inspiratory and expiratory efforts, and maximal abdominal expulsive efforts. The dynamic maneuvers were forced inspiratory and expiratory vital capacities and maximal voluntary ventilation. The patterns during the various respiratory maneuvers were relatively uniform. Although the number of subjects studied was small, our results would appear to give a general description of thoraco-abdominal mechanics, at least in trained subjects. breathing patterns; static respiratory maneuvers; maximal voluntary ventilation; forced inspiration and expiration; dynamic respiratory maneuvers; abdominal pressures and thoracic pressures at varying lung volumes Submitted on May 13, 1963


1990 ◽  
Vol 68 (2) ◽  
pp. 544-548 ◽  
Author(s):  
M. Manohar

The present study was carried out on seven healthy ponies to examine the extent of blood flow in various inspiratory and expiratory muscles at rest and during maximal exertion as well as to determine the proportion of cardiac output needed to perfuse respiratory muscles during these conditions. Tissue blood flow was studied with 15 micron-diameter radionuclide-labeled microspheres injected into the left ventricle during steady conditions. The inspiratory and expiratory muscles comprised 2.41 and 3.05% of body weight, respectively, and received 6.17 and 3.75% of the cardiac output at rest. With maximal exercise, heart rate (from 55 +/- 3 to 218 +/- 4 beats/min), mean aortic pressure (from 125 +/- 5 to 170 +/- 6 mmHg), and cardiac output (from 96 +/- 11 to 730 +/- 78 ml.min-1.kg-1) increased markedly. During exercise blood flow increased significantly in all respiratory muscles (P less than 0.0001) as vascular resistance decreased precipitously. Marked heterogeneity of perfusion existed among various inspiratory as well as expiratory muscles during exercise. Among the inspiratory muscles, the highest perfusion occurred in the diaphragm followed by serratus ventralis, and among the expiratory muscles, the highest perfusion occurred in the internal oblique abdominis and the transverse thoracis (triangularis sterni). Collectively, the inspiratory (8.44%) and expiratory (6.35%) muscle blood flow comprised 14.8 +/- 1.2% of the cardiac output during maximal exercise, a significant increase above resting value, whereas renal fraction of cardiac output decreased from 21% (at rest) to 0.72%.


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