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At least 145 records · Page 8Linked to original sources
PubMed1987

Cardiovascular effects of a new phenoxyalkylamine derivative, 2-isopropyl-5-[3-(2-methoxyphenoxy)propylamino]-2-(3,4,5-trimethoxy phenyl) valeronitrile fumarate (HV-525), in cross-circulated dog atrial preparations.

A newly developed phenoxyalkylamine derivative, 2-isopropyl-5-[3-(2-methoxyphenoxy)propylamino]-2-(3,4, 5-trimethoxyphenyl)-valeronitrile fumarate (HV-525), was investigated in intact dogs and in isolated dog atria perfused with anesthetized donor dog's arterial blood. When 0.3 mg/kg of HV-525 was intravenously administered to the donor dog, a depressor effect without significant changes in heart rate was observed in donor dogs and a decrease in developed tension was observed in the isolated atrium. At 1 mg/kg, HV-525 caused a depressor response in donor dogs and decreases in developed tension and atrial rate in isolated atria. The decrease in systemic blood pressure seen following 1 mg/kg of HV-525 was between 15-40 mmHg. These effects continued for about 60 min. When HV-525 was administered into the cannulated sinus node artery of the isolated atrium, dose related negative inotropic and chronotropic actions were observed. Occasionally, HV-525 induced slight, brief positive chronotropic and inotropic effects followed by long-lasting negative effects. The threshold dose for inducing the negative chronotropic effect was approximately 3 micrograms while the negative inotropic one was approximately 1 microgram. A large dose of 100 micrograms of HV-525 caused a profound deceleration but not atrial arrest. The order of potencies for inducing a negative chronotropic effect in dog atria was verapamil greater than propranolol much greater than HV-525 greater than or equal to lidocaine greater than or equal to quinidine greater than phenytoin greater than disopyramide greater than procainamide, and that for inducing a negative inotropic effect was verapamil greater than or equal to propranolol greater than HV-525 greater than lidocaine greater than phenytoin greater than disopyramide greater than procainamide greater than or equal to quinidine. HV-525 did not induce a significant effect on sinoatrial conduction time. HV-525 at the doses studied, uniformly suppressed the frequency-force relationship, while verapamil, one of the phenoxyalkylamine derivatives, caused a marked depression of high frequency-induced contraction. Thus, it is concluded that HV-525 has mild depressant properties on the cardiovascular system and may have characteristics different from those of verapamil.

Animals↗
PubMed1988

Interaction between diltiazem and halothane or enflurane in the canine blood-perfused papillary muscle and sinoatrial node preparations cross-circulated by chronically instrumented conscious donor dog.

Interaction of cardiovascular effects of diltiazem with those of halothane or enflurane was estimated in the canine isolated papillary muscle and sinoatrial node preparations perfused by arterial blood of the chronically instrumented conscious and halothane- or enflurane-anesthetized donor dog, into which diltiazem was infused i.v. at a rate of 20 micro g/kg/min for 60 min. One hour after diltiazem infusion, in the conscious donor dog, mean arterial pressure (MAP) and heart rate (DHR) were decreased to 84 +/- 3 and 84 +/- 2% and PQ interval (PQ) was prolonged to 148 +/- 5%, while in the isolated preparations, developed tension (DT) of the papillary muscle and sinoatrial rate (SAR) were decreased to 68 +/- 3 and 74 +/- 3% and blood flow (BF) was increased to 155 +/- 5% (n = 10). On the other hand, halothane (0.8%) anesthesia per se decreased MAP, DHR, DT and SAR to 89 +/- 8, 84 +/- 3, 79 +/- 3 and 89 +/- 5% (n = 7) of each basal value in conscious state 20 min after the inhalation. During halothane anesthesia, the same dose of diltiazem infused decreased MAP to 74 +/- 4 (n = 7), DHR to 66 +/- 4 (n = 6), DT to 62 +/- 7 (n = 7) and SAR to 69 +/- 1% (n = 3) of each value suppressed by halothane itself. Meanwhile, enflurane (1.7%) anesthesia itself decreased MAP, DHR, DT and SAR to 81 +/- 3, 85 +/- 2, 81 +/- 2 and 88 +/- 2% (n = 10) of each basal value in conscious state 30 min after enflurane inhalation. During enflurane anesthesia diltiazem decreased MAP to 74 +/- 3 (n = 10), DHR to 67 +/- 3 (n = 8), DT to 45 +/- 5 (n = 10) and SAR to 74 +/- 6% (n = 3) of each value under enflurane anesthesia alone. PQ interval of the donor dog heart was prolonged by halothane alone to 111 +/- 5% (n = 7) and by enflurane alone to 110 +/- 2% (n = 10) of the value before each anesthesia, and then diltiazem prolonged PQ interval to 160 +/- 8% (n = 6) and 174 +/- 10% (n = 8) of each value suppressed by the anesthetic itself during halothane- or enflurane-anesthesia, respectively. The second degree AV conduction block was induced in 1 of 7 halothane- and in 2 of 10 enflurane-anesthetized donor dogs, respectively. The sinus arrest was induced by diltiazem in 4 of 7 sinoatrial node preparations under halothane and in 7 of 10 ones during enflurane anesthesia. Moreover, plasma concentration of diltiazem 60 min after the start of infusion was 556 +/- 121 ng/ml in conscious dogs and tended to increase to 752 +/- 101 ng/ml in enflurane anesthetized donor dogs (n = 4), but there was no significant difference between two values (0.05 < P < 0.1). These results indicate that effects of diltiazem could be potentiated during halothane or enflurane anesthesia by elimination of compensatory reflex noted in conscious state, and that the negative inotropic effect of diltiazem was enhanced by enflurane anesthesia due to unknown mechanisms which probably include a slight but insignificant increase in plasma concentration.

Journal Article↗