Effects of diltiazem on the electrophysiological properties of cat ventricular muscle fibers during experimentally induced right ventricular systolic hypertension

S. S. Wong, Robert J Myerburg, A. M. Ezrin, M. S. Gaide, A. L. Bassett

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The electrophysiological effects of diltiazem were studied in right ventricular muscle fibers from normal cats and cats with experimentally induced right ventricular systolic hypertension (RVSH). Two types of action potential (AP) abnormalities were observed in preparations from cats with RVSH: Type I cells, found in most areas of the right ventricular free wall, demonstrated reduced maximum diastolic potential (MDP) (-64.4 mV) and V̇[max] (89.6 V/s) while Type II cells showed a 'slow response' AP configuration (MDP, -48.8 mV; AP amplitude, 48.9 mV; AP duration at 50% repolarization, 47.5 ms; AP duration at 90% repolarization, 90.2 ms; V̇[max], 13,1 V/s) and were often monitored near the tricuspid valve. Diltiazem (2.2 x 10 -7 and 2.2 x 10 -6 M) had no effect on MDP of normal, Type I, or Type II cells. Diltiazem at 2.2 x 10 -6 M significantly reduced AP amplitude and V̇[max] of both Type I and normal cells. In contrast, even at 2.2 x 10 -7 M, diltiazem significantly reduced AP amplitude and V[max] of the Type II cells. Diltiazem, 2.2 x 10 -6 M, would often abolish AP of Type II cells, while Type I cells were more sensitive to tetrodotoxin. AP duration of normal cells was unaffected by diltiazem while that of Type I and II cells was significantly shortened.

Original languageEnglish
Pages (from-to)986-993
Number of pages8
JournalJournal of Cardiovascular Pharmacology
Volume4
Issue number6
StatePublished - Dec 1 1982

Fingerprint

Diltiazem
Action Potentials
Cats
Hypertension
Muscles
Tricuspid Valve
Tetrodotoxin

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

Effects of diltiazem on the electrophysiological properties of cat ventricular muscle fibers during experimentally induced right ventricular systolic hypertension. / Wong, S. S.; Myerburg, Robert J; Ezrin, A. M.; Gaide, M. S.; Bassett, A. L.

In: Journal of Cardiovascular Pharmacology, Vol. 4, No. 6, 01.12.1982, p. 986-993.

Research output: Contribution to journalArticle

@article{2830426444b94d81993be5350af3e45c,
title = "Effects of diltiazem on the electrophysiological properties of cat ventricular muscle fibers during experimentally induced right ventricular systolic hypertension",
abstract = "The electrophysiological effects of diltiazem were studied in right ventricular muscle fibers from normal cats and cats with experimentally induced right ventricular systolic hypertension (RVSH). Two types of action potential (AP) abnormalities were observed in preparations from cats with RVSH: Type I cells, found in most areas of the right ventricular free wall, demonstrated reduced maximum diastolic potential (MDP) (-64.4 mV) and V̇[max] (89.6 V/s) while Type II cells showed a 'slow response' AP configuration (MDP, -48.8 mV; AP amplitude, 48.9 mV; AP duration at 50{\%} repolarization, 47.5 ms; AP duration at 90{\%} repolarization, 90.2 ms; V̇[max], 13,1 V/s) and were often monitored near the tricuspid valve. Diltiazem (2.2 x 10 -7 and 2.2 x 10 -6 M) had no effect on MDP of normal, Type I, or Type II cells. Diltiazem at 2.2 x 10 -6 M significantly reduced AP amplitude and V̇[max] of both Type I and normal cells. In contrast, even at 2.2 x 10 -7 M, diltiazem significantly reduced AP amplitude and V[max] of the Type II cells. Diltiazem, 2.2 x 10 -6 M, would often abolish AP of Type II cells, while Type I cells were more sensitive to tetrodotoxin. AP duration of normal cells was unaffected by diltiazem while that of Type I and II cells was significantly shortened.",
author = "Wong, {S. S.} and Myerburg, {Robert J} and Ezrin, {A. M.} and Gaide, {M. S.} and Bassett, {A. L.}",
year = "1982",
month = "12",
day = "1",
language = "English",
volume = "4",
pages = "986--993",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Effects of diltiazem on the electrophysiological properties of cat ventricular muscle fibers during experimentally induced right ventricular systolic hypertension

AU - Wong, S. S.

AU - Myerburg, Robert J

AU - Ezrin, A. M.

AU - Gaide, M. S.

AU - Bassett, A. L.

PY - 1982/12/1

Y1 - 1982/12/1

N2 - The electrophysiological effects of diltiazem were studied in right ventricular muscle fibers from normal cats and cats with experimentally induced right ventricular systolic hypertension (RVSH). Two types of action potential (AP) abnormalities were observed in preparations from cats with RVSH: Type I cells, found in most areas of the right ventricular free wall, demonstrated reduced maximum diastolic potential (MDP) (-64.4 mV) and V̇[max] (89.6 V/s) while Type II cells showed a 'slow response' AP configuration (MDP, -48.8 mV; AP amplitude, 48.9 mV; AP duration at 50% repolarization, 47.5 ms; AP duration at 90% repolarization, 90.2 ms; V̇[max], 13,1 V/s) and were often monitored near the tricuspid valve. Diltiazem (2.2 x 10 -7 and 2.2 x 10 -6 M) had no effect on MDP of normal, Type I, or Type II cells. Diltiazem at 2.2 x 10 -6 M significantly reduced AP amplitude and V̇[max] of both Type I and normal cells. In contrast, even at 2.2 x 10 -7 M, diltiazem significantly reduced AP amplitude and V[max] of the Type II cells. Diltiazem, 2.2 x 10 -6 M, would often abolish AP of Type II cells, while Type I cells were more sensitive to tetrodotoxin. AP duration of normal cells was unaffected by diltiazem while that of Type I and II cells was significantly shortened.

AB - The electrophysiological effects of diltiazem were studied in right ventricular muscle fibers from normal cats and cats with experimentally induced right ventricular systolic hypertension (RVSH). Two types of action potential (AP) abnormalities were observed in preparations from cats with RVSH: Type I cells, found in most areas of the right ventricular free wall, demonstrated reduced maximum diastolic potential (MDP) (-64.4 mV) and V̇[max] (89.6 V/s) while Type II cells showed a 'slow response' AP configuration (MDP, -48.8 mV; AP amplitude, 48.9 mV; AP duration at 50% repolarization, 47.5 ms; AP duration at 90% repolarization, 90.2 ms; V̇[max], 13,1 V/s) and were often monitored near the tricuspid valve. Diltiazem (2.2 x 10 -7 and 2.2 x 10 -6 M) had no effect on MDP of normal, Type I, or Type II cells. Diltiazem at 2.2 x 10 -6 M significantly reduced AP amplitude and V̇[max] of both Type I and normal cells. In contrast, even at 2.2 x 10 -7 M, diltiazem significantly reduced AP amplitude and V[max] of the Type II cells. Diltiazem, 2.2 x 10 -6 M, would often abolish AP of Type II cells, while Type I cells were more sensitive to tetrodotoxin. AP duration of normal cells was unaffected by diltiazem while that of Type I and II cells was significantly shortened.

UR - http://www.scopus.com/inward/record.url?scp=0020362981&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020362981&partnerID=8YFLogxK

M3 - Article

VL - 4

SP - 986

EP - 993

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 6

ER -