Nifedipine reduces arrhythmias but does not alter prostanoid release during coronary artery occlusion and reperfusion in anaesthetised greyhounds

Susan J. Coker, J. Parratt

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

We examined the effects of nifedipine, a calcium slow-channel blocking drug, on haemodynamics, blood gases, cardiac arrhythmias, and prostanoid release in anaesthetised greyhounds before, during, and after a 40-min occlusion of the left anterior descending coronary artery. Fifteen minutes after commencing treatment with nifedipine (5 μg/kg + 0.67 μg kg-1 min-1), there were significant reductions in arterial blood pressure, left ventricular end-diastolic pressure, and vascular resistance, with increases in cardiac output and stroke volume. Although coronary artery blood flow was unchanged, oxygen extraction was decreased, indicating that nifedipine reduced oxygen consumption. Nifedipine prevented the haemodynamic changes that occur in control dogs during acute myocardial ischaemia and markedly reduced the number of arrhythmias during coronary artery occlusion. The incidence of ventricular fibrillation induced by release of the occlusion was significantly reduced from 88 % in the control group to 22% in the group receiving nifedipine. The release of thromboxane B2 and 6-keto PGF (stable breakdown products of thromboxane A2 and prostacyclin, respectively) from the acutely ischaemic myocardium was not altered by nifedipine. It is concluded that this low dose of nifedipine had marked antiarrhythmic activity during both coronary artery occlusion and reperfusion. The relationship to dosage and possible mechanisms for this effect are discussed.

Original languageEnglish
Pages (from-to)406-417
Number of pages12
JournalJournal of Cardiovascular Pharmacology
Volume5
Issue number3
Publication statusPublished - 1983

Fingerprint

Myocardial Reperfusion
Coronary Occlusion
Nifedipine
Prostaglandins
Cardiac Arrhythmias
Coronary Vessels
Hemodynamics
Thromboxane B2
Cardiac Volume
Thromboxane A2
Calcium Channel Blockers
Ventricular Fibrillation
Epoprostenol
Oxygen Consumption
Cardiac Output
Vascular Resistance
Stroke Volume
Myocardial Ischemia
Myocardium
Arterial Pressure

Keywords

  • Arrhythmias
  • Coronary artery occlusion
  • Nifedipine
  • Prostacyclin
  • Reperfusion
  • Thromboxane

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

@article{94aaf1b4f09f43ffa13a75ede675904b,
title = "Nifedipine reduces arrhythmias but does not alter prostanoid release during coronary artery occlusion and reperfusion in anaesthetised greyhounds",
abstract = "We examined the effects of nifedipine, a calcium slow-channel blocking drug, on haemodynamics, blood gases, cardiac arrhythmias, and prostanoid release in anaesthetised greyhounds before, during, and after a 40-min occlusion of the left anterior descending coronary artery. Fifteen minutes after commencing treatment with nifedipine (5 μg/kg + 0.67 μg kg-1 min-1), there were significant reductions in arterial blood pressure, left ventricular end-diastolic pressure, and vascular resistance, with increases in cardiac output and stroke volume. Although coronary artery blood flow was unchanged, oxygen extraction was decreased, indicating that nifedipine reduced oxygen consumption. Nifedipine prevented the haemodynamic changes that occur in control dogs during acute myocardial ischaemia and markedly reduced the number of arrhythmias during coronary artery occlusion. The incidence of ventricular fibrillation induced by release of the occlusion was significantly reduced from 88 {\%} in the control group to 22{\%} in the group receiving nifedipine. The release of thromboxane B2 and 6-keto PGF1α (stable breakdown products of thromboxane A2 and prostacyclin, respectively) from the acutely ischaemic myocardium was not altered by nifedipine. It is concluded that this low dose of nifedipine had marked antiarrhythmic activity during both coronary artery occlusion and reperfusion. The relationship to dosage and possible mechanisms for this effect are discussed.",
keywords = "Arrhythmias, Coronary artery occlusion, Nifedipine, Prostacyclin, Reperfusion, Thromboxane",
author = "Coker, {Susan J.} and J. Parratt",
year = "1983",
language = "English",
volume = "5",
pages = "406--417",
journal = "Journal of Cardiovascular Pharmacology",
issn = "0160-2446",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Nifedipine reduces arrhythmias but does not alter prostanoid release during coronary artery occlusion and reperfusion in anaesthetised greyhounds

AU - Coker, Susan J.

AU - Parratt, J.

PY - 1983

Y1 - 1983

N2 - We examined the effects of nifedipine, a calcium slow-channel blocking drug, on haemodynamics, blood gases, cardiac arrhythmias, and prostanoid release in anaesthetised greyhounds before, during, and after a 40-min occlusion of the left anterior descending coronary artery. Fifteen minutes after commencing treatment with nifedipine (5 μg/kg + 0.67 μg kg-1 min-1), there were significant reductions in arterial blood pressure, left ventricular end-diastolic pressure, and vascular resistance, with increases in cardiac output and stroke volume. Although coronary artery blood flow was unchanged, oxygen extraction was decreased, indicating that nifedipine reduced oxygen consumption. Nifedipine prevented the haemodynamic changes that occur in control dogs during acute myocardial ischaemia and markedly reduced the number of arrhythmias during coronary artery occlusion. The incidence of ventricular fibrillation induced by release of the occlusion was significantly reduced from 88 % in the control group to 22% in the group receiving nifedipine. The release of thromboxane B2 and 6-keto PGF1α (stable breakdown products of thromboxane A2 and prostacyclin, respectively) from the acutely ischaemic myocardium was not altered by nifedipine. It is concluded that this low dose of nifedipine had marked antiarrhythmic activity during both coronary artery occlusion and reperfusion. The relationship to dosage and possible mechanisms for this effect are discussed.

AB - We examined the effects of nifedipine, a calcium slow-channel blocking drug, on haemodynamics, blood gases, cardiac arrhythmias, and prostanoid release in anaesthetised greyhounds before, during, and after a 40-min occlusion of the left anterior descending coronary artery. Fifteen minutes after commencing treatment with nifedipine (5 μg/kg + 0.67 μg kg-1 min-1), there were significant reductions in arterial blood pressure, left ventricular end-diastolic pressure, and vascular resistance, with increases in cardiac output and stroke volume. Although coronary artery blood flow was unchanged, oxygen extraction was decreased, indicating that nifedipine reduced oxygen consumption. Nifedipine prevented the haemodynamic changes that occur in control dogs during acute myocardial ischaemia and markedly reduced the number of arrhythmias during coronary artery occlusion. The incidence of ventricular fibrillation induced by release of the occlusion was significantly reduced from 88 % in the control group to 22% in the group receiving nifedipine. The release of thromboxane B2 and 6-keto PGF1α (stable breakdown products of thromboxane A2 and prostacyclin, respectively) from the acutely ischaemic myocardium was not altered by nifedipine. It is concluded that this low dose of nifedipine had marked antiarrhythmic activity during both coronary artery occlusion and reperfusion. The relationship to dosage and possible mechanisms for this effect are discussed.

KW - Arrhythmias

KW - Coronary artery occlusion

KW - Nifedipine

KW - Prostacyclin

KW - Reperfusion

KW - Thromboxane

UR - http://www.scopus.com/inward/record.url?scp=0020570435&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020570435&partnerID=8YFLogxK

M3 - Article

C2 - 6191139

AN - SCOPUS:0020570435

VL - 5

SP - 406

EP - 417

JO - Journal of Cardiovascular Pharmacology

JF - Journal of Cardiovascular Pharmacology

SN - 0160-2446

IS - 3

ER -