Acute effects of ethanol and acetaldehyde on blood pressure and heart rate in disulfiram-treated and control rats

Hellström, Ewa; Tottmar, Olof

doi:10.1016/0091-3057(82)90102-2

Cited by 28 publications

(12 citation statements)

References 33 publications

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“…Steady-state plasma ethanol concentrations were achieved over the duration of our study with a dose of 50mgkg-1 of 4-MP without any significant haemodynamic responses or changes in arterial blood gases. These findings are consistent with studies on 4-MP in rats by Hellstrom & Tottmar (1982).…”

Section: Discussionsupporting

confidence: 93%

Haemodynamic alterations in anaesthetized and acutely intoxicated newborn piglets

Chandler

Ong

Sitar

1990

British J Pharmacology

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1 We investigated the haemodynamic alterations in 2-day old anaesthetized piglets after acute ethanol intoxication using the microsphere technique. 2 After ethanol infusion, mean arterial blood pressure (MABP) decreased by 6%, cardiac output (CO) decreased by 26%, heart rate (HR) increased by 20% and systemic vascular resistance (SVR) increased by 36%. 3 Arterial perfusion to the kidneys, gastrointestinal (GI) organs and carcass decreased by 39%, 34% and 26%, respectively. 4 In piglets pretreated with 4-methylpyrazole (4-MP), an alcohol dehydrogenase inhibitor, the decrease in MABP and increase in HR were not observed after ethanol infusion, but the reduction in CO and increase in SVR were maintained. 5 Arterial blood flow to the GI organs and carcass, but not the kidneys, remained at significantly reduced levels. 6 These observations indicate that ethanol can adversely affect CO and arterial perfusion to GI and musculoskeletal structures while metabolites of ethanol, such as acetaldehyde, affect MABP and HR. Therefore, the clinical effects observed after acute ethanol intoxication in neonates may vary with their rate of ethanol metabolism.

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Section: Discussionsupporting

confidence: 93%

Haemodynamic alterations in anaesthetized and acutely intoxicated newborn piglets

Chandler

Ong

Sitar

1990

British J Pharmacology

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“…The cardiac effects of saturated aldehydes have been studied for over 40 years (Egle and Hudgins, 1974;Green and Egle, 1983;Hellstrom and Tottmar, 1982;James and Bear, 1967;James and Bear, 1968). Because acetaldehyde is the primary metabolite of ethanol, its effects on the cardiovascular system are of continued interest.…”

Section: Cardiac Effectsmentioning

confidence: 99%

“…Thus, it is difficult to differentiate between effects of airborne aldehydes and aldehydes generated endogenously (Dong and Moldoveanu, 2004a,b;Madden et al, 1999). Aliphatic aldehydes, such as acetaldehyde, butryaldehyde, and propionaldehyde, are strongly sympathomimetic in mammals in vivo through release of norepinephrine from sympathetic fibers (Green and Egle, 1983;Hellstrom and Tottmar, 1982;James and Bear, 1967;James and Bear, 1968). During intranodal perfusion in the heart, these aliphatic aldehydes stimulate positive chrontropic responses whereas at higher doses these aldehydes stimulate cardiac arrest ( James and Bear, 1968).…”

Section: Source Aldehyde(s) Concentrationmentioning

confidence: 99%

Aldehydes and Cardiovascular Disease

Conklin

Bhatnagar

2018

Comprehensive Toxicology

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“…Direct perfusion of the canine sinus node with acetaldehyde has been reported to elicit tachycardia that was inhibited by ␤-adrenergic blockade (James and Bear, 1967). Likewise, intravenous infusion of acetaldehyde in the rat caused tachycardia whose time course mimicked that of its blood level (Hellström and Tottmar, 1982). These effects were attributed to catecholamine release, because acetaldehyde seemed to enhance catecholamine secretion from bovine adrenal medulla (Schneider, 1971) and promote norepinephrine (NE) release from rat brain (Thadani and Truitt, 1977).…”

Section: Introductionmentioning

confidence: 99%

Aldehyde Dehydrogenase Type 2 Activation by Adenosine and Histamine Inhibits Ischemic Norepinephrine Release in Cardiac Sympathetic Neurons: Mediation by Protein Kinase Cε

Robador

Seyedi

Chan

et al. 2012

J Pharmacol Exp Ther

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During myocardial ischemia/reperfusion, lipid peroxidation leads to the formation of toxic aldehydes that contribute to ischemic dysfunction. Mitochondrial aldehyde dehydrogenase type 2 (ALDH2) alleviates ischemic heart damage and reperfusion arrhythmias via aldehyde detoxification. Because excessive norepinephrine release in the heart is a pivotal arrhythmogenic mechanism, we hypothesized that neuronal ALDH2 activation might diminish ischemic norepinephrine release. Incubation of cardiac sympathetic nerve endings with acetaldehyde, at concentrations achieved in myocardial ischemia, caused a concentration-dependent increase in norepinephrine release. A major increase in norepinephrine release also occurred when sympathetic nerve endings were incubated in hypoxic conditions. ALDH2 activation substantially reduced acetaldehyde-and hypoxia-induced norepinephrine release, an action prevented by inhibition of ALDH2 or protein kinase C (PKC). Selective activation of G i/o -coupled adenosine A 1 , A 3 , or histamine H 3 receptors markedly inhibited both acetaldehyde-and hypoxia-induced norepinephrine release. These effects were also abolished by PKC and/or ALDH2 inhibition. Moreover, A 1 -, A 3 -, or H 3 -receptor activation increased ALDH2 activity in a sympathetic neuron model (differentiated PC12 cells stably transfected with H 3 receptors). This action was prevented by the inhibition of PKC and ALDH2. Our findings suggest the existence in sympathetic neurons of a protective pathway initiated by A 1 -, A 3 -, and H 3 -receptor activation by adenosine and histamine released in close proximity of these terminals. This pathway comprises the sequential activation of PKC and ALDH2, culminating in aldehyde detoxification and inhibition of hypoxic norepinephrine release. Thus, pharmacological activation of PKC and ALDH2 in cardiac sympathetic nerves may have significant protective effects by alleviating norepinephrine-induced life-threatening arrhythmias that characterize myocardial ischemia/reperfusion.

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Acute effects of ethanol and acetaldehyde on blood pressure and heart rate in disulfiram-treated and control rats

Cited by 28 publications

References 33 publications

Haemodynamic alterations in anaesthetized and acutely intoxicated newborn piglets

Haemodynamic alterations in anaesthetized and acutely intoxicated newborn piglets

Aldehydes and Cardiovascular Disease

Aldehyde Dehydrogenase Type 2 Activation by Adenosine and Histamine Inhibits Ischemic Norepinephrine Release in Cardiac Sympathetic Neurons: Mediation by Protein Kinase Cε

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