Sympathetic stimulation and norepinephrine infusion modulate extracellular potassium concentration during acute myocardial ischemia

Margaret R. Warner, Timothy S. Kroeker, Douglas P. Zipes

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The purpose of this study was to investigate whether sympathetic stimulation modulated the rise in extracellular K+ concentration ([K+]o) evoked by acute myocardial ischemia. In 35 α-chloralose-anesthetized dogs, we measured changes in [K+]o during acute myocardial ischemia in the presence and absence of sympathetic stimulation or norepinephrine infusion. A series of four 5-minute occlusions of the distal left anterior descending coronary artery (LAD) was completed in 18 dogs. Thirty minutes of reperfusion separated each LAD occlusion. Four to five K+-sensitive electrodes were inserted into the left ventricular midmyocardium that was perfused by the distal LAD. Lead II of the electrocardiogram, arterial pressure, and [K+]o were recorded, and the right atrium was paced at a constant cycle length. The first, second, and fourth LAD occlusions were done in the absence of sympathetic stimulation or norepinephrine infusion. The changes in [K+]o evoked by the first LAD occlusion differed (p<0.05) from those elicited by the second and fourth occlusions. However, the changes in [K+]o during the second and fourth LAD occlusions were similar (p>0.2) and served as controls for the responses obtained during the third occlusion. Two minutes before the third LAD occlusion, sympathetic stimulation (4 Hz) or norepinephrine infusion (0.25-0.5 μg/kg per minute i.v.) was begun and was continued until 2 minutes after reperfusion. We found that sympathetic stimulation and norepinephrine infusion increased (p<0.05) myocardial blood flow in both normal and ischemic tissue. The mean response recorded by 23 K+-sensitive electrodes in 11 dogs showed that sympathetic stimulation increased (p<0.001) the [K+]o at 1, 2, 3, 4, and 5 minutes after the onset of LAD occlusion compared with the second and fourth occlusions. In contrast, the mean response recorded by 20 K+-sensitive electrodes in seven dogs showed that norepinephrine infusion reduced (p<0.02) the [K+]o at 4 and 5 minutes after the onset of LAD occlusion. These data show that sympathetic stimulation increased the [K+]o evoked by acute myocardial ischemia, an effect that was not mimicked by the intravenous administration of norepinephrine.

Original languageEnglish
Pages (from-to)1078-1087
Number of pages10
JournalCirculation Research
Volume71
Issue number5
StatePublished - Nov 1992

Fingerprint

Myocardial Ischemia
Norepinephrine
Potassium
Dogs
Electrodes
Reperfusion
Chloralose
Heart Atria
Intravenous Administration
Coronary Vessels
Arterial Pressure
Electrocardiography

Keywords

  • Extracellular potassium concentration
  • Myocardial ischemia
  • Norepinephrine
  • Potassium
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Sympathetic stimulation and norepinephrine infusion modulate extracellular potassium concentration during acute myocardial ischemia. / Warner, Margaret R.; Kroeker, Timothy S.; Zipes, Douglas P.

In: Circulation Research, Vol. 71, No. 5, 11.1992, p. 1078-1087.

Research output: Contribution to journalArticle

Warner, Margaret R. ; Kroeker, Timothy S. ; Zipes, Douglas P. / Sympathetic stimulation and norepinephrine infusion modulate extracellular potassium concentration during acute myocardial ischemia. In: Circulation Research. 1992 ; Vol. 71, No. 5. pp. 1078-1087.
@article{9b54cd5c73fb4ff8960b8fbb9a2e8316,
title = "Sympathetic stimulation and norepinephrine infusion modulate extracellular potassium concentration during acute myocardial ischemia",
abstract = "The purpose of this study was to investigate whether sympathetic stimulation modulated the rise in extracellular K+ concentration ([K+]o) evoked by acute myocardial ischemia. In 35 α-chloralose-anesthetized dogs, we measured changes in [K+]o during acute myocardial ischemia in the presence and absence of sympathetic stimulation or norepinephrine infusion. A series of four 5-minute occlusions of the distal left anterior descending coronary artery (LAD) was completed in 18 dogs. Thirty minutes of reperfusion separated each LAD occlusion. Four to five K+-sensitive electrodes were inserted into the left ventricular midmyocardium that was perfused by the distal LAD. Lead II of the electrocardiogram, arterial pressure, and [K+]o were recorded, and the right atrium was paced at a constant cycle length. The first, second, and fourth LAD occlusions were done in the absence of sympathetic stimulation or norepinephrine infusion. The changes in [K+]o evoked by the first LAD occlusion differed (p<0.05) from those elicited by the second and fourth occlusions. However, the changes in [K+]o during the second and fourth LAD occlusions were similar (p>0.2) and served as controls for the responses obtained during the third occlusion. Two minutes before the third LAD occlusion, sympathetic stimulation (4 Hz) or norepinephrine infusion (0.25-0.5 μg/kg per minute i.v.) was begun and was continued until 2 minutes after reperfusion. We found that sympathetic stimulation and norepinephrine infusion increased (p<0.05) myocardial blood flow in both normal and ischemic tissue. The mean response recorded by 23 K+-sensitive electrodes in 11 dogs showed that sympathetic stimulation increased (p<0.001) the [K+]o at 1, 2, 3, 4, and 5 minutes after the onset of LAD occlusion compared with the second and fourth occlusions. In contrast, the mean response recorded by 20 K+-sensitive electrodes in seven dogs showed that norepinephrine infusion reduced (p<0.02) the [K+]o at 4 and 5 minutes after the onset of LAD occlusion. These data show that sympathetic stimulation increased the [K+]o evoked by acute myocardial ischemia, an effect that was not mimicked by the intravenous administration of norepinephrine.",
keywords = "Extracellular potassium concentration, Myocardial ischemia, Norepinephrine, Potassium, Sympathetic nervous system",
author = "Warner, {Margaret R.} and Kroeker, {Timothy S.} and Zipes, {Douglas P.}",
year = "1992",
month = "11",
language = "English",
volume = "71",
pages = "1078--1087",
journal = "Circulation Research",
issn = "0009-7330",
publisher = "Lippincott Williams and Wilkins",
number = "5",

}

TY - JOUR

T1 - Sympathetic stimulation and norepinephrine infusion modulate extracellular potassium concentration during acute myocardial ischemia

AU - Warner, Margaret R.

AU - Kroeker, Timothy S.

AU - Zipes, Douglas P.

PY - 1992/11

Y1 - 1992/11

N2 - The purpose of this study was to investigate whether sympathetic stimulation modulated the rise in extracellular K+ concentration ([K+]o) evoked by acute myocardial ischemia. In 35 α-chloralose-anesthetized dogs, we measured changes in [K+]o during acute myocardial ischemia in the presence and absence of sympathetic stimulation or norepinephrine infusion. A series of four 5-minute occlusions of the distal left anterior descending coronary artery (LAD) was completed in 18 dogs. Thirty minutes of reperfusion separated each LAD occlusion. Four to five K+-sensitive electrodes were inserted into the left ventricular midmyocardium that was perfused by the distal LAD. Lead II of the electrocardiogram, arterial pressure, and [K+]o were recorded, and the right atrium was paced at a constant cycle length. The first, second, and fourth LAD occlusions were done in the absence of sympathetic stimulation or norepinephrine infusion. The changes in [K+]o evoked by the first LAD occlusion differed (p<0.05) from those elicited by the second and fourth occlusions. However, the changes in [K+]o during the second and fourth LAD occlusions were similar (p>0.2) and served as controls for the responses obtained during the third occlusion. Two minutes before the third LAD occlusion, sympathetic stimulation (4 Hz) or norepinephrine infusion (0.25-0.5 μg/kg per minute i.v.) was begun and was continued until 2 minutes after reperfusion. We found that sympathetic stimulation and norepinephrine infusion increased (p<0.05) myocardial blood flow in both normal and ischemic tissue. The mean response recorded by 23 K+-sensitive electrodes in 11 dogs showed that sympathetic stimulation increased (p<0.001) the [K+]o at 1, 2, 3, 4, and 5 minutes after the onset of LAD occlusion compared with the second and fourth occlusions. In contrast, the mean response recorded by 20 K+-sensitive electrodes in seven dogs showed that norepinephrine infusion reduced (p<0.02) the [K+]o at 4 and 5 minutes after the onset of LAD occlusion. These data show that sympathetic stimulation increased the [K+]o evoked by acute myocardial ischemia, an effect that was not mimicked by the intravenous administration of norepinephrine.

AB - The purpose of this study was to investigate whether sympathetic stimulation modulated the rise in extracellular K+ concentration ([K+]o) evoked by acute myocardial ischemia. In 35 α-chloralose-anesthetized dogs, we measured changes in [K+]o during acute myocardial ischemia in the presence and absence of sympathetic stimulation or norepinephrine infusion. A series of four 5-minute occlusions of the distal left anterior descending coronary artery (LAD) was completed in 18 dogs. Thirty minutes of reperfusion separated each LAD occlusion. Four to five K+-sensitive electrodes were inserted into the left ventricular midmyocardium that was perfused by the distal LAD. Lead II of the electrocardiogram, arterial pressure, and [K+]o were recorded, and the right atrium was paced at a constant cycle length. The first, second, and fourth LAD occlusions were done in the absence of sympathetic stimulation or norepinephrine infusion. The changes in [K+]o evoked by the first LAD occlusion differed (p<0.05) from those elicited by the second and fourth occlusions. However, the changes in [K+]o during the second and fourth LAD occlusions were similar (p>0.2) and served as controls for the responses obtained during the third occlusion. Two minutes before the third LAD occlusion, sympathetic stimulation (4 Hz) or norepinephrine infusion (0.25-0.5 μg/kg per minute i.v.) was begun and was continued until 2 minutes after reperfusion. We found that sympathetic stimulation and norepinephrine infusion increased (p<0.05) myocardial blood flow in both normal and ischemic tissue. The mean response recorded by 23 K+-sensitive electrodes in 11 dogs showed that sympathetic stimulation increased (p<0.001) the [K+]o at 1, 2, 3, 4, and 5 minutes after the onset of LAD occlusion compared with the second and fourth occlusions. In contrast, the mean response recorded by 20 K+-sensitive electrodes in seven dogs showed that norepinephrine infusion reduced (p<0.02) the [K+]o at 4 and 5 minutes after the onset of LAD occlusion. These data show that sympathetic stimulation increased the [K+]o evoked by acute myocardial ischemia, an effect that was not mimicked by the intravenous administration of norepinephrine.

KW - Extracellular potassium concentration

KW - Myocardial ischemia

KW - Norepinephrine

KW - Potassium

KW - Sympathetic nervous system

UR - http://www.scopus.com/inward/record.url?scp=0026712985&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026712985&partnerID=8YFLogxK

M3 - Article

C2 - 1394871

AN - SCOPUS:0026712985

VL - 71

SP - 1078

EP - 1087

JO - Circulation Research

JF - Circulation Research

SN - 0009-7330

IS - 5

ER -