Nov 25, 2019 · The automatic regulation of breathing is controlled by lung receptors and chemoreceptors. Lung receptors protect respiratory structures and the three types are J receptors (sense lung congestion), stretch receptors (monitor lung inflation), and irritant receptors (protect against toxic inhalants). Chemoreceptors monitor the gas exchange by sensing changes in the …
There are three types of lung receptors: stretch receptors, which monitor lung inflation; irritant receptors, which protect against the damaging effects of toxic inhalants; and J receptors, which are thought to sense lung congestion.
Base of the lung is the concave inferior portion that fits over the convex. Base of the lung is the concave inferior portion that. School Portland State University; Course Title ACTG 493; Uploaded By danielbrian269. Pages 23 This preview shows page 6 ...
The stretch receptors which monitor the lungs’ inflation, the irritant receptors protect against the effect of toxins entering the lungs, and J receptors which are believed to sense lung congestion. (Grossman & Porth, 2013) When the parasympathetic nervous system is stimulated airways constrict and glandular secretion is increased.
Receptors, called spindles, in the respiratory muscles measure muscle length and increase motor discharge to the diaphragm and intercostal muscles when increased stiffness of the lung or resistance to the movement of air caused by disease impedes muscle shortening.
There are also receptors in the airways and in the alveoli that are excited by rapid lung inflations and by chemicals such as histamine, bradykinin, and prostaglandins. The most important function of these receptors, however, may be to defend the lung against noxious material in the atmosphere.
These receptors are particularly important when lung function is impaired, since they can help maintain tidal volume and ventilation at normal levels. Changes in the length of a muscle affect the force it can produce when stimulated. Generally there is a length at which the force generated is maximal. Receptors, called spindles, in the respiratory ...
Many of the upper airway muscles, like the tongue and laryngeal adductors, undergo phasic changes in their electrical activity synchronous with respiration, and the reduced activity of these muscles during sleep may lead to upper airway closure. Neil S. Cherniack. Load Next Page.
During sleep, body metabolism is reduced, but there is an even greater decline in ventilation so that the partial pressure of carbon dioxide in arterial blood rises slightly and arterial partial pressure of oxygen falls. The effects on ventilatory pattern vary with sleep stage. In slow-wave sleep, breathing is diminished but remains regular, while in rapid eye movement sleep, breathing can become quite erratic. Ventilatory responses to inhaled carbon dioxide and to hypoxia are less in all sleep stages than during wakefulness. Sufficiently large decreases in the partial pressure of oxygen or increases in the partial pressure of carbon dioxide will cause arousal and terminate sleep.
The main effect of stimulating these receptors is a slowing of respiratory frequency by increasing expiratory time. This is known as the Hering-Breuer inflation reflex.2. Irritant receptors lie between airway epithelial cells and are stimulated by noxious gases, cold, and inhaled dusts.
Among the determinants of inspiratory time and tidal volume are the feedback signals from pulmonary stretch receptors tracking changes in lung volume and central control from the PC. The relative importance of the vagal afferents to eupneic breathing pattern seems to vary among species (as noted long ago by Widdicombe, 1964) and also between adult and neonatal animals ( Tables 4 and 5 ). There have been three methods used to assess the role of vagal afferent information in the regulation of breathing pattern. One has been to look at the nature of the change in patterns when that afferent traffic is interrupted (e.g., by vagotomy or vagal cooling), and the other two approaches attempt to assess the strength of the Hering-Breuer inflation-inhibiting reflex. This is sometimes expressed in terms of the inhibition ratio, which is the ratio of the duration of the apnea induced by inflation to the average duration of the previous breath cycles, as represented in Table 5 (except for the data on pigs and baboons ( Huszczuk et al., 1977 ), which are uniquely expressed as the ratio of the duration of the apnea following occlusion at peak inspiration to the duration of the control expiratory pause). Younes et al. (1974) pointed out that the duration of apnea following lung inflation is not a good quantifier of strength of the Hering-Breuer reflex, because it will be affected not only by the inspiration-inhibiting activity of pulmonary stretch receptors, but also by the interaction of that inhibition with rising inspiratory excitation influences, such as the rising Pa CO2 during the breath-hold period. The time course of these interactions may vary between individuals or species. Hence, a better approach may be to occlude the airway at end expiration so that the subsequent inspiration will lack afferent information from lung expansion. The extent to which the inspiratory effort following occlusion is prolonged compared to control inspirations that are terminated by inhibitory volume feedback becomes a measure of the strength of those inhibitory mechanisms (expressed as 1–T I control/T I occluded × 100, or simply as T I o/T I c). This approach was used, for example, in comparing the strength of the Hering-Breuer reflex between premature and full-term human infants by Olinsky et al. (1974), who found that this index was greater in premature (58%) than in full-term infants (25%).
Usually, inspiration increases and expiration decreases the heart rate (sinus arrhythmia). This phenomenon is mediated primarily by the vagus nerve. Pulmonary stretch receptors and cardiac mechanoreceptors, as well as baroreceptors, contribute to its generation. The variation of heart rate in inspiration and expiration is age-dependent and is reduced in elderly people (e.g., normal maximal-to-minimal variation in people 10 to 40 years old is >18 beats per minute, but in people 61 to 70 years old, it declines to >8 beats per minute). The test is easy to perform with a commercial ECG machine or appropriately set electromyography (EMG) equipment. While supine with the head elevated to 30 degrees, the patient breathes deeply at 6 respirations per minute (usually for 8 cycles), and minimal and maximal heart rate within each respiratory cycle (5 seconds inspiration followed by 5 seconds expiration) is measured. The simplest index is the heart rate variability (maximum heart rate minus minimum heart rate). Another index, the E/I ratio, is determined by the longest R-R interval on ECG (slow heart rate) divided by the shortest R-R interval (fast heart rate). An abnormal test indicates parasympathetic dysfunction.
The dorsal–medial medulla contains an elongated nucleus of cells called the nucleus tractus solitarius (NTS), which is the terminus of nearly all of the cardiovascular afferents including the baroreceptors, cardiopulmonary afferents, arterial chemoreceptors, and pulmonary stretch receptors.
Three kinds of receptors with vagal afferents are located in the lungs and play a role in ventilatory control. The pulmonary stretch receptors are nerves ending in the tracheal and bronchial smooth muscles.
Vagal efferents originating mainly in the nucleus ambiguus, but some in the dorsal motor nucleus of the vagus in the medulla, inhibit the heart rate by reducing the slope of the pacemaker potential in SA nodal cells. Baroreceptors tonically activate cells in the NTS, and this tonic excitation is relayed to the nucleus ambiguus where vagal efferents are tonically active. Thus in humans there is a constant vagal tone that continuously inhibits the heart rate. Reductions in blood pressure relieve this tonic inhibition, thereby accelerating the heart rate by removing parasympathetic tone. This completes a negative feedback loop: the accelerated heart rate increases the cardiac output and tends to restore the blood pressure. When blood pressure rises, the reverse occurs: NTS stimulates the NA more and there is greater vagal inhibition of heart rate (see Figure 5.13.5 ).
Irritant receptors have a minor role in the control of breathing. They are located between and below the epithelial cells of the airways (larynx, trachea, bronchi, and intrapulmonary airways).