Articles: vagus-nerve-physiopathology.
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J. Auton. Nerv. Syst. · Mar 1994
Role of vagal afferents in the haemodynamic response to acute central hypovolaemia in unanaesthetized rabbits.
In unanaesthetized mammals, including rabbits, the response to acute central hypovolaemia is biphasic. An initial phase of baroreflex-mediated systemic vasoconstriction is succeeded by an abrupt failure of sympathetic vasoconstrictor drive and haemodynamic decompensation. We have tested whether a signal travelling in the cervical vagus nerves is responsible for the second phase. ⋯ Vagotomy had no effect on Phase I, but the onset of Phase II was delayed until CI had fallen by approximately 53% in 6 rabbits. In 1 rabbit, Phase II did not occur, even though CI had fallen by 67%. We conclude that an afferent vagal signal does not contribute to the compensatory Phase I, and is not essential for the occurrence of the decompensatory Phase II, of acute central hypovolaemia in unanaesthetized rabbits.
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The present investigation was undertaken to evaluate the vagal function of trained (T) and sedentary (S) rats by use of different approaches in the same animal. After 13 wk of exercise training (treadmill for 1 h 5 times/wk at 26.8 m/min and 15% grade), T rats had a resting heart rate (HR) slightly but significantly lower than S rats (299 +/- 3 vs. 308 +/- 3 beats/min). T rats had marked reduction of the intrinsic HR (329 +/- 4 vs. 369 +/- 5 beats/min) after blockade by methylatropine and propranolol. ⋯ Baroreflex bradycardia (phenylephrine injections) was reduced, bradycardic responses produced by electrical stimulation of the vagus were depressed, and responses to methacholine injection were decreased in T rats. Therefore several evidences of vagal function impairment were observed in T rats. The resting bradycardia after exercise training is more likely to be dependent on alterations of the pacemaker cells, inasmuch as the intrinsic HR was markedly reduced.
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Immunohistochemical visualization of Fos protein, the nuclear phosphoprotein product of the early-immediate gene c-fos, permits identification of populations of neurons that are activated in response to a variety of stimuli. This study examined the distribution of Fos-like immunoreactive (FLI) neurons in the spinal cord and the nucleus tractus solitarii (NTS) of the caudal medulla evoked by a noxious visceral stimulus in the unanesthetized rat. It also compared the inhibition of pain behavior and Fos expression by a mu-selective opioid agonist, morphine, and a kappa-selective opioid agonist, U-50,488. ⋯ Both morphine (1-10 mg/kg s.c.) and U-50,488 (3-30 mg/kg s.c.) produced a dose-dependent inhibition of the pain behavior in these animals and a dose-dependent suppression of the number of FLI neurons in both the spinal cord and in the NTS; complete suppression of FLI neurons was, however, not necessary for the production of antinociception. Furthermore, although equianalgesic doses of morphine and U-50,488 reduced the number of labelled neurons in the spinal cord to a comparable extent, morphine reduced the number of immunoreactive neurons in the NTS to a greater extent than did U-50,488. These results suggest that morphine and U-50,488 have comparable effects on the transmission of visceral nociceptive messages by spinal neurons, but differentially affect the autonomic response to noxious visceral stimuli.
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In unilaterally vagotomized rabbits, changes in single vagal nerve fibers from the lung stretch and irritant receptors were studied during the cough reflex following ammonia vapour administered into the lungs. The discharge rates of slowly adapting pulmonary stretch receptors (SARs) before the onset of cough and at the onset of cough did not change significantly. In contrast, the occurrence of cough after ammonia inhalation was usually preceded by vigorous stimulation of the rapidly adapting pulmonary stretch receptors (RARs). These results suggest that the genesis of cough provoked by ammonia is mainly mediated by afferent input from RARs.
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Clinical cardiology · Jun 1985
Case ReportsParoxysmal vagally mediated AV block with recurrent syncope.
Paroxysmal complete atrioventricular (AV) block without associated electrocardiographic (ECG) abnormality is not a well recognized entity. A mother and her daughter had recurrent syncopal episodes, but a normal ECG. The episodes were preceded by nausea and vomiting. ⋯ Paroxysmal AV block was vagally mediated in one of the patients, as indicated by prompt response to atropine. In the second case, the vagal dependence could not be proved but appears to be the most likely explanation. It thus appears that paroxysmal, vagally mediated complete AV block should be seriously considered in patients with unexplained syncope.