Electrophysiologic effects of civamide (zucapsaicin) on canine cardiac tissue in vivo and in vitro

David O. Arnar, John J. Cai, Hon Chi Lee, James B. Martins

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The cardiac electrophysiologic effects of civamide (zucapsaicin), the cis-isomer of the alkyl vanillylamide, capsaicin, were evaluated in intact dogs and isolated Purkinje fibers. In anesthetized dogs, the mechanism of ventricular tachycardia inducible from 1 to 3 h after coronary artery occlusion was determined by activation mapping. Of 16 dogs studied, nine had ventricular tachycardia of focal endocardial origin; four, a reentrant mechanism; and three had no inducible arrhythmia. Civamide (50 μg/kg) was administered to 10 of 13 dogs that were inducible, but three dogs were used as time controls. Transmural activation times were unaltered by civamide, but mean arterial pressure decreased from 76 μ 10 to 66 μ 10 mm Hg (p < 0.05), and muscle refractory periods shortened from 138 μ 3 to 132 μ 4 ms (p < 0.05). Civamide altered inducibility in five of six dogs with ventricular tachycardia of focal endocardial origin, but those with epicardial reentrant mechanisms were not affected in three of four dogs. With microelectrode techniques in vitro, civamide (10-5 M) shortened the action-potential duration at 50% repolarization (APD50) from 193 μ 13 to 177 μ 12 ms (p < 0.01) and APD90 from 260 μ 15 to 248 μ 13 ms (p < 0.01) in isolated Purkinje fibers (n = 10). Nifedipine prevented the effects of civamide in vitro. These results show that civamide may alter inducibility of ventricular tachycardia with focal endocardial origin and shorten APD of Purkinje fibers in vitro. The effects of civamide in vitro are prevented by preexposure of the Purkinje fibers to nifedipine, suggesting that the electrophysiologic effects of civamide may be mediated through blockade of calcium channels.

Original languageEnglish (US)
Pages (from-to)875-883
Number of pages9
JournalJournal of Cardiovascular Pharmacology
Volume32
Issue number6
DOIs
StatePublished - Dec 1998
Externally publishedYes

Fingerprint

Canidae
Purkinje Fibers
Dogs
Ventricular Tachycardia
pamidronate
Nifedipine
In Vitro Techniques
zucapsaicin
Coronary Occlusion
Capsaicin
Microelectrodes
Calcium Channels
Action Potentials
Cardiac Arrhythmias
Coronary Vessels
Arterial Pressure
Muscles

Keywords

  • Action- potential durations
  • Calcium channel blockade
  • Civamide
  • Inducible ventricular tachycardia
  • Ischemia
  • Zucapsaicin

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Electrophysiologic effects of civamide (zucapsaicin) on canine cardiac tissue in vivo and in vitro. / Arnar, David O.; Cai, John J.; Lee, Hon Chi; Martins, James B.

In: Journal of Cardiovascular Pharmacology, Vol. 32, No. 6, 12.1998, p. 875-883.

Research output: Contribution to journalArticle

@article{543bf4240561442b8fe0acf3b3fb0f70,
title = "Electrophysiologic effects of civamide (zucapsaicin) on canine cardiac tissue in vivo and in vitro",
abstract = "The cardiac electrophysiologic effects of civamide (zucapsaicin), the cis-isomer of the alkyl vanillylamide, capsaicin, were evaluated in intact dogs and isolated Purkinje fibers. In anesthetized dogs, the mechanism of ventricular tachycardia inducible from 1 to 3 h after coronary artery occlusion was determined by activation mapping. Of 16 dogs studied, nine had ventricular tachycardia of focal endocardial origin; four, a reentrant mechanism; and three had no inducible arrhythmia. Civamide (50 μg/kg) was administered to 10 of 13 dogs that were inducible, but three dogs were used as time controls. Transmural activation times were unaltered by civamide, but mean arterial pressure decreased from 76 μ 10 to 66 μ 10 mm Hg (p < 0.05), and muscle refractory periods shortened from 138 μ 3 to 132 μ 4 ms (p < 0.05). Civamide altered inducibility in five of six dogs with ventricular tachycardia of focal endocardial origin, but those with epicardial reentrant mechanisms were not affected in three of four dogs. With microelectrode techniques in vitro, civamide (10-5 M) shortened the action-potential duration at 50{\%} repolarization (APD50) from 193 μ 13 to 177 μ 12 ms (p < 0.01) and APD90 from 260 μ 15 to 248 μ 13 ms (p < 0.01) in isolated Purkinje fibers (n = 10). Nifedipine prevented the effects of civamide in vitro. These results show that civamide may alter inducibility of ventricular tachycardia with focal endocardial origin and shorten APD of Purkinje fibers in vitro. The effects of civamide in vitro are prevented by preexposure of the Purkinje fibers to nifedipine, suggesting that the electrophysiologic effects of civamide may be mediated through blockade of calcium channels.",
keywords = "Action- potential durations, Calcium channel blockade, Civamide, Inducible ventricular tachycardia, Ischemia, Zucapsaicin",
author = "Arnar, {David O.} and Cai, {John J.} and Lee, {Hon Chi} and Martins, {James B.}",
year = "1998",
month = "12",
doi = "10.1097/00005344-199812000-00003",
language = "English (US)",
volume = "32",
pages = "875--883",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Electrophysiologic effects of civamide (zucapsaicin) on canine cardiac tissue in vivo and in vitro

AU - Arnar, David O.

AU - Cai, John J.

AU - Lee, Hon Chi

AU - Martins, James B.

PY - 1998/12

Y1 - 1998/12

N2 - The cardiac electrophysiologic effects of civamide (zucapsaicin), the cis-isomer of the alkyl vanillylamide, capsaicin, were evaluated in intact dogs and isolated Purkinje fibers. In anesthetized dogs, the mechanism of ventricular tachycardia inducible from 1 to 3 h after coronary artery occlusion was determined by activation mapping. Of 16 dogs studied, nine had ventricular tachycardia of focal endocardial origin; four, a reentrant mechanism; and three had no inducible arrhythmia. Civamide (50 μg/kg) was administered to 10 of 13 dogs that were inducible, but three dogs were used as time controls. Transmural activation times were unaltered by civamide, but mean arterial pressure decreased from 76 μ 10 to 66 μ 10 mm Hg (p < 0.05), and muscle refractory periods shortened from 138 μ 3 to 132 μ 4 ms (p < 0.05). Civamide altered inducibility in five of six dogs with ventricular tachycardia of focal endocardial origin, but those with epicardial reentrant mechanisms were not affected in three of four dogs. With microelectrode techniques in vitro, civamide (10-5 M) shortened the action-potential duration at 50% repolarization (APD50) from 193 μ 13 to 177 μ 12 ms (p < 0.01) and APD90 from 260 μ 15 to 248 μ 13 ms (p < 0.01) in isolated Purkinje fibers (n = 10). Nifedipine prevented the effects of civamide in vitro. These results show that civamide may alter inducibility of ventricular tachycardia with focal endocardial origin and shorten APD of Purkinje fibers in vitro. The effects of civamide in vitro are prevented by preexposure of the Purkinje fibers to nifedipine, suggesting that the electrophysiologic effects of civamide may be mediated through blockade of calcium channels.

AB - The cardiac electrophysiologic effects of civamide (zucapsaicin), the cis-isomer of the alkyl vanillylamide, capsaicin, were evaluated in intact dogs and isolated Purkinje fibers. In anesthetized dogs, the mechanism of ventricular tachycardia inducible from 1 to 3 h after coronary artery occlusion was determined by activation mapping. Of 16 dogs studied, nine had ventricular tachycardia of focal endocardial origin; four, a reentrant mechanism; and three had no inducible arrhythmia. Civamide (50 μg/kg) was administered to 10 of 13 dogs that were inducible, but three dogs were used as time controls. Transmural activation times were unaltered by civamide, but mean arterial pressure decreased from 76 μ 10 to 66 μ 10 mm Hg (p < 0.05), and muscle refractory periods shortened from 138 μ 3 to 132 μ 4 ms (p < 0.05). Civamide altered inducibility in five of six dogs with ventricular tachycardia of focal endocardial origin, but those with epicardial reentrant mechanisms were not affected in three of four dogs. With microelectrode techniques in vitro, civamide (10-5 M) shortened the action-potential duration at 50% repolarization (APD50) from 193 μ 13 to 177 μ 12 ms (p < 0.01) and APD90 from 260 μ 15 to 248 μ 13 ms (p < 0.01) in isolated Purkinje fibers (n = 10). Nifedipine prevented the effects of civamide in vitro. These results show that civamide may alter inducibility of ventricular tachycardia with focal endocardial origin and shorten APD of Purkinje fibers in vitro. The effects of civamide in vitro are prevented by preexposure of the Purkinje fibers to nifedipine, suggesting that the electrophysiologic effects of civamide may be mediated through blockade of calcium channels.

KW - Action- potential durations

KW - Calcium channel blockade

KW - Civamide

KW - Inducible ventricular tachycardia

KW - Ischemia

KW - Zucapsaicin

UR - http://www.scopus.com/inward/record.url?scp=0031672238&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031672238&partnerID=8YFLogxK

U2 - 10.1097/00005344-199812000-00003

DO - 10.1097/00005344-199812000-00003

M3 - Article

C2 - 9869492

AN - SCOPUS:0031672238

VL - 32

SP - 875

EP - 883

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 6

ER -