Carotid body denervation

Bureau MA, Lamarche J, Foulon P, Dalle D. Postnatal maturation of respiration in intact and carotid body-chemodenervated lambs. J Appl Physiol 1985 59 869-874. Bureau MA, Lamarche J, Foulon P, Dalle D. The ventilatory response to h poxia in the newborn lamb after carotid body denervation. Respir Physiol 1985 60 109-119. Hofer MA. Sleep-wake state organization in infant rats with episodic respiratory disturbance following sinoaortic denervation. Sleep 1985 8 40 8. 

Serra A, Brozoski D, Hedin N, Franciosi R, Forster HV Mortality after carotid body denervation in rats. J Appl Physiol 2001 91 1298-1306. 

Bureau MA, Lamarche J, Foulon P, Dalle D. The ventilatory response to hypoxia in the newborn lamb after carotid body denervation. Respir Physiol 1985 60(1) 109-119. 

Martin-Body RL, Robson GJ, Sinclair JD. Restoration of hypoxic respiratory responses in the awake rat after carotid body denervation by sinus nerve section. J Physiol 1986 380 61-73. 

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). 

The hypotension is not exclusively due to the bradycardia, because the latter is abolished by atropine, but the hypotension persists. The hypertension is due to the reflex stimulation of the vasomotor center by (1) the chemoceptors of the carotid body, (2) the direct excitation of the center, (3) by stimulation of the sympathetic ganglia (74), and (4) a discharge of adrenaline from the adrenal medulla (75). Hypertension is seen even if the adrenal gland is denervated (76). 

The mechanism of the respiratory stimulation involves the action of Conium alkaloid on the sensory elements of the carotid body. The stimulating doses are of the order of 2-5 mg./kg. in the normal dog. According to Dautrebande and Philippot (105), this stimulatory action is abolished by denervation of both carotid sinuses. 

Martin-Body RL. Brain transections demonstrate the central origin of hypoxic ventilatory depression in carotid hody-denervated rats. J Physiol Lond 1988 407 41-52. 

Holton P, Wood JB. The effects of bilateral removal of the carotid bodies and denervation of the carotid sinuses in two human subjects. J Physiol (Lond) 1965 181 365-378. 

Hess A. Chronically denervated rat carotid bodies. Acta Anat 1977 97 307-316. Hellstrom S. Putative neurotransmitters in the carotid body, mass fiagmentographic studies. Adv Biochem Psychopharmacol 1977 16 257-263. 

Buerk DG, Nair PK, Whalen WJ. Evidence for second metabolic pathway for O2 from Pti02 measurements in denervated cat carotid body. J Appl Physiol 1989 67 1578-1584. 

Wang ZZ, Dinger B, Fidone SJ, Stensaas LJ. Changes in tyrosine hydroxylase and substance P immunoreactivity in the cat carotid body following chronic hypoxia and denervation. Neuroscience 1998 83 1273-1281. 

Ryan ML, Hedrick MS, Pizarro J, Bisgard GE. Effects of carotid body sympathetic denervation on ventilatory accbmatization to hypoxia in the goat. Respir Physiol 1995 99 215-224. 

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