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PubMed1989

Effects of amrinone on twitch, tetanus and shortening kinetics in mammalian skeletal muscle.

The contractile effects of amrinone were studied on twitch and tetanus responses of mouse lumbrical muscles. Amrinone (1.1 mM) increased the maximum force level during the tetanus, reduced the rate of rise of force during the onset of tetanus and prolonged the time from the last stimulus to half-relaxation. The rate of redevelopment of force after a release during the tetanus plateau was likewise reduced. Amrinone (greater than or equal to 0.5 mM) increased the time to peak twitch force and the time to half-relaxation during the twitch. The peak twitch force was not significantly changed. The force-velocity relation was markedly affected by amrinone: there was a decrease in maximum velocity of shortening, an increase in maximum isometric force and a decrease in curvature of the force-velocity relation. The results suggest that amrinone modulates the kinetic properties of the myosin cross-bridges by exerting a specific effect upon the myofilament system. The latter effects are mainly responsible for the contractile changes produced by amrinone in mouse skeletal muscle. Amrinone appears to have little effect on the metabolism of activator calcium in this particular preparation.

Amrinone↗
PubMed1982

Relaxant effects of amrinone upon pulmonary smooth muscle.

Amrinone, a cardiac positive inotropic agent, inhibited histamine-induced bronchoconstriction in a dose-related manner in dogs when administered intra-duodenally at doses ranging from 0.3 to 10 mg/kg. This bronchodilatory property of amrinone in vivo was confirmed in vitro: amrinone relaxed carbachol-induced contractions and it inhibited Ba2+- or histamine-induced contractions of guinea pig tracheas. When amrinone was examined for its inhibition of histamine contractions under modified Ca2+ availability, the EC25 and EC75 of amrinone were 76 and 8 times smaller, respectively, under conditions of intracellular rather than normal Ca2+ availability. The corresponding decreases for verapamil were 12,414 and 33 times. No meaningful changes in the potencies of amrinone or verapamil were seen when normal Ca2+ availability was changed to extracellular Ca2+ availability. These data suggest that verapamil, and partially amrinone, inhibit histamine-induced tracheal contractions by reducing the bioavailability of intracellular Ca2+.

Airway Resistance↗
PubMed1995

Amrinone increases ventricular contractility and diastolic compliance in endotoxemia.

Systolic and diastolic dysfunction occur during human septic shock, and sensitivity to beta-adrenergic agents is reduced. We sought to determine whether amrinone, an inotropic agent independent of beta-receptors, increases left-ventricular contractility or diastolic compliance after endotoxin infusion. We measured left-ventricular volume (using a conductance catheter) and pressure (using a Millar catheter) before and after administering amrinone (4.5 mg/kg i.v., then 10 micrograms/kg/min) to six endotoxemic and seven control pigs. The slope of the end-systolic pressure-volume relationship, Ees, was used as the primary measure of contractility. Diastolic stiffness was characterized using stiffness parameters taken from pressure-volume relationships (k) and from pressure-volume strain relationships. Amrinone increased Ees from a median of 10.4 mm Hg/ml (interquartile range, 7.2 to 12.3) to 16.4 (13.7 to 18.6) (p < 0.05) in the endotoxin group (p < 0.05). Amrinone decreased diastolic stiffness (k) in the endotoxin group by 35 +/- 18% (p < 0.05). Amrinone did not significantly change Ees or k in the control group. Mean arterial pressure decreased after endotoxin infusion from 117 +/- 23 mm Hg to 76.5 +/- 14.9 mm Hg (p < 0.05), and decreased further after amrinone to 62.0 +/- 14.8 mm Hg (p < 0.05). We conclude that in this model of sepsis, amrinone may beneficially increase systolic contractility and diastolic compliance, but may dangerously decrease an already low mean arterial pressure.

Amrinone↗
PubMed1993

Early administration of amrinone does not impair regional metabolism of O2 or lactate and, by improving myocardial performance, preserves myocardial blood flow in the ischemic canine heart.

The inotropic and vasodilating effects of amrinone can upset the balance of O2 supply and demand by changing those components in opposite directions simultaneously. We used a canine model of acute coronary artery occlusion to test our hypothesis that early administration of amrinone (before failure of the heart) would have beneficial effects on hemodynamic status and regional metabolism during ischemia, even before heart failure. Twenty dogs anesthetized with thiamylal were subjected to 50%, 75%, and 100% occlusion of the left anterior descending coronary artery. Half of the dogs were given a bolus injection of amrinone (0.75 mg/kg) 1-2 min before each occlusion, immediately followed by continuous infusion (10 micrograms.kg-1 x min-1) during occlusion; the other half did not receive amrinone (control). Hemodynamic and metabolic variables were measured in the ischemic area (the left anterior descending coronary artery) and in a nonischemic area (the circumflex vein). Amrinone not only decreased heart rate, left ventricular systolic and end-diastolic pressures, and mean pulmonary arterial pressure during constrictions but also maintained contractility, stroke volume index, and stroke volume index/left ventricular end-diastolic pressure before and during constrictions. Regional myocardial blood flow in ischemic areas decreased with amrinone during constrictions but was still higher than in untreated animals. Regional ischemic and nonischemic metabolic variables (metabolism of intracoronary potassium, CO2, O2, glucose, and lactate) were similar for both groups and changed to the same extent. Amrinone appears to improve left ventricular performance and increase blood flow to ischemic myocardium while not worsening regional metabolic effects during various grades of ischemia in the dog.

Amrinone↗
PubMed1998

[Effects of amrinone on renal blood flow and cardiac function, in comparison with those of milrinone and olprinone, in anesthetized dog].

Amrinone, one of the phosphodiesterase III inhibitors, is clinically used for acute heart failure and possesses diuretic action, which is not observed in other phosphodiesterase III inhibitors. To clarify the mechanism of the diuretic action of amrinone, we investigated its effects on renal blood flow and some other hemodynamic parameters in comparison with the effects of milrinone and olprinone in anesthetized dogs. Amrinone increased both renal and femoral blood flow in a dose-dependent manner. On the other hand, milrinone and olprinone increased only femoral blood flow and had no effect on renal blood flow. Amrinone, milrinone and olprinone dose-dependently increased left ventricular max dp/dt, and the estimated slope of the dose-response curve for olprinone was significantly sharper than that of amrinone. Furthermore, these three drugs increased the cardiac index and decreased systemic vascular resistance (SVR) significantly. The action of amrinone on SVR was more potent than those of milrinone and olprinone. These results suggest that the diuretic action of amrinone is involved in augmentation of renal blood flow and may support useful effects on acute heart failure.

Amrinone↗
PubMed1992

Calcium inhibits the cardiac stimulating properties of dobutamine but not of amrinone.

To contrast the effect of increasing blood calcium concentrations on the cardiovascular actions of intravenous beta-adrenergic agonists and phosphodiesterase inhibitors, 46 patients recovering from aortocoronary bypass surgery received either dobutamine or amrinone both in the presence and absence of a calcium infusion. Cardiac output, systemic arterial pressure, pulmonary arterial pressure, central venous pressure, pulmonary artery occlusion pressure, heart rate, and blood ionized calcium concentration were measured before and during infusions of dobutamine (2.5 and 5.0 micrograms/kg/min) and amrinone (0.75 mg/kg bolus + 10 micrograms/kg/min or 2.25 mg/kg bolus + 20 micrograms/kg/min). After the initial dobutamine infusion period, patients were randomly and blindly assigned to receive either a calcium or placebo infusion, and the dobutamine infusions were repeated. Because of the long duration of amrinone's actions, the amrinone maintenance infusion was continued while randomized, blinded infusion of either calcium or placebo was added. Dobutamine (5 micrograms/kg/min) increased cardiac output from 7.1 +/- 0.3 L/min to 9.1 +/- 0.4 L/min, and increased heart rate from 93 +/- 4 beats/min to 107 +/- 4 beats/min. Systemic vascular resistance decreased and stroke volume increased. Dobutamine had no significant effects on other hemodynamic values. Amrinone (2.25 mg/kg bolus + 20 micrograms/kg/min) increased cardiac output from 5.6 +/- 0.4 L/min to 6.9 +/- 0.5 L/min, and increased heart rate from 87 +/- 3 beats/min to 98 +/- 3 beats/min. Amrinone decreased mean arterial pressure, systemic vascular resistance, pulmonary artery occlusion pressure, central venous pressure, and pulmonary artery pressure. Calcium infusion increased arterial pressure (8 to 13 percent) but had no significant effects on any other hemodynamic parameters. Calcium reduced the increase in cardiac output produced by dobutamine by 30 percent, but it did not alter the cardiotonic actions of amrinone. Thus, calcium inhibits the cardiotonic actions of certain beta-adrenergic agonists, most likely by interfering with signal transduction through the beta-adrenergic receptor complex.

Amrinone↗
PubMed1992

Effect of amrinone on tumor necrosis factor production in endotoxic shock.

Tumor necrosis factor (TNF) is a macrophage-derived mediator responsible for many of the pathophysiologic manifestations of endotoxic shock. We now demonstrate that amrinone, a noncatechol inotrope, strongly inhibits lipopolysaccharide (LPS)-induced TNF production at concentrations readily achieved in vivo. This inhibition is apparent in murine macrophages, in macrophage cell lines, in vivo, and in cell lines containing a reporter gene construct that substitutes the chloramphenicol acetyl transferase (CAT) coding sequence for the TNF coding sequence and introns. Inhibition by amrinone (like inhibition by pentoxifylline) is manifested at the level of mRNA accumulation, in contrast to inhibition caused by dexamethasone. Combined application of dexamethasone and amrinone caused additive inhibition of TNF biosynthesis in vitro. Furthermore, treatment of mice with amrinone immediately prior to endotoxin challenge led to significantly improved survival. These findings suggest that amrinone possesses antiinflammatory as well as inotropic properties that may make it an appropriate agent for use in septic shock or other serious bacterial infections. Abrupt removal of amrinone or pentoxifylline from the culture medium prior to LPS stimulation, however, caused significantly augmented TNF production. Therefore, amrinone and other phosphodiesterase inhibitors may also enhance sensitivity to LPS during a period of time following discontinuation of therapy.

Amrinone↗
PubMedDate not supplied

Programmed electrical stimulation in conscious dogs: electropharmacologic testing of amrinone.

In order to assess possible proarrhythmic properties of amrinone, serial programmed electrical stimulation was performed via several previously implanted electrodes in 12 conscious dogs during the late reperfusion phase following experimental myocardial infarction. In 6 dogs, programmed electrical stimulation was carried out before and following the administration of amrinone (Wincoram) at cumulative doses of 0.3, 1 and 3 mg/kg, i.v., while the rest served as control group and received matching volumes of saline. Amrinone decreased atrioventricular refractoriness but did not alter ventricular refractory periods in both normal and infarct zones. Amrinone (3 mg/kg) substantially enhanced intraventricular conduction. Induction of ventricular arrhythmias was attempted only at base line and following 3 mg/kg of amrinone. Inducibility was unaltered by amrinone. However, in two experiments we observed more severe forms of arrhythmia to be inducible following drug administration. The number of extrastimuli necessary for the induction of arrhythmias was decreased in two cases during treatment. In the control group, neither the nature of induced arrhythmias nor the number of extrastimuli was changed. We conclude that, in our model, amrinone exerts a moderate proarrhythmic effect when assessed by programmed electrical stimulation. This arrhythmogenic property may be due to an enhancement of intraventricular conduction.

Amrinone↗
PubMed1988

Amrinone administration in endotoxin shock.

This study explored the hemodynamic effects of amrinone, a phosphodiesterase inhibitor, in association with intravenous fluids, in the treatment of endotoxin shock. Mongrel dogs were anesthetized with pentobarbital and mechanically ventilated with room air. Treatment was started 30 min after slow intravenous administration of 3 mg/kg of E. coli endotoxin. In the first part of the study, ten dogs were resuscitated for 30 min with intravenous saline alone (10 ml/kg) and for the next 3 h by saline (10 ml/kg/h) and amrinone 40 micrograms/kg/min. During this latter period, arterial pressure remained stable while cardiac output significantly increased from 3.1 +/- 0.5 to 5.2 +/- 0.7 l/min (P less than 0.01), and oxygen delivery increased from 616 +/- 92 to 983 +/- 156 ml/min (P less than 0.01). Comparison with control animals revealed that amrinone infusion prevented the decrease in left ventricular stroke work and markedly increased oxygen delivery. In the second part of the study, 18 dogs were treated by saline infusion titrated to maintain pulmonary artery balloon-occluded pressure at baseline level. In ten dogs, amrinone was added 60 min after endotoxin administration at a dose of 40 micrograms/kg/min. Total amount of fluids infused averaged 87 +/- 14 ml in the amrinone-treated dogs and 64 +/- 15 ml in the control dogs (differences nonsignificant). Oxygen delivery and oxygen consumption increased significantly in the amrinone-treated dogs (from 541 +/- 36 to 1063 +/- 176 ml/min, P less than 0.01, and from 145 +/- 23 to 202 +/- 38 ml/min, P less than 0.01, respectively) but not in the control dogs. The amrinone-treated dogs had lower PaO2 and higher venous admixture than the control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Amrinone↗
PubMed1995

[Hemodynamic effects of amrinone during emergence from cardiopulmonary bypass].

Amrinone, a phosphodiesterase III inhibitor, is known to exert inotropic and vasodilating effects. This study was undertaken to investigate the hemodynamic effects and optimal dose of amrinone in patients undergoing coronary artery bypass surgery. Seventeen patients with ejection fraction > 0.45 were included. In both group B and C, amrinone 0.5 mg.kg-1 was administered in the venous reservoir near the end of cardiopulmonary bypass (CPB), and doses of 1 and 5 micrograms.kg-1.min-1 by an intravenous infusion. Additional group of A did not receive amrinone. In group B, amrinone increased cardiac index by 79% and stroke index by 81% while decreased mean arterial pressure by 19% and systemic vascular resistance by 59% in comparison with group A. Heart rate did not increase. In group C, changes of hemodynamic variables were almost the same compared with group B. These data suggests that amrinone improves left ventricular performance without increasing myocardial oxygen demand while recovering from CPB. However, a high dose of amrinone should be used in combination with catecholamines because its vasodilating action is potentiated by hyperdynamic state after CPB.

Aged↗
PubMed1996

[Amrinone administration exerts no deleterious effect on platelet counts and blood transfusion volume during CABG].

The purpose of this study was to examine retrospectively the effect of amrinone on platelet counts and blood transfusion volume during CABG. Patients were divided into two groups. Amrinone group included 40 patients and for comparison another group included 33 patients who had undergone CABG without amrinone. Anesthesia and surgical procedures were standardized and similar for all patients. Platelet counts and hematocrit levels were measured in the arterial blood before CPB, at the end of CPB (after treatment with amrinone in amrinone group), 1 day, 3 days, and 7 days after surgery. Time course of changes in platelet counts was the same between the groups at the following points: before CPB, after CPB, 1 day, 3 days, and 7 days after surgery. We administered amrinone to patients who underwent CABG. The titrated dose of amrinone (about 29mg.kg-1) has not affected the time course of changes in platelet counts and blood transfusion volume.

Aged↗
PubMed1996

[Hemodynamic effects of amrinone, phosphodiesterase inhibitor, early after coronary artery bypass grafting].

This study was conducted to evaluate the hemodynamic effects of amrinone early after open-heart surgery. Eighteen patients who underwent coronary artery bypass grafting were randomly divided into two groups: ten patients (group A) were administered 5 micrograms/kg/min of amrinone, and eight patients (group B) were administered 10 micrograms/kg/min. No bolus of amrinone was administered before continuous infusion. The mean and systolic arterial pressure and systemic vascular resistance index were significantly decreased (p < 0.05) after infusion of amrinone in both groups. Cardiac index was not increased in group A, but was significantly increased in group B without increase in the double product. There were no significant changes in heart rate, mean pulmonary arterial pressure or pulmonary capillary wedge pressure in either group. Pulmonary vascular resistance index tended to decrease in either group. Transient hypotension after infusion of amrinone was a serious clinical problem. Of the eight patients with systemic vascular resistance index less than 2000 dyne*sec*cm-5*m2 before infusion, blood pressure decreased below 100 mmHg in five patients. Administration of amrinone was discontinued in two patients in group B and one patient in group A because of transient hypotension. In this study, continuous infusion of amrinone (10 micrograms/kg/min) had both positive inotropic and vasodilating properties; however, transient hypotension must be monitored carefully.

Aged↗
PubMed1997

[Effect of amrinone and vagotomy on airway constriction in dogs: analysis by respiratory system impedance method].

Amrinone, a selective phosphodiesterase III inhibitor, is a positive inotropic agent with vasodilating effect which is attributable to an increase in cyclic AMP in vascular smooth muscle. Little is known about the effect of amrinone on airway mechanics. The purpose of this study was to clarify the bronchodilating effect of amrinone in dogs, when bronchoconstriction was induced by methacholine infusion. We also evaluated the effect of amrinone on bronchoconstriction in vagotomized dogs. To evaluate the effect of amrinone on respiratory function, the total respiratory system impedance was measured using forced oscillation method by imposing a random noise. The analysis was performed by dynamic models and a second-order system curve fitting. From the study, we conclude that amrinone 0.5 mg.kg-1.1.0 mg.kg-1 or 2.0 mg.kg-1 attenuates methacholine-induced bronchoconstriction in a dose-related manner. In vagotomized dogs, amrinone also had the same effect on methacholine induced bronchoconstriction.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1997

Effect of amrinone on murine viral myocarditis.

Management of acute viral myocarditis is still controversial. Amrinone, a noncatecholamine nonglycoside bipyridine agent, produces sustained improvement of cardiac function and symptomatology in congestive heart failure (CHF). Amrinone demonstrates phosphodiesterase inhibitory activity that is relatively selective for the major phosphodiesterase isozyme in cardiac muscles, PDE III, which specifically hydrolyzes cyclic 3'5' adenosine monophosphate (cAMP). We investigated the effects of amrinone in an animal model of acute CHF related to myocarditis caused by the encephalomyocarditis virus (EMCV). Female C3H mice were inoculated intraperitoneally (i.p.) with 500 plaque-forming units of EMCV in 0.1 ml of saline. A total of 96 mice were randomly assigned to four groups. Each animal was administered 0.2 ml of phosphate-buffered saline (PBS) containing amrinone at a concentration of 1, 10, or 50 mg/kg, or PBS as an infected control, injected i.p. once daily for 21 days, starting on day 1 after viral inoculation. Each group contains 20 to 30 mice. Infected untreated mice survived at 80% (n = 16), however, only 13% (n = 16) of mice treated with amrinone (50 mg/kg) survived (p < 0.01). Downregulation of cardiac cAMP occurred 1 day after the viral infection. Although amrinone (10 and 50 mg/kg) treatment significantly (p < 0.05) increased the cardiac cAMP content and the dose of 10 mg/kg could potentially retard death from CHF due to viral myocarditis. The higher (50 mg/kg) doses of amrinone may produce unfavorable effects when used to treat mammals with viral myocarditis and CHF.

Acute Disease↗
PubMed1997

The cardiac effects of pimobendan (but not amrinone) are preserved at rest and during exercise in conscious dogs with pacing-induced heart failure.

We compared the effects of pimobendan (0.25 mg/kg i.v.), a Ca++ sensitizer, with some phosphodiesterase-III inhibition effects, and amrinone (1 mg/kg plus 10 microg/kg/min i.v.), a PDE-III inhibitor, on left ventricular (LV) systolic and diastolic performance, both at rest and during exercise, in seven conscious dogs before and after pacing-induced congestive heart failure (CHF). Before CHF, under resting conditions, both pimobendan and amrinone caused a similar significant decrease in left ventricle size and end-systolic pressure, arterial elastance, and the time constant of LV relaxation. Similar results were obtained during exercise. Both agents also produced a similar increase in E(ES), the slope of the LV end-systolic pressure-volume relation (3.4 +/- 1.5 vs. 4.2 +/- 1.1 mm Hg/ml; amrinone vs. pimobendan). After CHF, the vasodilatory effects of amrinone and pimobendan were preserved both at rest and during exercise; however, the inotropic actions were different. After CHF, pimobendan increased E(ES) (3.9 +/- 0.5 vs. 5.7 +/- 0.4 mm Hg/ml, P < .05), decreased the time constant of LV relaxation, increased the maximum rate of LV filling (37 +/- 19 ml/sec) (P < .05) and produced a downward shift of the early diastolic portion of LV pressure-volume loop. Pimobendan also augmented LV contractile performance during CHF exercise. In contrast, after CHF, amrinone no longer produced a positive inotropic effect. Amrinone improved LV relaxation and filling, both at rest and during exercise after CHF, but significantly less than pimobendan. We conclude that after CHF, the cardiac response to a PDE-III inhibitor is attenuated, but the response to Ca++ sensitizer is preserved. Thus, after CHF, pimobendan is more effective than amrinone in enhancing LV contractile state, LV relaxation and LV filling both at rest and during exercise.

Amrinone↗
PubMed1988

The effects of amrinone, cyclophosphamide and anti-platelet serum on platelet production in the Gunn rat.

The effect of amrinone on platelet production was differentiated from that of a known bone-marrow cytotoxic agent (cyclophosphamide) and anti-platelet serum (APS). The rate of platelet production has been observed over a 4-day period in the Gunn rat using [75Se]selenomethionine cohort labelling of platelets following administration of either amrinone, 160 mg kg-1 day-1, cyclophosphamide, 30 mg kg-1 day-1 or APS, 0.75 ml. Platelet numbers were reduced by amrinone, cyclophosphamide and APS. The rate of platelet production was increased following APS and suppressed by cyclophosphamide, but the rate of platelet production when expressed as the selenomethionine incorporation in counts per minute (cpm) per 10(8) platelets appeared to be increased in amrinone-treated animals. When these values are expressed as radioactivity per unit platelet volume the difference between the control and the amrinone-treated group was reduced but the difference between the control, APS- and cyclophosphamide-treated groups remained unchanged. It is concluded that in the Gunn rat amrinone affects platelet production by producing fewer, larger platelets.

Amrinone↗
PubMed1995

Elimination of amrinone during continuous veno-venous haemofiltration after cardiac surgery.

We studied the elimination of amrinone during continuous veno-venous haemofiltration (CVVHF) in three anuric patients after cardiac surgery. The patients had developed low cardiac output followed by acute prerenal failure. Plasma amrinone levels measured by HPLC were fitted to a two-compartment model. We found significant amrinone clearance, with a mean sieving coefficient (S) of 0.44%, which correlates with the protein-unbound, pharmacologically effective fraction of amrinone. The AUC of the arterial plasma concentration-time curve was decreased by 49.8%. All pharmacokinetic parameters showed wide interindividual variation. To ensure the therapeutic effect of amrinone and to avoid toxic adverse effects monitoring of plasma amrinone levels is necessary.

Amrinone↗
PubMed1993

Amrinone, in combination with norepinephrine, is an effective first-line drug for difficult separation from cardiopulmonary bypass.

A crucial element for weaning patients from cardiopulmonary bypass (CPB) rests on the selection of an appropriate therapeutic regimen. Amrinone, a phosphodiesterase III inhibitor, combines inotropic support with pulmonary and systemic vasodilatation, without increasing heart rate (HR) or myocardial oxygen consumption. These characteristics should be useful in the failing heart during weaning from CPB. Nineteen patients were included in this prospective, open-labelled, phase IV study when systolic blood pressure (DPAP) > 15 mmHg or central venous pressure (CVP) > 15 mmHg, during progressive separation from CPB. At that moment, CPB flow was increased to alleviate heart failure and amrinone administered as a bolus (0.75 mg.kg-1) followed by an infusion (10 micrograms.kg-1.min-1). Weaning from CPB was then resumed and haemodynamic variables (SBP, DPAP, CVP and HR) were compared with those measured at CPB flow when failure had first occurred. Failure to wean from CPB occurred at 57 +/- 28% of full pump flow. After the amrinone bolus, DPAP and CVP decreased by 20% and 21% respectively. Subsequently, 16 patients required the infusion of norepinephrine (4-8 micrograms.min-1) to maintain a SBP > 80 mmHg. Heart rate remained unchanged after the bolus of amrinone, after separation from CPB, and no arrhythmias were noted. Successful weaning from CPB was possible 12 +/- 8 min after the amrinone bolus. Weaning resulted in a cardiac index similar to that measured pre-bypass. Amrinone is rapidly effective during weaning from CPB and, in combination with norepinephrine, provides the necessary inotropic support during this unstable period.

Aged↗