Summary
Effect of Verapamil (V) on impulse conduction in the acutely ischemic myocardium was tested in ten dogs (5 control and 5 treated) after ligation of left anterior descending artery (LAD). In the treated group V was given 0.15 mg/kg IV bolus at a rate of 2 mg/min immediately after LAD occlusion and was followed by an IV infusion at a dose of 7.5 μg/kg/min. In each dog, LAD was ligated below the second diagonal initially and 30 min later below the first diagonal. From multiple needle electrodes, endocardial bipolar (0.5 mm apart) electrograms (40–500 Hz 10 mm = 0.5 mV) were recorded prior to ligation and at 5, 15, and 30 min after each LAD occlusion. Constant rate atrial pacing (200/min.) was performed and premature stimuli were delivered at fixed coupling (50%) intervals. Conduction times (defined as the interval from premature pacing stimulus to the earliest high frequency deflection in the endocardial electrograms) were measured within the ischemic zone and within normal zone in both groups of dogs. Results showed that (1) prior to LAD ligation, the conduction within the normal myocardium was similar between the control and V treated groups of dogs; (2) following LAD ligation, conduction within the ischemic zone slowed significantly in the control group of dogs; (3) in the V treated dogs, conduction within the ischemic zone did not alter from the pretreatment values and was significantly different to the corresponding values in the control group. We conclude that post occlusion intravenous verapamil prevents deterioration of impulse conduction that normally occurs as a result of acute ischemia. This observation suggests a possible new mechanism of antiarrhythmic action of verapamil in acute ischemia and that a racemic mixture of verapamil may possess more than simple calcium antagonistic properties.
Zusammenfassung
Wir prüften die Wirkung von Verapamil (V) auf die Reizleitungszeit innerhalb des akut ischämischen Myokards bei 10 Hunden (5 Kontrollgruppe, 5 behandelt mit V) nach Unterbindung des RIVA. Verapamil wurde in einer Dosis von 0,15 mg/kg intravenös als Bolus, unmittelbar nach Koronarverschluß bei 5 Hunden verabreicht; anschließend wurde eine Dosis von 7,5 μg/kg/Min infundiert. Die Unterbindung des RIVA erfolgte in zwei Stufen: in einer ersten Phase distal vom 2. R. diagonalis und in einer zweiten Stufe 30 Min später distal vom 1. R. diagonalis. Endokardiale bipolare Elektrokardiogramme wurden mittels mehrerer Nadelelektroden vor sowie 5, 15 und 30 Min nach jeder Unterbindung aufgezeichnet. Die Untersuchung wurde bei konstanter Vorhofstimulation (200/Min) und vorzeitigen Stimuli mit einem Kopplungsintervall von 50% durchgeführt. Die Reizleitungszeit (definiert als der Zeitintervall zwischen der vorzeitigen Schrittmacherstimulation und der ersten hochfrequenten Schwingung im endokardialen EKG) wurde im ischämischen sowie normalen Muskelareal beider Untersuchungsgruppen gemessen. Ergebnis: (1) Vor Koronarverschluß war die Reizleitungszeit innerhalb des normalen Myokardiums bei beiden Untersuchungsgruppen gleich. (2) Nach Verschluß des RIVA verzögerte sich die Reizleitungszeit signifikant innerhalb des ischämischen Areals bei der Kontrollgruppe. (3) In der mit Verapamil behandelten Gruppe unterschied sich die Reizleitungszeit innerhalb des ischämischen Myokards nicht signifikant von Werten vor dem Koronarverschluß. Dies war signifikant unterschiedlich von Werten in der Vergleichsgruppe.
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Peter, T., Hamamoto, H., McCullen, A., Yamaguchi, I., Mandel, W.J. (1980). Verapamil Effects in the Setting of Acute Experimental Myocardial Ischemia. In: Fleckenstein, A., Roskamm, H. (eds) Calcium-Antagonismus. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-67595-9_8
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DOI: https://doi.org/10.1007/978-3-642-67595-9_8
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