Vagal Mediation of the Effect of Alcohol on Heart Rate

Newlin, David B.; Byrne, Evan; Porges, Stephen W.

doi:10.1111/j.1530-0277.1990.tb00498.x

Cited by 39 publications

(25 citation statements)

References 10 publications

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“…Decreases in vagal tone index of similar magnitude 5 min after smoking marijuana cigarettes have been noted previously . Although the cardiovascular effects of morphine, alcohol, nicotine, methylphenidate, and pentobarbitol were not as pronounced, all of these substances have been reported (Newlin et al 1990;Pretorius et al 1991;Wong et al 1991) to decrease vagal tone index in humans. Therefore, it is possible that withdrawal of vagal tone is a common factor in the response to abused drugs.…”

Section: Discussionmentioning

confidence: 96%

Intravenous Cocaine Decreases Cardiac Vagal Tone, Vagal Index (Derived in Lorenz Space), and Heart Period Complexity (Approximate Entropy) in Cocaine Abusers

Newlin

Wong

Stapleton

et al. 2000

Neuropsychopharmacology

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We assessed the effects of i.v. cocaine on parasympathetic and sympathetic nervous system activity, and on the complexity vs. regularity of changes in heart rate over time. Fourteen otherwise healthy men with histories of i.v. cocaine abuse received bolus injections of cocaine (20 mg or 40 mg) and placebo (saline) on different days.Cardiovascular measures derived from the electrocardiogram, including heart rate, Porges' vagal tone (respiratory sinus arrhythmia), the 0.10 Hz rhythm, Toichi's vagal index, Toichi's sympathetic index, and approximate entropy (ApEn), were measured continuously. As predicted, cocaine produced tachycardia, accompanied by pronounced decreases in response to 40 mg cocaine in two different vagal tone indexes that precisely mirrored the increases in heart rate. The measure of sympathetic (and vagal) neural influences on the heart (0.10 Hz wave) also decreased in response to cocaine. Converging evidence from Toichi's vagal index supported the conclusion that the tachycardia from cocaine was due to withdrawal of cardiac vagal tone. These findings, and evidence that cocaine decreased cardiovascular complexity, contradict the prevailing assumption that the mechanism by which cocaine produces tachycardia is sympathetic (beta-adrenergic Cocaine is a widely abused drug with pronounced subjective and cardiovascular effects (Fischman et al. 1976;Johanson and Fischman 1989). Early human research on cocaine (Fischman et al. 1976;Resnick et al. 1977) revealed dose-dependent positive chronotropic effects on the heart, reaching a mean increase in heart rate of 38 bpm in response to 32 mg i.v. cocaine. Effects on the cardiovascular system can be remarkable in some subjects. Increases in heart rate have been reported to occur in response to doses as low as 13 mg i.v. cocaine; these increases ranged from 15 to 46 bpm (Ambre et al. 1988). The magnitude of these effects has led to the conclusion that cardiotoxicity from cocaine may be a major factor in death due to cocaine overdose (Billman 1990).The cardiotoxicity of cocaine has directed interest toward the autonomic mechanism by which the drug produces cardiovascular arousal. It has been assumed (Billman 1990;Ritchie and Greene 1990) that the cardiovascular response to cocaine is due primarily to activation of sympathetic autonomic mechanisms. This view stems in part from evidence that cocaine directly blocks reuptake of catecholamines in the periphery (Ritchie and Greene 1990 that propranolol (a beta-adrenergic blocker) and phentolamine (an alpha-adrenergic blocker) may partially reverse cardiovascular arousal in cocaine overdose (Rappolt et al. 1977). However, controlled studies at moderate dosages of cocaine in humans would be needed to confirm these observations. Furthermore, there is conflicting evidence in animal research concerning the role of the sympathetic nervous system in the response to cocaine in the intact organism. Recent findings indicate that central administration of cocaine actually decreases peripheral sympathetic neural activity in c...

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Section: Discussionmentioning

confidence: 96%

Intravenous Cocaine Decreases Cardiac Vagal Tone, Vagal Index (Derived in Lorenz Space), and Heart Period Complexity (Approximate Entropy) in Cocaine Abusers

Newlin

Wong

Stapleton

et al. 2000

Neuropsychopharmacology

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“…However, Kirschbaum et al (1993) demonstrated that HR was back to baseline levels 15 min after stress exposition, which is much shorter than what it took until our baseline started. However, the observed alcohol stimulated baseline HR increase may have been a mixture of several effects, including gustatory responses following the consumption of beverages like bitter lemon, which could have acted towards decreasing heart rate in some subjects (Newlin et al, 1990). To our surprise, DOAs showed the expected HR increases from sober to intoxicated baseline conditions, but lacked dampening effects under stress conditions.…”

Section: Discussionmentioning

confidence: 82%

Alcohol-induced heart rate response dampening during aversive and rewarding stress paradigms in subjects at risk for alcoholism

Croissant

Rist²,

Demmel³

et al. 2006

International Journal of Psychophysiology

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“…Numerous investigations support the contention that acute alcohol ingestion results in a decrease of heart rate variability, which is partially mediated by brainstem centers via the vagal nerve [24,35,45,56]. For example, Weise et al [56] reported that acute alcohol (0.7 g ethanol/ kg bodyweight) decreased heart rate variability.…”

Section: Introductionmentioning

confidence: 85%

“…The significant negative correlation between RSA and the lipoproteins (LDL, CHOL, TG and VLDL) closely mirrors a risk for development of coronary artery disease due to a reduced cardiac parasympathetic modulation. Newlin et al [35] and Weise et al [56], using spectral analysis, found RSA in healthy subjects to be reduced after moderate alcohol consumption. With the time domain method, we did not find a significant decrease in RSA or a change in IBI after moderate alcohol intake, whereas RSA with acoustic stimulation did change significantly.…”

Section: Rsa With Auditory Stimulation In Healthy Subjects and The Rimentioning

confidence: 99%

“…For example, Weise et al [56] reported that acute alcohol (0.7 g ethanol/ kg bodyweight) decreased heart rate variability. Similarly, Newlin et al [35] found that the physiologically normal response to food or beverage intake, of an increased vagal tone is inhibited by moderate doses of alcohol (0.5 g ethanol/kg bodyweight). Respiratory sinus arrhythmia (RSA), i.e.…”

Section: Introductionmentioning

confidence: 99%

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Acute Moderate Alcohol Consumption Affects Cardiovascular Responses in Healthy Males with Different Tolerance Levels

Schulte¹,

Warzel²,

Westphal³

et al. 2002

Neuropsychobiology

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We investigated the effect of acute moderate alcohol consumption or placebo on respiratory sinus arrhythmia (RSA) in 48 healthy participants with different levels of alcohol tolerance but no abuse. In the electrocardiogram recording, auditory stimuli were presented at defined points in the respiratory cycle, which allows a non-invasive measure of CNS control over RSA. After alcohol consumption we found a decrease in RSA with auditory stimulation. Moreover, individuals with low tolerance showed only a slight change in the RSA after alcohol intake compared to baseline, whereas the placebo drink led to a reduced RSA. In subjects with high alcohol tolerance, alcohol consumption led to a reduction of RSA, with no change after placebo. These results suggest a centrally driven influence on RSA that is changed by alcohol ingestion depending upon subjects’ levels of alcohol tolerance.

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Vagal Mediation of the Effect of Alcohol on Heart Rate

Cited by 39 publications

References 10 publications

Intravenous Cocaine Decreases Cardiac Vagal Tone, Vagal Index (Derived in Lorenz Space), and Heart Period Complexity (Approximate Entropy) in Cocaine Abusers

Intravenous Cocaine Decreases Cardiac Vagal Tone, Vagal Index (Derived in Lorenz Space), and Heart Period Complexity (Approximate Entropy) in Cocaine Abusers

Alcohol-induced heart rate response dampening during aversive and rewarding stress paradigms in subjects at risk for alcoholism

Acute Moderate Alcohol Consumption Affects Cardiovascular Responses in Healthy Males with Different Tolerance Levels

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