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Major contribution of vasospasm-induced coronary blood flow reduction to anaphylactic ventricular dysfunction assessed in isolated blood-perfused rat heart
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Abstract
Background: Cardiac anaphylaxis is accompanied by coronary spasm and decreased left ventricular (LV) contractility. However, it has not been determined experimentally whether LV dysfunction during anaphylaxis is induced mainly by reduced coronary blood flow (CBF) or direct negative inotropic actions of chemical mediators. To demonstrate the major role of CBF reduction in anaphylactic LV dysfunction, we determined LV contractility during anaphylaxis and forcible CBF reduction maneuver to reproduce the anaphylaxis-induced CBF reduction in isolated blood-perfused rat hearts.
Methods: Isolated hearts from Wistar rats in the ovalbumin-sensitized anaphylaxis, non-sensitized flow reduction, and non-sensitized time control group were subjected to coronary perfusion with blood at a constant pressure and measurements of CBF and LV pressure. Cardiac anaphylaxis was induced by intracoronary injections of ovalbumin antigen.
Results: In response to antigen administrations, sensitized anaphylaxis group rat hearts showed decreases in CBF and the maximum increasing rate of systolic LV pressure (dP/dtmax) with an increased coronary vascular resistance as evidence of coronary spasm. The non-sensitized flow reduction group rat hearts whose CBF was forcibly reduced as in anaphylaxis showed the same degree of dP/dtmax reduction.
Conclusions: The contractile failure during cardiac anaphylaxis is caused mainly by decreased CBF due to coronary spasm.
Abstract
Background: Cardiac anaphylaxis is accompanied by coronary spasm and decreased left ventricular (LV) contractility. However, it has not been determined experimentally whether LV dysfunction during anaphylaxis is induced mainly by reduced coronary blood flow (CBF) or direct negative inotropic actions of chemical mediators. To demonstrate the major role of CBF reduction in anaphylactic LV dysfunction, we determined LV contractility during anaphylaxis and forcible CBF reduction maneuver to reproduce the anaphylaxis-induced CBF reduction in isolated blood-perfused rat hearts.
Methods: Isolated hearts from Wistar rats in the ovalbumin-sensitized anaphylaxis, non-sensitized flow reduction, and non-sensitized time control group were subjected to coronary perfusion with blood at a constant pressure and measurements of CBF and LV pressure. Cardiac anaphylaxis was induced by intracoronary injections of ovalbumin antigen.
Results: In response to antigen administrations, sensitized anaphylaxis group rat hearts showed decreases in CBF and the maximum increasing rate of systolic LV pressure (dP/dtmax) with an increased coronary vascular resistance as evidence of coronary spasm. The non-sensitized flow reduction group rat hearts whose CBF was forcibly reduced as in anaphylaxis showed the same degree of dP/dtmax reduction.
Conclusions: The contractile failure during cardiac anaphylaxis is caused mainly by decreased CBF due to coronary spasm.
Keywords
anaphylactic shock, acute coronary syndrome, coronary blood flow, left ventricular contractility, cross-circulation method
About this articleTitle
Major contribution of vasospasm-induced coronary blood flow reduction to anaphylactic ventricular dysfunction assessed in isolated blood-perfused rat heart
Journal
Issue
Pages
11-17
Published online
2013-04-26
Page views
1475
Article views/downloads
1371
DOI
10.5603/CJ.a2013.0047
Bibliographic record
Cardiol J 2014;21(1):11-17.
Keywords
anaphylactic shock
acute coronary syndrome
coronary blood flow
left ventricular contractility
cross-circulation method
Authors
Yuhichi Kuda
Yasutaka Kurata
Mofei Wang
Mamoru Tanida
Toshishige Shibamoto
