Chemoreceptor Aortic

Chemoreceptors. The peripheral chemoreceptors include the carotid bodies, located at the bifurcation of the common carotid arteries, and the aortic bodies, located in the aortic arch. These receptors are stimulated by a decrease in arterial oxygen (hypoxia), an increase in arterial carbon dioxide (hypercapnia),... 

The peripheral chemoreceptors include the carotid and aortic bodies. The carotid bodies, which are more important in humans, are located near the bifurcation of the common carotid arteries. The aortic bodies are located in the arch of the aorta. The peripheral chemoreceptors respond to a decrease in P02/ an increase in PC02, and a decrease in pH (increase in H+ ion concentration) of the arterial blood. 

HCN is a systemic poison toxicity is due to inhibition of cytochrome oxidase, which prevents cellular utilization of oxygen. Inhibition of the terminal step of electron transport in cells of the brain results in loss of consciousness, respiratory arrest, and ultimately, death. Stimulation of the chemoreceptors of the carotid and aortic bodies produces a brief period of hyperpnea cardiac irregularities may also occur. The biochemical mechanisms of cyanide action are the same for all mammalian species. HCN is metabolized by the enzyme rhodanese which catalyzes the transfer of sulfur from thiosulfate to cyanide to yield the relatively nontoxic thiocyanate. 

Results of in vitro studies suggest an interaction between calcium ions and cyanide in cardiovascular effects (Allen and Smith 1985 Robinson et al. 1985a). It has been demonstrated that exposure to cyanide in metabolically depleted ferret papillary muscle eventually results in elevated intracellular calcium levels, but only after a substantial contracture develops (Allen and Smith 1985). The authors proposed that intracellular calcium may precipitate cell damage and arrhythmias. The mechanism by which calcium levels are raised was not determined. Franchini and Krieger (1993) produced selective denervation of the aortic and carotid bifurcation areas, and confirmed the carotid body chemoreceptor origin of cardiovascular, respiratory and certain behavioral responses to cyanide in rats. Bradycardia and hyperventilation induced by cyanide are typical responses evoked by carotid body chemoreceptor stimulation (Franchini and Krieger 1993). 

Chapter 28). Stimulation of nicotinic receptors in adrenergic nerve terminals leads to the release of norepinephrine and activation of nicotinic chemoreceptors in the aortic arch and carotid bodies causes nausea and vomiting. Nicotinic receptors in the central nervous system mediate a complex range of excitatory and inhibitory effects. 

Low doses of nicotine stimulate respiration through activation of chemoreceptors in the aortic arch and carotid bodies, while high doses directly stimulate the respiratory centers. In toxic doses, nicotine depresses respiration by inhibiting the respiratory centers in the brainstem and by a complex action at the receptors at the neuromuscular junction of the respiratory muscles. At these neuromuscular receptors, nicotine appears to occupy the receptors, and the end plate is depolarized. After this, the muscle accommodates and relaxes. These central and peripheral effects paralyze the respiratory muscles. 

Q5 Alkalosis can be caused by both metabolic and respiratory problems. Apart from hyperventilation, respiratory alkalosis can be produced by hypoxia, for example, when a person moves to high altitude with a reduced arterial P02, stimulation of respiration occurs via the peripheral chemoreceptors in the carotid and aortic bodies, which respond to the low arterial P02. Increased rate and depth of respiration causes an increased quantity of C02 to be lost from the body, and so pH rises. 

Doses from/with smoking. Nicotine causes release of catecholamines in the CNS, also serotonin, and antidiuretic hormone, corticotrophin and growth hormone. The effects of nicotine on viscera are probably largely reflex, from stimulation of sensory receptors (chemoreceptors) in the carotid and aortic bodies, pulmonary circulation and left ventricle. Some of the results are mutually antagonistic. 

For example, chemoreceptors, called peripheral chemoreceptors, located in carotid arteries and aortic arteries, monitor changes in oxygen pressure in the arteries. If oxygen pressure falls below 60 mm Hg, the peripheral chemoreceptors send a message to the respiratory center in the medulla to increase ventilation. 

Doxapram (respiratory stimulant that activates peripheral aortic and carotid body chemoreceptors) behaves as a physiological antagonist when used to reverse central respiratory depression caused by barbiturates or inhalational anaesthetic agents. 

Although CN can disperse rapidly at high temperatures, at lower temperatures CN provides stimulation of the chemoreceptors in the aortic arch activating a reflex respiratory gasp. It has been shown that it is not possible in the conscious human to prevent subsequent gasps following stimulation of the chemoreceptors. If the concentration of CN is sufficient, the subsequent inhalation of additional CN leads to unconsciousness, convulsion, and possibly death. 

Aortic chemoreceptors which show feehle response to CO2 were enhanced after treating the aortic hody with oUgomycin (Erhan et al., 1981). The overshoot of chemosensory response was abolished hy the carbonic anhydrase inhibitor, indicating that the hypercapnic response was due to H being responsible. This shows (O Figure S-6) dominance of COi/H response. 

Erhan B, Mulligan S, Lahiri S. 1981. Metabolic regulation of aortic chemoreceptor response to CO2. Neurosci Lett 24 143-147. 

A decrease in PaC02 may occur in patients with cardiogenic, hypovolemic, or septic shock because oxygen delivery to the carotid and aortic chemoreceptors is reduced. This relative deficit in Pa02 stimulates an increase in ventilation. The hyperventilation in sepsis is also mediated via a central mechanism. Hyperventilation-induced respiratory alkalosis with an elevation in cardiac index and hypotension without peripheral vasoconstriction may therefore be an early sign of sepsis. 

In conclusion, low-level acute exposure to CN has been characterized by a respiratory gasp, which is believed to be cansed by stimnlation of chemoreceptors in the aortic arch. The chronic conseqnences of this type of acnte exposure to CN are largely unknown. Since there are normal cellnlar mechanisms that maintain the balance between CN and sulfur, the equilibrium of the systems is thought to be well controlled. 

Chemoreceptors. Early investigators assumed that the chemically sensitive areas controlling respiration were located in the brain. In 1926 De Castro (15) suggested that the carotid bodies, located near the carotid bifurcation of each common carotid artery, also could be important chemoreceptors. Shortly thereafter, Heymans and Heymans (16) found that ventilation was stimulated when the aortic arch of an animal was perfused with blood from an animal breathing a low oxygen air mixture. This study established the existence and general location of chemosensi-tive bodies in the aortic arch (the aortic bodies). Additional studies by Heymans and co-workers (17) delineated the location and function of the carotid bodies and demonstrated that they were stimulated by hypoxia and hypercapnia. The exact location and function of the aortic bodies was described by Comroe (18). 

The chemosensitive cells of carotid and aortic bodies (the peripheral chemoreceptors) are stimulated by decreases in the 02 tension of arterial blood perfusing the peripheral chemoreceptors and by increases in arterial pCo2 or arterial [H+]. The stimulation resulting from increased arterial pco2 Is probably an indirect result of increased [H+] from the acidifying action of C02 in the vicinity of the chemosensitive cells. It now seems that these bodies respond to changes in their extracellular [H+] and can respond to even the most acute metabolic acid-base disturbance without significant delay (19). 

The influence of ACh and parasympathetic innervation on various organs and tissues is discussed in detail in Chapter 6. ACh and its analogs stimulate secretion by all glands that receive parasympathetic innervation, including the lacrimal, tracheobronchial, salivary, and digestive glands. The effects on the respiratory system, in addition to increased tracheobronchial secretion, include hronchoconstriction and stimulation of the chemoreceptors of the carotid and aortic bodies. When instilled into the eye, muscarinic agonists produce miosis (see Chapter 63). 

In general, the cardiovascular responses to nicotine are due to stimulation of sympathetic ganglia and the adrenal medulla, together with the discharge of catecholamines from sympathetic nerve endings. Also contributing to the sympathomimetic response to nicotine is the activation of chemoreceptors of the aortic and carotid bodies, which reflexly results in vasoconstriction, tachycardia, and elevated blood pressure. 

In a small number of patients whose respiratory center is depressed by long-term retention of carbon dioxide, injury, or drugs, ventilation is maintained largely by stimulation of carotid and aortic chemoreceptors, commonly referred to as the hypoxic drive. The provision of too much oxygen can depress this drive, resulting in respiratory acidosis. In these cases, supplemental oxygen should be titrated carefully to ensure adequate arterial saturation. If hypoventilation results, then mechanical ventilatory support with or without tracheal intubation should be provided. 

Respiratory chemoreceptors exist peripherally in the aortic arch and carotic bodies and centrally in the ventral medulla oblongata of the brain. These receptors are sensitive to partial pressures of CO2 and O2 and to blood pH. 

The two major peripheral chemoreceptors are the carotid and the aortic bodies. The central chemoreceptors are probably localized close to the respiratory center in the medulla. 

Between 1927 and 1930, Heymans discovered the chemoreceptor reflexes in the carotid and aortic bodies. He showed that when stimulated, these receptors excite the respiratory center. 

The histological structure of the carotid bodies is very typical. The chemoreceptor cell contains unstable granules that disappear when the nerve endings of the carotid bodies are stimulated. The mechanism by which the chemical stimulus is converted to an electrical impulse is not known. Aortic chemoreceptors are found between the aortic arch and the pulmonary artery on the dorsal aspect of the pulmonary artery. 

For a long time, lobeiine was known as a powerful respiratory stimulant. This important property has been explained by the activation of the carotid and aortic body chemoreceptors at therapeutic doses. 

Bartelds B, Van Bel F, Teitel D, Rudolph A. Carotid, not aortic, chemoreceptors mediate the fetal cardiovascular response to acute h poxaemia in lambs. Pediatr Res... 

The fetus is living at low PO2 Mount Everest in utero and is at birth suddenly exposed to high PO2. This transition requires a change of setting of oxygen sensitivity. The carotid and aortic bodies are the main peripheral O2 sensors. While the carotid bodies seem to be the main peripheral chemoreceptors involved in respiratory control, the aortic bodies are more involved in cardiovascular homeostasis in the fetus (1). They have a low hypoxic sensitivity and their involvement in the hypoxic ventilatory response is controversial (2). 

Perhaps surprisingly, given their importance in the developing infant, the carotid chemoreceptors have minimal sensitivity to hypoxia at birth and become more sensitive over the first few days or weeks of life (10-16). Increasing hypoxia sensitivity of the arterial chemoreceptors after birth is termed resetting, and it occurs in both carotid and aortic chemoreceptors (17). Carotid chemoreceptor resetting appears to be modulated by the 4-fold rise in arterial O2 tension that occurs at birth (18-22), raising the possibility that peri- and postnatal hypoxia may impair carotid chemoreceptor development. In addition, perinatal hyperoxia causes... 

Kumar P, Hanson MA. Re-setting of the hypoxic sensitivity of aortic chemoreceptors in the new-born lamb. J Dev Physiol 1989 11 (4) 199-206. 

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