
Effects of Polyamines on Ethylmorphine N-Demethylation in Rat Liver Microsomes
Author(s) -
Haruaki Nakaya,
Yoshiyuki Hattori,
Morio Kanno
Publication year - 1980
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.30.587
Subject(s) - ischemia , anesthesia , verapamil , medicine , lidocaine , occlusion , cardiology , coronary occlusion , calcium
Effects of calcium antagonists and lidocaine on the conduction delay observed in the ischemic myocardium were studied in 24 open-chest anesthetized dogs. Acute myocardial ischemia was produced by complete occlusion of the left anterior descending coronary artery (LAD) for 5 to 10 minutes. The conduction time was measured from the initial deflection of V waves on the His bundle electrograms to the major deflection of the bipolar electrograms recorded from the ischemic and non-ischemic subepicardium under a constant atrial pacing. LAD occlusion produced conduction delay in the ischemic zone (14.3 +/- 2.3 msec, p less than 0.001) with no effect on the normal zone. This ischemia-induced conduction delay was reversible and rate-dependently increased. Administration of lidocaine (2 mg/kg bolus, 4.3 mg/kg/hr constant infusion) prior to the second occlusion increased conduction delay by 12.9 +/- 1.9 msec (p less than 0.001) whereas diltiazem (0.4 mg/kg i.v.) and verapamil (0.3 mg/kg i.v.) reduced the ischemia-induced conduction delay by 12.7 +/- 4.9 msec (p less than 0.05) and 8.4 +/- 1.8 msec (p less than 0.001), respectively. These results indicate that slow channel blocking agents reduce the conduction delay induced by the myocardial ischemia, in contrast with the prolonging effect of lidocaine.