Reduction of sympathetic inotropic response after ischemia in dogs. Contributor to stunned myocardium

A. A. Ciuffo, P. Ouyang, L. C. Becker, L. Levin, M. L. Weisfeldt

Research output: Contribution to journalArticle

Abstract

Eight open chest dogs underwent 25 min of coronary occlusion to determine whether brief myocardial ischemia disrupts the normal myocardial inotropic response to sympathetic nervous stimulation. If so, this could represent a mechanism contributing to postischemic myocardial dysfunction. Myocardial segment shortening was measured using ultrasonic dimension crystals before and after coronary artery occlusion and reperfusion. Left ansa subclavia stimulation and systemic norepinephrine (NE) infusion were used to test the myocardial inotropic response to neural stimulation and direct exposure to the sympathetic mediator, respectively. Before coronary artery occlusion, base-line preischemic segment shortening (12.5±1.6%) (SEM) increased during both sympathetic stimulation (20.2±1.4%) and NE infusion (19.7±1.1%). The control segment responded similarly. After ischemia and reperfusion there was no significant change in heart rate, aortic or left ventricular pressures, nor changes in control segment shortening. In contrast, shortening in the postischemic segment was markedly reduced compared to baseline (4.1±2.4%), and no longer responded to sympathetic stimulation (2.4±2.8%), while responsiveness to systemic NE was maintained (12.9±2.0%), P

Original languageEnglish (US)
Pages (from-to)1504-1509
Number of pages6
JournalJournal of Clinical Investigation
Volume75
Issue number5
StatePublished - 1985

Fingerprint

Myocardial Stunning
Coronary Occlusion
Norepinephrine
Ischemia
Dogs
Coronary Vessels
Myocardial Reperfusion
Ventricular Pressure
Ultrasonics
Reperfusion
Myocardial Ischemia
Thorax
Heart Rate

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Reduction of sympathetic inotropic response after ischemia in dogs. Contributor to stunned myocardium. / Ciuffo, A. A.; Ouyang, P.; Becker, L. C.; Levin, L.; Weisfeldt, M. L.

In: Journal of Clinical Investigation, Vol. 75, No. 5, 1985, p. 1504-1509.

Research output: Contribution to journalArticle

@article{62bebb72cd20450da770c307be94e93b,
title = "Reduction of sympathetic inotropic response after ischemia in dogs. Contributor to stunned myocardium",
abstract = "Eight open chest dogs underwent 25 min of coronary occlusion to determine whether brief myocardial ischemia disrupts the normal myocardial inotropic response to sympathetic nervous stimulation. If so, this could represent a mechanism contributing to postischemic myocardial dysfunction. Myocardial segment shortening was measured using ultrasonic dimension crystals before and after coronary artery occlusion and reperfusion. Left ansa subclavia stimulation and systemic norepinephrine (NE) infusion were used to test the myocardial inotropic response to neural stimulation and direct exposure to the sympathetic mediator, respectively. Before coronary artery occlusion, base-line preischemic segment shortening (12.5±1.6{\%}) (SEM) increased during both sympathetic stimulation (20.2±1.4{\%}) and NE infusion (19.7±1.1{\%}). The control segment responded similarly. After ischemia and reperfusion there was no significant change in heart rate, aortic or left ventricular pressures, nor changes in control segment shortening. In contrast, shortening in the postischemic segment was markedly reduced compared to baseline (4.1±2.4{\%}), and no longer responded to sympathetic stimulation (2.4±2.8{\%}), while responsiveness to systemic NE was maintained (12.9±2.0{\%}), P",
author = "Ciuffo, {A. A.} and P. Ouyang and Becker, {L. C.} and L. Levin and Weisfeldt, {M. L.}",
year = "1985",
language = "English (US)",
volume = "75",
pages = "1504--1509",
journal = "Journal of Clinical Investigation",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "5",

}

TY - JOUR

T1 - Reduction of sympathetic inotropic response after ischemia in dogs. Contributor to stunned myocardium

AU - Ciuffo, A. A.

AU - Ouyang, P.

AU - Becker, L. C.

AU - Levin, L.

AU - Weisfeldt, M. L.

PY - 1985

Y1 - 1985

N2 - Eight open chest dogs underwent 25 min of coronary occlusion to determine whether brief myocardial ischemia disrupts the normal myocardial inotropic response to sympathetic nervous stimulation. If so, this could represent a mechanism contributing to postischemic myocardial dysfunction. Myocardial segment shortening was measured using ultrasonic dimension crystals before and after coronary artery occlusion and reperfusion. Left ansa subclavia stimulation and systemic norepinephrine (NE) infusion were used to test the myocardial inotropic response to neural stimulation and direct exposure to the sympathetic mediator, respectively. Before coronary artery occlusion, base-line preischemic segment shortening (12.5±1.6%) (SEM) increased during both sympathetic stimulation (20.2±1.4%) and NE infusion (19.7±1.1%). The control segment responded similarly. After ischemia and reperfusion there was no significant change in heart rate, aortic or left ventricular pressures, nor changes in control segment shortening. In contrast, shortening in the postischemic segment was markedly reduced compared to baseline (4.1±2.4%), and no longer responded to sympathetic stimulation (2.4±2.8%), while responsiveness to systemic NE was maintained (12.9±2.0%), P

AB - Eight open chest dogs underwent 25 min of coronary occlusion to determine whether brief myocardial ischemia disrupts the normal myocardial inotropic response to sympathetic nervous stimulation. If so, this could represent a mechanism contributing to postischemic myocardial dysfunction. Myocardial segment shortening was measured using ultrasonic dimension crystals before and after coronary artery occlusion and reperfusion. Left ansa subclavia stimulation and systemic norepinephrine (NE) infusion were used to test the myocardial inotropic response to neural stimulation and direct exposure to the sympathetic mediator, respectively. Before coronary artery occlusion, base-line preischemic segment shortening (12.5±1.6%) (SEM) increased during both sympathetic stimulation (20.2±1.4%) and NE infusion (19.7±1.1%). The control segment responded similarly. After ischemia and reperfusion there was no significant change in heart rate, aortic or left ventricular pressures, nor changes in control segment shortening. In contrast, shortening in the postischemic segment was markedly reduced compared to baseline (4.1±2.4%), and no longer responded to sympathetic stimulation (2.4±2.8%), while responsiveness to systemic NE was maintained (12.9±2.0%), P

UR - http://www.scopus.com/inward/record.url?scp=0021837641&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021837641&partnerID=8YFLogxK

M3 - Article

C2 - 3998147

AN - SCOPUS:0021837641

VL - 75

SP - 1504

EP - 1509

JO - Journal of Clinical Investigation

JF - Journal of Clinical Investigation

SN - 0021-9738

IS - 5

ER -