somewhere in the medulla ( it should be noted that usage of anesthesia causes some distortion. Therefore,there is no wonder (that the picture which emerges from anesthetized experimental animals, to some extent differs from what is in conscious man. L FACTORS INFLUENCING RESPIRATORY CENTER (RC) Three sets of factors. as indicated in the beginning of this chapter, influence the RC These are, (i) peripheral reflexes, (ii) chemical control and (iii) influences from the higher center. PERIPHERAL REFLEXES I. HeringBreuer reflex. According to the classical concept, the picture is as follows Receptors are present in the smooth muscles of the finer bronchioles. When the lung is inflated these (stretch) receptors are stimulated impulse generated these impulses are carried by the vegal (afferent) nerve fibers which emerge from these receptors impulses ultimately cause inhibition of the inspiratory center (I neurons) inspiration stops and expiration starts no stretching of these receptors now therefore, no inhibition on the neurons now inspiratory center again begins to send impulse the next cycle begins, his is called Hering-Breuer inflation reflex. According to the classical view, the Hering-Breuer
inflation reflex is an important cause of rhythmicity of the respiration, importance of the Hering-Breuer reflex. For a long time, it (the Hering-Breuer reflex) used to be thought to be of great importance for the maintenance of tha rhythmicity of the respiration. In absence of Hering-Breuer reflex, it was thought, respiratory frequency will diminish but the individual respirations would be deeper. The position has changed in recent times. It is now believed, that the Heing-Breuer reflex does not play a significant role, at least in man. m ordinary tidal volume breathing of the heathy resting individual (eupnea). It becomes important only when the respiratory excursions become violent as in hyperpnea ( = excessive breathing) of muscular exercise. In a case of hyperpnea. the Hering-Breuer reflex becomes active and the excessive prolongation of contractions of the inspiratory muscles are prevented; this causes rise in the rate of respiration but fall in the amplitude of individual excursions. Question arises, how the body is benefited by reducing the period of contraction of the inspiratory muscles in excercise hyperpnea, when the need of the air is great? The answer seems to be that towards the end of a deep inspiration, stretchability of the lung is reduced, as explained earlier while discussing the compliance of the lung (fig 4.2.3.), so that a stage comes, when the inspiratory muscles are working but there is no real entry of air into the lungs. In this stage the contraction of the muscles produces only expenditure of energy but no (or little) gain in respiration. Thus the body prevents excessive cost for the breathing during muscular exercise. Also, during enercise, it is necessary that excess CO2 produced should be removed, by expired air. Activation of Hering -Breuer reflex ensures increased frequency of expiration increased washing out of CO2. In short. Hering-Breuer reflex is weak in resting adult human beings. It becomes active when the tidal volumes exceed one liter (normal. 500 ml). Hering Breuer deflation reflex. If the lungs are greatly deflated, impulses are set up in another type of receptor which travel up via vagus to stimulate inspiration. This is Hering-Breuer deflation re-flex. In ordinary tidal air volume breathing (eupnea) this is not called into action but in such conditions like collapse of the lung (atelectesis) this reflex is activated and inspiratory drives are increased. The teleology is obvious. In a case of collapse of the lung, increase in inspiratory drive will cause more air entry into the healthy parts of the lung, and will thus compens ate for the functional loss of lung tissue. II. Propnoceptors in the chest wall ( "load detecting mechanism") if the compliance of the lung is decreased (eg. in lung fibrosis), the expansion of the chest wall becomes difficult Or. if the airway resistance increases (e.g. emphysema) air flow becomes difficult. In such conditions, there is an intrinsic mechanism [which involves the mechanoreceptors like muscle spindles, joint receptors and tendon receptors of Golgi (for details of them see chap 2, sec XC)] by which the thoracic cage detects that the thoracic cage expansion, ie , tidal air volume is not adequate (ie, the needs of the body are not fully satisfied) and the muscles of inspirations work harder (= contract more vigorosly) this state (= muscle contraction) continued until the filling of the lungs is adequate. It appears that afferent nerve fibers from the mechano receptors of these muscles of inspiration reach the cerebral cortex. (The organs Iike muscle spindles detect the fact that contraction of the muscles of inspiration is not adequate (i.e. the spindles detect the load), send the information to the anterior horn cell of the spinal cord (fig 10C. 2. 1). Collaterals arising from these nerve fibers go to the cerebral cortex). It is possible, one of the mechanisms by which we become conscious to the need of more sustained effort to inspire (dyspnea) is the firing of these collaterals to the cerebral cortex. In short, activation of these corticopetal (= cerebral cortex seeking) fibers is one of the mechanisms of dyspnea. III. J. receptors. J. reflex. In 1955 A.S. Paintal established the existence of another kind of receptors, the j receptors, which when stimulated produce widespread changes in the respiratory. cardiovascular and skeleto muscular system. These receptors are situated in close relation to the pulmonary capillaries.
inflation reflex is an important cause of rhythmicity of the respiration, importance of the Hering-Breuer reflex. For a long time, it (the Hering-Breuer reflex) used to be thought to be of great importance for the maintenance of tha rhythmicity of the respiration. In absence of Hering-Breuer reflex, it was thought, respiratory frequency will diminish but the individual respirations would be deeper. The position has changed in recent times. It is now believed, that the Heing-Breuer reflex does not play a significant role, at least in man. m ordinary tidal volume breathing of the heathy resting individual (eupnea). It becomes important only when the respiratory excursions become violent as in hyperpnea ( = excessive breathing) of muscular exercise. In a case of hyperpnea. the Hering-Breuer reflex becomes active and the excessive prolongation of contractions of the inspiratory muscles are prevented; this causes rise in the rate of respiration but fall in the amplitude of individual excursions. Question arises, how the body is benefited by reducing the period of contraction of the inspiratory muscles in excercise hyperpnea, when the need of the air is great? The answer seems to be that towards the end of a deep inspiration, stretchability of the lung is reduced, as explained earlier while discussing the compliance of the lung (fig 4.2.3.), so that a stage comes, when the inspiratory muscles are working but there is no real entry of air into the lungs. In this stage the contraction of the muscles produces only expenditure of energy but no (or little) gain in respiration. Thus the body prevents excessive cost for the breathing during muscular exercise. Also, during enercise, it is necessary that excess CO2 produced should be removed, by expired air. Activation of Hering -Breuer reflex ensures increased frequency of expiration increased washing out of CO2. In short. Hering-Breuer reflex is weak in resting adult human beings. It becomes active when the tidal volumes exceed one liter (normal. 500 ml). Hering Breuer deflation reflex. If the lungs are greatly deflated, impulses are set up in another type of receptor which travel up via vagus to stimulate inspiration. This is Hering-Breuer deflation re-flex. In ordinary tidal air volume breathing (eupnea) this is not called into action but in such conditions like collapse of the lung (atelectesis) this reflex is activated and inspiratory drives are increased. The teleology is obvious. In a case of collapse of the lung, increase in inspiratory drive will cause more air entry into the healthy parts of the lung, and will thus compens ate for the functional loss of lung tissue. II. Propnoceptors in the chest wall ( "load detecting mechanism") if the compliance of the lung is decreased (eg. in lung fibrosis), the expansion of the chest wall becomes difficult Or. if the airway resistance increases (e.g. emphysema) air flow becomes difficult. In such conditions, there is an intrinsic mechanism [which involves the mechanoreceptors like muscle spindles, joint receptors and tendon receptors of Golgi (for details of them see chap 2, sec XC)] by which the thoracic cage detects that the thoracic cage expansion, ie , tidal air volume is not adequate (ie, the needs of the body are not fully satisfied) and the muscles of inspirations work harder (= contract more vigorosly) this state (= muscle contraction) continued until the filling of the lungs is adequate. It appears that afferent nerve fibers from the mechano receptors of these muscles of inspiration reach the cerebral cortex. (The organs Iike muscle spindles detect the fact that contraction of the muscles of inspiration is not adequate (i.e. the spindles detect the load), send the information to the anterior horn cell of the spinal cord (fig 10C. 2. 1). Collaterals arising from these nerve fibers go to the cerebral cortex). It is possible, one of the mechanisms by which we become conscious to the need of more sustained effort to inspire (dyspnea) is the firing of these collaterals to the cerebral cortex. In short, activation of these corticopetal (= cerebral cortex seeking) fibers is one of the mechanisms of dyspnea. III. J. receptors. J. reflex. In 1955 A.S. Paintal established the existence of another kind of receptors, the j receptors, which when stimulated produce widespread changes in the respiratory. cardiovascular and skeleto muscular system. These receptors are situated in close relation to the pulmonary capillaries.
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