Role of cardiac vagal c-fibers in cardiovascular control

Thorén, Peter

doi:10.1007/bfb0031531

Cited by 437 publications

(174 citation statements)

References 293 publications

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“…Later, bradycardia and hypotension from the stimulation of cardiac chemoreceptors and mechanoreceptors were established. 7,8,15 Cardiac vagal afferents are located mainly in the inferoposterior wall of the left ventricle 1 but are present in all cardiac chambers. 15 Stimulation of these receptors increases parasympathetic activity and inhibits sympathetic activity producing bradycardia, vasodilation, hypotension, and inhibition of renal sympathetic activity.…”

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confidence: 99%

“…7,8,15 Cardiac vagal afferents are located mainly in the inferoposterior wall of the left ventricle 1 but are present in all cardiac chambers. 15 Stimulation of these receptors increases parasympathetic activity and inhibits sympathetic activity producing bradycardia, vasodilation, hypotension, and inhibition of renal sympathetic activity. 11,16 The reflex can be abolished by cervical vagotomy and the bradycardia can be blocked with anticholinergic drugs, but the efferent pathway of the sympathoinhibition remains unknown.…”

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confidence: 99%

“…19 In animals, exogenous epinephrine has been noted to augment the BJR induced by veratridine. 15 In addition, significantly elevated epinephrine levels preceding syncope have been demonstrated in susceptible individuals during tilttable testing. 20 Hence, the combination of hypovolemia and increased plasma epinephrine levels appear to be associated with imminent neurocardiogenic syncope in susceptible individuals.…”

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confidence: 99%

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Witnessed asystole during spinal anesthesia treated with atropine and ondansetron: a case report

Martinek

2004

Can J Anesth/J Can Anesth

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P Pu ur rp po os se e: : To present a case of asystole during spinal anesthesia that responded to atropine and ondansetron and to discuss the possible pathophysiology with special emphasis on the Bezold-Jarisch reflex and the role of 5-HT 3 receptors in mediating bradycardia and sympathoinhibition.C Cl li in ni ic ca al l f fe ea at tu ur re es s: : A 50-yr-old, 97-kg, healthy male presented for elective left high tibial osteotomy. Spinal anesthesia was induced uneventfully at L3-4 with 11.25 mg of hyperbaric 0.75% bupivacaine and morphine 0.25 mg. Thirteen minutes after induction, the incision site was infiltrated with 20 mL of 0.5% bupivacaine with epinephrine 5 µg·mL -1 for intraoperative hemostasis, resulting in an increase in heart rate from 74 to 90 beats·min -1 . Three minutes after infiltration of the incision site, the patient's heart rate dropped to 48 beats·min -1 , accompanied by a blood pressure of 107/51 mmHg, SpO 2 97%, and a sinus bradycardia on the electrocardiogram. The electrocardiographic complexes suddenly disappeared with loss of the pulse oximeter waveform. Pre-drawn atropine 0.6 mg iv and ondansetron 4 mg iv were administered within seven seconds of the event. After an asystolic period of 30 to 40 sec, but before chest compressions were initiated, vital signs returned to normal with no other sequelae. C Co on nc cl lu us si io on n: : Exogenous epinephrine may have triggered the Bezold-Jarisch reflex and subsequent asystole. It is postulated that the combination of atropine and ondansetron may have played a key role in resuscitation by blocking the serotonergic and cholinergic receptors in the afferent and efferent limbs of this vagally-mediated reflex. HE risk of sudden cardiac arrest in healthy patients during spinal anesthesia is well documented 1-4 with a quoted incidence of seven per 10,000 spinal anesthetics. Objectif

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confidence: 99%

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Witnessed asystole during spinal anesthesia treated with atropine and ondansetron: a case report

Martinek

2004

Can J Anesth/J Can Anesth

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“…The simultaneous decreases in HR and MAP elicited by these doses of chloroephedrine resemble those produced by activation of the Bezold-Jarisch reflex (Somers and Mark, 1996;Thoren, 1979). This vaso-vagal cardiac reflex is initiated by the chemical or mechanical stimulation of cardiac vagal afferents and subsequent activation of cardiac vagal efferents which slow HR, decrease cardiac output and lower AP (Thoren, 1979). The ability of atropine to significantly attenuate the initial decrease in HR and completely abolish the decrease in MAP elicited by 10 mg/kg of ( − )-chloroephedrine, indicates that high doses of chloroephedrine produce vagal activation.…”

Section: Discussionmentioning

confidence: 83%

Chloroephedrine: contaminant of methamphetamine synthesis with cardiovascular activity

Varner¹,

Hein²,

Ogden³

et al. 2001

Drug and Alcohol Dependence

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Chloroephedrine is an intermediate and possible contaminant formed when methamphetamine is manufactured using ephedrine or pseudoephedrine as precursors. The purpose of this study was to determine whether this contaminant has biological activity and might contribute to methamphetamine-induced cardiovascular toxicity. In conscious rats, the ( − ) and ( + ) isomers of chloroephedrine (0.1 and 1.0 mg/kg, i.v.) dose-dependently increased mean arterial pressure (MAP) and heart rate (HR). The potency of the pressor effects of ( −) and (+)-chloroephedrine was between that of ephedrine and pseudoephedrine. The increases in HR elicited by the four stimulants were similar except that the tachycardia elicited by all doses of ephedrine and pseudoephedrine were preceded by a brief decrease in HR. The i.v. administration of 10 mg/kg of (+ ) or (− )-chloroephedrine produced biphasic (decrease followed by increase) the MAP and HR responses. Ephedrine and pseudoephedrine did not decrease MAP at any dose tested. The initial decrease in HR elicited by ( − )-chloroephedrine was significantly reduced and the hypotensive response abolished by atropine, indicating that these components of the MAP and HR responses resulted from vagal activation. The secondary pressor response elicited by ( − )-chloroephedrine was significantly reduced and the tachycardia significantly increased by pretreatment with phentolamine (3 mg/kg, i.v.). The increase in HR was reversed by propranolol. These results indicate that ( − ) and (+)-chloroephedrine have sympathomimetic properties similar to other known sympathomimetic stimulants. In addition, larger doses of chloroephedrine can activate the vagus nerve. The combination of ( +)-methamphetamine and ( −)-chloroephedrine did not markedly alter the magnitude of the MAP and HR responses of ( + )-methamphetamine alone except at high doses of ( −)-chloroephedrine (10 mg/kg). Contamination of illicit methamphetamine with chloroephedrine may have toxic consequences.

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“…Alternatively, we may suggest that ABV injection may stimulate terminals of the cardiopulmonary afferents in the heart and activate the Bezold-Jarisch reflex, which presents bradycardia and hypotension as a typical response due to sympathetic inhibition and parasympathetic excitation 4,5,17 . ABV contains histamine and serotonin 10 , which are used experimentally to activate the BezoldJarisch reflex 26 .…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular profile after intravenous injection of Africanized bee venom in awake rats

Guimarães

Costa

Machado

et al. 2004

Rev. Inst. Med. trop. S. Paulo

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SUMMARYThe manifestations caused by Africanized bee stings depend on the sensitivity of the victim and the toxicity of the venom. Previous studies in our laboratory have demonstrated cardiac changes and acute tubular necrosis (ATN) in the kidney of rats inoculated with Africanized bee venom (ABV). The aim of the present study was to evaluate the changes in mean arterial pressure (MAP) and heart rate (HR) over a period of 24 h after intravenous injection of ABV in awake rats. A significant reduction in basal HR as well as in basal MAP occurred immediately after ABV injection in the experimental animals. HR was back to basal level 2 min after ABV injection and remained normal during the time course of the experiment, while MAP returned to basal level 10 min later and remained at this level for the next 5 h. However, MAP presented again a significant reduction by the 7 th and 8 th h and returned to the basal level by the 24 th h. The fall in MAP may contribute to the pathogenesis of ATN observed. The fall in MAP probably is due to several factors, in addition to the cardiac changes already demonstrated, it is possible that the components of the venom themselves or even substances released in the organism play some role in vascular beds.

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Role of cardiac vagal c-fibers in cardiovascular control

Cited by 437 publications

References 293 publications

Witnessed asystole during spinal anesthesia treated with atropine and ondansetron: a case report

Witnessed asystole during spinal anesthesia treated with atropine and ondansetron: a case report

Chloroephedrine: contaminant of methamphetamine synthesis with cardiovascular activity

Cardiovascular profile after intravenous injection of Africanized bee venom in awake rats

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