Action of cocaine and chronic sympathetic denervation on vagal escape

Campos, H. A.; Urquilla, Pedro R.

doi:10.1113/jphysiol.1969.sp008695

Cited by 2 publications

(2 citation statements)

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“…Thereafter, vagal stimulation was performed repeatedly for 10 min-periods with stimulation alternating with 10-min periods without stimulation, to avoid nerve damage by prolonged electrical stimulation. The effectiveness of the vagal stimulation was attested by the characteristic transient bradycardia and hypotension, named ‘vagal escape’ [19] (see Figure S2 ). The vagally-induced bronchospasm was observed when ventilation was not yet injurious (see Figure S3 ).…”

Section: Methodsmentioning

confidence: 99%

Activation of Nicotinic Cholinergic Receptors Prevents Ventilator-Induced Lung Injury in Rats

et al. 2011

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Respiratory distress syndrome is responsible for 40 to 60 percent mortality. An over mortality of about 10 percent could result from additional lung injury and inflammation due to the life-support mechanical ventilation, which stretches the lung. It has been recently demonstrated, in vitro, that pharmacological activation of the alpha 7 nicotinic receptors (α7-nAChR) could down regulate intracellular mediators involved in lung cell inflammatory response to stretch. Our aim was to test in vivo the protective effect of the pharmacological activation of the α7-nAChR against ventilator-induced lung injury (VILI). Anesthetized rats were ventilated for two hours with a high stretch ventilation mode delivering a stroke volume large enough to generate 25-cmH2O airway pressure, and randomly assigned to four groups: pretreated with parenteral injection of saline or specific agonist of the α7-nAChR (PNU-282987), or submitted to bilateral vagus nerve electrostimulation while pre-treated or not with the α7-nAChR antagonist methyllycaconitine (MLA). Controls ventilated with a conventional stroke volume of 10 mL/kg gave reference data. Physiological indices (compliance of the respiratory system, lung weight, blood oxygenation, arterial blood pressure) and lung contents of inflammatory mediators (IL-6 measured by ELISA, substance P assessed using HPLC) were severely impaired after two hours of high stretch ventilation (sham group). Vagal stimulation was able to maintain the respiratory parameters close to those obtained in Controls and reduced lung inflammation except when associated to nicotinic receptor blockade (MLA), suggesting the involvement of α7-nAChR in vagally-mediated protection against VILI. Pharmacological pre-treatment with PNU-282987 strongly decreased lung injury and lung IL-6 and substance P contents, and nearly abolished the increase in plasmatic IL-6 levels. Pathological examination of the lungs confirmed the physiological differences observed between the groups. In conclusion, these data suggest that the stimulation of α7-nAChR is able to attenuate VILI in rats.

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Section: Methodsmentioning

confidence: 99%

Activation of Nicotinic Cholinergic Receptors Prevents Ventilator-Induced Lung Injury in Rats

et al. 2011

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“…Cer tainly, such a concept is as plausible as the cholinergic link hypo thesis. Chronic sympathetic denervation of the heart markedly impaired the recovery from the inhibitory action of vagal stimula tion, suggesting that catecholamines liberated during vagal escape originate for the most part from sympathetic nerves supplying the heart [8], These observations are in agreement with the finding that the cardioslimulant action of acetylcholine in the cat heart requires the presence of intact postganglionic sympathetic fibers [6J. Although the present studies do not deny the presence or relevance of cholinergic-adrenergic interactions in different spe cies or in different organ-systems, they do insist that cognizance he taken of the anatomical and functional presence of both adrenergic and cholinergic fibers in the efferent cardiac nerves, including, of course, the vagosympathetic trunk.…”

Section: Discussionmentioning

confidence: 99%