Key result
Forcible reduction of coronary blood flow in isolated rat hearts produced the same degree of left ventricular contractile failure as ovalbumin-induced anaphylaxis, demonstrating that anaphylactic ventricular dysfunction is primarily caused by coronary spasm.
Why the study?
Does forcible coronary blood flow reduction reproduce the left ventricular dysfunction seen in cardiac anaphylaxis in isolated rat hearts?
Does forcible coronary blood flow reduction reproduce the left ventricular dysfunction seen in cardiac anaphylaxis in isolated rat hearts?
Contractile failure during cardiac anaphylaxis is primarily caused by decreased coronary blood flow due to coronary spasm rather than direct negative inotropic effects of chemical mediators.
Coronary spasm may mediate anaphylactic LV dysfunction in isolated rat hearts; leaves open relevance to human anaphylaxis and clinical practice.
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.
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Kuda et al. (2013) studied Cardiac anaphylaxis (n=21). Forcible coronary blood flow reduction vs. Ovalbumin-induced anaphylaxis was evaluated on Maximum increasing rate of systolic LV pressure (dP/dtmax). Forcible reduction of coronary blood flow in isolated rat hearts produced the same degree of left ventricular contractile failure as ovalbumin-induced anaphylaxis, demonstrating that anaphylactic ventricular dysfunction is primarily caused by coronary spasm.
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