Characterization and Modulation of Antigen-Induced Effects in Isolated Rat Heart

Major Contribution of Vasospasm-Induced Coronary Blood Flow Reduction to Anaphylactic Ventricular Dysfunction Assessed in Isolated Blood-Perfused Rat Heart

“…As mentioned above, anaphylactic LV dysfunction was not persistent but only transient, with LV function completely recovering within 10 min along with CBF recovery, whereas the previous experimental studies using crystalloid perfusion reported incomplete recovery of LV contractility during cardiac anaphylaxis for longer periods (~60 min) of measurements [10,11]. This inconsistency may be at least in part related to the difference in perfusate, i.e., blood vs. crystalloid: the use of more physiological perfusate of blood might enhance the release of chemical mediators or modulators to yield coronary vasodilation and/or positive inotropic effects.…”

“…Following the baseline measurements, the antigen (ovalbumin 1.2 mg) dissolved in 300 μL saline was administered into the coronary artery, which yielded the forcible constriction of the left coronary Yuhichi Kuda et al, Cardiac contractility and coronary flow during anaphylaxis artery (main trunk) only in the sensitized hearts. Direct injection of the antigen ovalbumin into coronary arteries of isolated sensitized rat hearts is a well-established experimental method to create rat cardiac anaphylaxis models efficiently [10,11]. The variables were continuously measured for 10 min after the antigen administration.…”

“…Allergic activation of cardiac must cells is known to be of particular importance as a cause of the acute coronary syndrome, which is called "Kounis syndrome" [9]. Anaphylaxis-induced coronary vasoconstriction and cardiac dysfunction have also been demonstrated experimentally [10,11]: in excised rat hearts, ovalbumin-induced anaphylaxis caused cardiac dysfunction characterized by the decreases in the systolic LV pressure (LVP) and the maximum incre-asing rate of LVP (dP/dt max ) along with coronary vasoconstriction. These findings strongly suggest that coronary vasoconstriction-induced myocardial ischemia and reduced LV contractility are involved in the pathogenesis of anaphylactic shock.…”

Latex anaphylaxis causing heart block: role of ranitidine

“…1,6 In the guinea pig, the onset of cardiac rhythm changes occurs approximately 20 sec after antigenic challenge, at the same time as the initial change in blood pressure, and immediately before the anaphylactic increase in bronchial resistance. 1 In man, anaphylactic reactions have been accompanied by electrocardiographic changes, including cardiac arrhythmias, heart block, and acute myocardial infarction and cardiac failure, which may occur without preceding respiratory distress which might otherwise be the cause of secondary cardiac symptoms, z Histamine induces atrioventricular conduction delay and constriction of epicardial coronary vessels by stimulating H~ receptors, and H 2 receptor stimulation mediates coronary vasodilatation and an increase in heart rate and myocardial contractility.…”

Induction of Cardiovascular Anaphylaxis and Basic Pharmacological Analysis of Involved Mediators in Pithed Rats

“…In contrast, Sprague-Dawley rats have been utilized to a limited extent in allergy-related experiments: the reason for this may be related to the relative instability of reproducible antigen-antibody reactions in this strain. Wistar rats, in contrast, predominantly have been used as the standard strain for this purpose (Church, 1975;Gomes et al, 1994;Kamei et al, 1993;Katayama et al, 1978;Misawa, 1988;Vleeming et al, 1991).…”