INFLUENCE FROM THE HIGHER CENTERS

cells. In short, in spite of the tremendous vascularity these glomus cells are prone to hypoxia so that slight fall of Pa 02 causes hypoxia in them stimulus. 2. These glomus cells are stimulated when there is a fall of ATP production in them. The efficiency of ATP production of these cell being not high, even slight hypoxia causes their stimulation. 3. The CB is very vascular, so vascular that the dissolved 02 in the arterial blood alone is sufficient (02 bound as Hb02 is not required). This results in a delicate situation. While this means that CB is not stimulated by fall of Hb % (thus, of Hb02), it also means slight fall of blood supply or slightest arterial hypoxia (= a condition where Pa 02 is low, typical example, high altitude sickness where PI02 is low) can cause stimulation. 4. Sympathetic stimulation can cause reduction of blood supply to the CB by vasoconstriction of vasa vasorum of CB stimulation. The student, at this stage may recall some fascinating examples: (1) Excitement usually causes hyperpnea. A fat middle aged aristocratic lady, when slighted, becomes strongly excited and begins to pant. This is due to sympathetic stimulation (n) Muscular exercise causes violent rise of This may be due to (a) sympathetic stimulation or (b) very slight (so slight that we cannot detect by our laboratory instruments; recall, muscular exercise does not cause a detectable fall of Pa02 and yet there is hyperventilation) fall of Pa 02 can be detected by the CB and that is enough for its stimulation. Such very slight. (and undetectable in the laboratory) fall of Pa 02 may be present during exercise (in) in anemia there is usually at rest no dyspnea (recall, CB is fed only by dissolved 02 n the plasma and this dissolved 02is normal in anemia). The CB also sensors high Pa C02 and CH. But high Pa C02 acts mostly via central chemoreceptor (CC) cells. High CH (=1 ow pH) acts via both the CB as well as the CC. H+ ion concentration Rise of H+ion concentration in the blood (= fall of blood pH) causes hyperventilation. Teleology is obvious. Hyperventilation removal of body C02 reduction of H2C03 and thus of H+. Thus, hyperventilation is a compensatory mechanism against acidosis. Our body, normally, produces large quantities of acids (H+ions) from protein metabolism. H+ ions of these acids, called 'fixed acids' are normally removed by the kidney. Renal failure, thus is an important cause of acidosis (and is called renal acidosis). Alternatively, in diabetic acidosis, large quantities of p hydroxy butyric acid and related products are produced causing acidosis. The renal acidosis and diabetic acidosis come under the category of 'metabolic acidosis'. On the other hand, in advanced emphysema (leading to 'cor pulmonale' ) there is retention of C02 (hypercapnia) leading to overproduction of H2C03 and thus H+ions. This type of acidosis is called respiratory acidosis. In both the forms (metabolic and respiratory) of acidosis, clinically there is hyperventilation (E)- However, cause of this E in metabolic acidosis is rise of H* ion concentration, [ H+ , in the blood. H+ions act on boththe peripheral chemoreceptors, PC, as well as on central chemore eptors, CC, and thus produce On the other hand in advanced emphysema/cor pulmonale, the respiratory drive is, as already stated, mainly due to Pa 02. Coronary chemoreceptors Special types of chemoreceptors, called 'coronary chemoreceptors' are present in the distribution of coronary artery as well as pulmonary artery. When stimulated, they produce a triad of effects, (i) hypopnea (or apnea), (n) brady cardia and (in) hypotension. These chemoreceptors can be stimulated, by veratrum alkaloids. What is their exact physiological role is uncertain, (see, for further details, 'Bezold-Jarisch reflex' chap 4, sec V). Drugs Many drugs are known which depress or stimulate the respiratory center. Thus, doxapram (dopram) and mkethamide (coramme) stimulate the respiratory center. However they also stimulate other areas of brain and a sufficiently effective dose may produce convulsion. M oreover their beneficial ef fects pass off quickly. For these reasons, these drugs are of limited therapeutic values in cases of respiratory failure. In addition to a direct stimulating effect on the respiratory center, they probably act also via the peripheral chemoreceptors. Barbiturates and morphine (opium) on the other hand, depress the respiratory centers. With both the drugs, the sensitivity of the C02 sensitive chemoreceptors in the brain are depressed but the carotid bodies retain their sensitivity for a long time and respiration continues because of the hypoxic drive. In India, suicides by morphine or barbiturate poisoning are common. Once upon a time, the use of mkethamide was very popular in cases of severe respiratory depression by. barbiturate poisoning. For reasons mentioned above, this is no longer so. INFLUENCE FROM THE HIGHER CENTERS The cerebral cortex is able to influence the respiration. Thus, stimulation of premotor cortex leads to tachypnea. Stimulation of gyrus cmguh, which is situated on the medial aspect of the cerebral hemisphere (fig. IDA. 1. 1) and is a part of cerebral cortex, leads to cessation of respiration. When the animal opossum (habitat, South America) is confronted by grave enemy, it often collapses, stops respiration and apparently looks dead; stimulation of the gyrus cmguh can also lead to this state, so that this can be called 'reaction opossum' (also called, 'playing dead, or playing 'opossum'). Teleologically, this can be viewed as a last ditch attempt by the animal's system to save himself, (for the appearance of it being.