Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Amrinone”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1992

Effects of Amrinone on shortening velocity, force development and ATPase activity of demembranated preparations of rat ventricular myocardium.

This study analyses the effects of Amrinone (bipyridine derivative with phosphodiesterase inhibitor properties) on the myofibrillar apparatus of rat myocardium. Thin trabeculae were isolated from the right ventricle and chemically demembranated. Force development and shortening velocity were measured during maximal calcium activations (pCa = 4.45) in control conditions and in the presence of 1-3 mM Amrinone. Maximum shortening velocity was obtained both from extrapolation of the force-velocity curve and with the slack test method. Amrinone was found to significantly reduce maximum shortening velocity and force development. Myofibrils and myosin were prepared from rat ventricular myocardium and their ATPase activity was assessed in control conditions and in the presence of Amrinone (0.3-6 mM). Ca-Mg dependent myofibrillar ATPase activity which was determined at low ionic strength was depressed by Amrinone in a dose-dependent way. Ca-stimulated ATPase activity determined at high ionic strength in myofibril or myosin preparations was not affected. Furthermore, Amrinone did not influence the pCa-ATPase activity curve of the myofibrillar preparations. A comparison between the inhibitory effects of Amrinone on myofibrils prepared from euthyroid rats and myofibrils prepared from hypothyroid rats was carried out. The ATPase activity was significantly less depressed in myofibrils prepared from hypothyroid rats than in those prepared from euthyroid rats. These results provide the first evidence of an effect of Amrinone on ATP splitting and force generation in the myofilament system of cardiac muscle.

Adenosine Triphosphatases↗
PubMed1994

Effect of intracoronary infusions of amrinone and dobutamine on segment shortening, blood flow, and oxygen consumption in in situ canine hearts.

Previous in vivo studies assessing the effects of amrinone on myocardial contractility used intravenous infusions, and thus were complicated by varying cardiac loading conditions. Accordingly, the present study was performed in 15 open-chest, anesthetized (fentanyl and midazolam) dogs using infusions of amrinone and dobutamine directly into the left anterior descending artery (LAD). In the LAD bed, percentage of segment shortening (%SS), an index of local myocardial contractility, was assessed with ultrasonic crystals. Coronary blood flow was measured electromagnetically and used to calculate myocardial oxygen consumption and infused drug concentrations. Amrinone and dobutamine were infused separately into the LAD at rates yielding calculated arterial blood concentrations in the clinical range (100, 150, and 200 micrograms/min, and 2.5, 5.0, and 7.5 micrograms/min, respectively). A mixture of amrinone and dobutamine was also infused into LAD and changes in %SS compared with the sum of the their individual effects. In six of the dogs, an extracorporeal system was used to maintain constant coronary blood flow during amrinone infusions. Amrinone and dobutamine caused individually increases in %SS that were comparable (range, 20%-45%). Myocardial oxygen consumption increased in parallel with %SS for both amrinone and dobutamine. For amrinone, coronary blood flow increased more than myocardial oxygen consumption, resulting in a modest (at highest dose approximately 10%) decrease in oxygen extraction; whereas for dobutamine, coronary blood flow increased in proportion to myocardial oxygen consumption, resulting in no change in oxygen extraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Amrinone↗
PubMed1998

[Effects of amrinone, an inhibitor of c-AMP-specific phosphodiesterases, on neointimal hyperplasia after balloon injury in rats].

Amrinone(5-amino(3,4'-bibyridin)6-(1H)-one), an inhibitor of c-AMP-specific phosphodiesterases, has been used clinically as an inodilator. We have investigated the effect of amrinone on neointimal hyperplasia in rat carotid artery after balloon injury. When amrinone was administered subcutaneously to rats at a dose of 10 mg/kg/day for 14 days, significant reduction of neointimal thickness was noted. Four days treatment with amrinone, however, failed to reduce the intimal thickness. To investigate the mode of action to reduce intimal thickness, we tried to study the effects of amrinone on platelet aggregation and the proliferation of aortic smooth muscle cells. Amrinone produced a dose-dependent inhibition of ADP-induced rat platelet aggregation in vitro as well as ex vivo in rats. The proliferation of human aortic smooth muscle cells in culture stimulated with FBS or PDGF was also inhibited by amrinone. These results indicate that amrinone may have potential to prevent vascular neointimal hyperplasia in clinical balloon injury through inhibition of vascular smooth muscle cell growth and platelet aggregation.

Amrinone↗
PubMed1995

Comparative vasoactive effects of amrinone on systemic and pulmonary arteries in rabbits.

Amrinone has been increasingly used in management of low cardiac output syndrome during anesthesia, particularly when associated with right heart failure and pulmonary hypertension. This in vitro study was performed to determine and compare the direct vasoactive effects of amrinone on isolated rabbit systemic and pulmonary arteries. Responses of aortic and pulmonary artery rings from New Zealand white rabbits were assessed in the presence and absence of intact endothelium and with or without precontraction by norepinephrine (NE, 3 x 10(-6)M) or potassium chloride (KCl, 3 x 10(-2)M). Using a tissue bath preparation, cumulative concentration response curves of amrinone were obtained at different concentrations after a period of stabilization. Amrinone caused a dose-related vasodilation of NE-precontracted aortic and pulmonary arteries. It elicited about 65% and 90% relaxation, respectively, at a concentration of 300 mumol/L. Amrinone also induced a dose-related vasodilation of KCl-precontracted aortic and pulmonary arteries but to a lesser degree. All these effects were endothelium independent. By comparison, amrinone caused more relaxation in both NE- and KCl-precontracted pulmonary artery than aortic rings. In conclusion, amrinone has significant endothelium-independent, direct vasodilatory effects on isolated rabbit systemic and pulmonary arteries, more pronounced in the latter, particularly NE-precontracted vessels. Amrinone may have some calcium channel-blocking effect.

Amrinone↗
PubMed1991

Effects of amrinone on cardiac index, venous oxygen saturation and venous admixture in patients recovering from cardiac surgery.

The hemodynamic and oxygen transport effects of low-dose (0.75 mg/kg loading dose + 10 micrograms/kg/min infusion, n = 12) and high-dose (2.25 mg/kg loading dose + 20 micrograms/kg/min infusion, n = 12) amrinone were evaluated in extubated patients 24 h after CABG. At both doses, amrinone significantly (p less than 0.05) increased HR, but decreased mean arterial, mean pulmonary artery, central venous and pulmonary artery occlusion pressures. High-dose amrinone significantly decreased systemic vascular resistance. Arterial oxygen saturation decreased significantly following both low- (97.8 +/- 0.4 to 95.6 +/- 0.9 percent) and high- (98.8 +/- 3.4 to 93.9 +/- 1.2 percent) dose amrinone. Pulmonary shunt increased significantly following low-dose amrinone and markedly increased Qs/Qt after high-dose amrinone. Although amrinone significantly increased cardiac index in a dose-dependent fashion (low:3.0 +/- 0.2 to 3.3 +/- 0.3 L/min/m2; high:2.7 +/- 0.2 to 3.4 +/- 0.2 L/min/m2), mixed venous oxygen saturation did not change. Thus, mixed venous oxygen saturation may not predict the hemodynamic response to amrinone infusion in postoperative surgical patients.

Amrinone↗
PubMed1983

Amrinone dilates pulmonary vessels and blunts hypoxic vasoconstriction in isolated rat lungs.

The direct effects of the cardiotonic agent amrinone (WIN 40680) on pulmonary vasoreactivity were studied in isolated, blood-perfused, rat lungs. Lungs were perfused at constant flow and ventilated with normoxic gas, while mean pulmonary arterial pressure was monitored. Pressor responses to hypoxic gas (3% O2, 5% CO2) and angiotensin II (0.25 microgram/0.1 ml) were elicited after amrinone or saline was added to the perfusate. Pressor responses were blunted when calculated amrinone perfusate concentration was increased to 10 micrograms/ml. Pressor responses to hypoxia fell from 8 +/- 1 mm Hg (mean +/- SE, n = 8) before, to 2 +/- 1 mm Hg after amrinone (10 micrograms/ml), while responses to angiotensin II fell from 7 +/- 1 to 3 +/- 1 mm Hg (n = 8). Pressor responses in saline controls did not change. Pulmonary arterial pressure dropped within minutes following injection of amrinone (300 micrograms) into the pulmonary arterial cannula, with a greater drop during hypoxia than during normoxia. Meclofenamate did not prevent blunting of pressor responses by amrinone. Amrinone is a rapidly acting vasodilator which blunts vasoconstriction due to hypoxia or angiotensin II. Since it combines cardiotonic and pulmonary vasodilator actions, amrinone may have therapeutic potential for patients with cor pulmonale and pulmonary hypertension.

Aminopyridines↗
PubMed1987

Amrinone blunts cardiac depression caused by enflurane or isoflurane anesthesia in the dog.

The effects of two infusion rates of amrinone, a positive inotrope and vasodilator, were studied during high and low concentrations of either enflurane or isoflurane anesthesia in a canine model. The anesthetic concentrations used were: "low" = 2.1-2.2% enflurane or 1.7-1.8% isoflurane, and "high" = 3.4-3.5% enflurane or 3.0-3.1% isoflurane. The two infusion rates of amrinone were: "low" = 2 mg/kg plus 30 micrograms X kg-1 X min-1 and "high" = 4 mg/kg plus 100 micrograms X kg-1 X min-1. In the present study, amrinone, in sufficient doses, blunted the deleterious effects of enflurane or isoflurane on myocardial function, reduced systemic vascular resistance (SVR) and pulmonary capillary wedge pressure, restored left ventricular dP/dtmax (LVdP/dtmax), and maintained cardiac index, even at the high concentrations of enflurane or isoflurane that caused marked cardiac depression. However, with reduced SVR, mean arterial pressure remained low. With lower enflurane or isoflurane, high concentrations of amrinone elevated LVdP/dtmax and heart rate above baseline, which might be of concern if myocardial oxygen supply were limited. No arrhythmias were observed at any time in this study. Amrinone did not increase plasma catecholamine levels with either anesthetic. Elevated amrinone plasma concentrations persisted for at least 1 hr after cessation of the high amrinone infusion and continued stimulatory effects on the cardiovascular system were observed. These results suggest that in selected patients amrinone may be beneficial in the short-term treatment of perioperative depression of cardiac performance.

Amrinone↗
PubMed1986

The effects of amrinone and related drugs on intracellular calcium in isolated mammalian cardiac and vascular smooth muscle.

The effects of amrinone and related agents were studied in mammalian cardiac and vascular smooth muscle preparations loaded intracellularly with aequorin, a bioluminescent calcium indicator that emits light when it combines with Ca++. In cat papillary muscles, the effects of amrinone on the amplitude and time course of the aequorin light signal, as they relate to changes in uptake and release of calcium from the sarcoplasmic reticulum and to changes in the sensitivity of the myofilaments to Ca++, were consistent with reports that, in positive inotropic doses, the predominant action of amrinone is to increase intracellular concentrations of cyclic AMP. However, amrinone also produced dose-related caffeine-like effects on the aequorin light signal, suggesting additional subcellular actions. The positive inotropic effects of amrinone were most pronounced at low frequencies of stimulation (0.01 to 0.25 Hz) and were nearly obliterated at more physiologic heart rates (0.5 to 1.25 Hz). Toxic doses of amrinone were associated with development of a Ca++-overload state characterized by the presence of afterglimmers, aftercontractions, and arrhythmias. Amrinone's relaxant effect on ferret aortic and portal vein strips was associated with a corresponding decrease in intracellular Ca++ levels, and minimally effective relaxant doses were 10 to 100 times lower than positive inotropic doses reported for ferret heart. The vascular effects of amrinone were different from other agents known to increase intracellular cyclic AMP concentrations, suggesting multiple subcellular actions.

Actin Cytoskeleton↗
PubMed1985

Amrinone effects on electromechanical coupling and depolarization-induced automaticity in ventricular muscle of guinea pigs and ferrets.

The effects of the cardiotonic agent, amrinone (0.05-4 mM), on electrical and mechanical activities of ferret and guinea-pig papillary muscles were studied using current and voltage clamp (single sucrose gap) techniques. In current clamp studies, amrinone increased, in a dose-dependent manner, contractile force elicited by action potential in both species. Depolarization-induced automaticity was facilitated in ferret muscles at all maximum diastolic potentials between -70 and -15 mV. Facilitation of automaticity in guinea-pig muscles occurred only at potentials more negative than -35 mV and was suppressed at more positive potentials. Cimetidine (10 microM) partially reversed the effects of amrinone on automaticity in both species. In voltage clamp studies, amrinone increased the slow inward current. Steady-state outward current was increased in guinea-pig but not in ferret muscles. A dual effect of amrinone on tension was observed. Amrinone was found to increase phasic tension of ferret papillary muscles only for depolarizations lasting less than 250 to 300 msec. For longer depolarizations, amrinone decreased the phasic tension (in a dose-dependent manner), whereas the tonic tension was not modified. The decrease as well as the increase in tension was associated with an increase of the slow inward current. The results suggest that amrinone may be arrhythmogenic and may have an intracellular action at the sarcoplasmic reticulum level (partial inhibition) in addition to its action on the calcium current.

Action Potentials↗
PubMed1997

[Hemodynamic effects of amrinone in children during cardiopulmonary bypass and postoperative 12 hours].

Hemodynamic effects of amrinone in children during cardiopulmonary bypass (CPB) and postoperative 12 hours were studied. In 10 patients undergoing open heart surgery, 1 mg/kg of amrinone was infused as the initial CPB dose and 5 - 10 micrograms/kg/min of amrinone was continuously administered as the maintenance dose during CPB and postoperative 12 hours. Amrinone levels ranged from 0.9 to 1.4 micrograms/ml during CPB and postoperative 12 hours. After infusion of amrinone, mean arterial blood pressure decreased significantly, but other parameters did not show remarkable change. The administration of amrinone during CPB showed enough vasodilating effect and decreased the need of conventionally used other vasodilators (nitroglycerin or prostaglandin E1). The postoperative course of 10 patients was clinically uneventful. The administration of amrinone in 10 patients did not produce thrombocytopenia compared with the control group (5 patients) in the postoperative period. In conclusion, the administration of amrinone during CPB and postoperative 12 hours in children was useful in producing enough vasodilating effect without major side effect.

Amrinone↗
PubMed1997

Effect of amrinone on portal hemodynamics and tissue blood flow in the isolated perfused rat liver.

We studied the effect of amrinone on portal perfusion pressure, perfusion flow, and tissue blood flow using an isolated perfused rat liver model. In the constant perfusion flow model, amrinone effectively decreased perfusion pressure in the precontracted state by adenosine triphosphate (ATP) or norepinephrine. Amrinone dose-dependently decreased portal perfusion pressure increased by calcium chloride. Similarly, amrinone dose-dependently increased portal perfusion flow decreased by ATP in the constant perfusion pressure model. Amrinone effectively increased tissue blood flow decreased by ATP or norepinephrine measured by laser-Doppler flowmetry. A specific inhibitor of the biosynthesis of nitric oxide, N omega-nitro-L-arginine, did not affect the hemodynamic effect of amrinone, suggesting that nitric oxide is not involved in the portal vasodilating effect of amrinone. We conclude that amrinone increases portal blood flow by decreasing perfusion pressure and contributes to increasing tissue blood flow of the liver without the involvement of nitric oxide.

Amrinone↗
PubMed1979

Cardiotonic activity of amrinone--Win 40680 [5-amino-3,4'-bipyridine-6(1H)-one].

The cardiotonic activity of a new, noncatechol, nonglycoside agent, amrinone, was investigated in vitro and in anesthestized and unanesthetized dogs. Amrinone (3-100 microgram/ml) caused a dose-dependent increase in papillary muscle developed tension and df/dt without significant changes in duration of the contractile cycle or time-to-peak tension. Amrinone induced slight increases in right atrial rate with no changes in electrophysiological properties of the cat papillary muscle or dog Purkinje fibers. In anesthetized dogs, intravenous bolus injections of amrinone at doses ranging from 1 to 10 mg/kg caused increases in cardiac contractile force and left ventricular dp/dt max with relatively small changes in heart rate and blood pressure. No significant changes in lead II ECG were observed. In unanesthetized dogs, intravenous infusion of amrinone (10-100 microgram/kg per min) caused increases in left ventricular dp/dt max and only small changes in heart rate and blood pressure. Amrinone, tested orally in this model at doses of 2-10 mg/kg, produced a positive inotropic effect with a rapid onset and long duration of action. The inotropic response to amrinone was not blocked by propranolol, dibenzyline, chlorisondamine, atropine, metiamide, or reserpine. Amrinone's inotropic response was not associated with significant alterations in cardiac norepinephrine, phosphodiesterase, cyclic AMP, or Na+, K+-activated ATPase.

Adenosine Triphosphatases↗
PubMed1996

Growth factor expression and effects of amrinone in monocrotaline-induced pulmonary hypertension in rats.

Platelet-derived growth factor (PDGF) and basic fibroblast growth factor (bFGF) have been implicated in myointimal proliferative arteriopathy, a lesion seen in monocrotaline-induced pulmonary hypertension (MIPH). The purpose of this study was to examine the expression of PDGF and bFGF in the lungs of rats given monocrotaline and to examine the effects of amrinone on the hearts and lungs of these rats. Twenty-four 26-day-old rats were randomized to receive either monocrotaline (approximately 3.6 mg/kg/d) or no monocrotaline and concomitantly to receive either amrinone (100 mg/kg/d) or no amrinone for 21 days. Lungs were examined for immunohistochemical evidence of PDGF and bFGF, and hearts were examined for effects of pulmonary hypertension and amrinone. Immunohistochemical staining of lungs showed no evidence of PDGF except in bronchioles. bFGF staining was similar between groups (no monocrotaline 25%, monocrotaline 27%, monocrotaline and amrinone 22%), and the staining was confined to the arterial walls. Rats given monocrotaline showed significantly greater right ventricular (RV) weight (0.13 +/- 0.02 g versus 0.23 +/- 0.04 g [mean +/- SD], P < 0.001), right ventricular/left ventricular (RV/LV) weight ratio (0.29 +/- 0.06 versus 0.59 +/- 0.1, P < 0.001), and lung/body weight ratio (0.006 +/- 0.001 versus 0.01 +/- 0.003, P < 0.05) than controls. Rats given monocrotaline and amrinone were not significantly different from rats given only monocrotaline with regard to RV weight, RV/LV weight ratio, or lung/body weight ratio. We conclude that the vasculopathy seen in MIPH is not associated with the presence of PDGF or bFGF, suggesting that other growth factors may mediate this process. The course of MIPH is not altered by amrinone.

Amrinone↗
PubMed1998

Amrinone, a selective phosphodiesterase III inhibitor, improves microcirculation and flap survival: a comparative study with prostaglandin E1.

BACKGROUND: Amrinone, a selective phosphodiesterase (PDE) III inhibitor, is a newly developed agent that possesses a combination of positive inotropic and vasodilating properties as a result of preventing the degradation of cAMP and it has recently been licensed for treatment of heart failure alone. Amrinone is expected to be useful for the treatment not only of heart failure but also of peripheral circulatory disorders, including vascular disease, and for ischemic flaps, because it improves microcirculatory hemodynamics. To investigate potential therapeutic applications of amrinone, we evaluated its ability to improve microcirculatory hemodynamics and flap survival. MATERIALS AND METHODS: The rat skinfold chamber technique was employed to quantify microcirculation directly in vivo. The improved survival area of random flaps in rats treated with amrinone was examined to assess therapeutic efficacy of this drug. Its effects were compared with those of prostaglandin E1 (PGE1), which has been widely approved as an agent for improving hemodynamics. RESULTS: Microcirculatory blood flow and flap survival area were significantly increased in both amrinone- and PGE1-treated animals, compared to the saline-treated controls. The ameliorating effects of amrinone were comparable to those of PGE1. CONCLUSIONS: The results of this study suggest amrinone to be a potentially useful drug not only for treating heart failure but also for improving microcirculation in patients with vascular diseases and for postoperative care after reconstructive surgery.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2000

Topical application of amrinone (a selective phosphodiesterase III inhibitor) for relief of vasospasm.

BACKGROUND: Amrinone, a selective phosphodiesterase III inhibitor, is an agent that possesses a combination of positive inotropic and vasodilating properties as a result of preventing the degradation of cAMP, and it has recently been licensed for the treatment of heart failure. The aim of this study was to investigate the potential therapeutic application of amrinone to resolve vasospasm, which is the major problem in reconstructive surgery. In this study its effect was compared with that of lidocaine, the most commonly used topical vasodilating agent clinically. MATERIALS AND METHODS: The probe of an ultrasonic transit-time volume flowmeter was applied to the femoral artery of rats to measure blood flow. After a baseline recording was obtained, 0.03 ml of epinephrine was applied topically to induce vasospasm. The vessels were then immersed in 1 ml of amrinone (5 mg/ml), 10% lidocaine hydrochloride, or normal physiological saline solution for 1 min in an attempt to resolve the spasm. In another group of animals, no solution was used following administration of epinephrine to allow observation of spontaneous resolution of the vasospasm over time. RESULTS: The results showed an essentially immediate spasm-resolving effect in both the amrinone group and the lidocaine group. The amrinone group showed a significantly greater degree of maximum increase in blood flow than the lidocaine group. The effect of lidocaine decreased with time, whereas amrinone had a more lasting effect. CONCLUSIONS: The findings suggest that amrinone could be used as an effective topical vasodilating agent to resolve vasospasm in reconstructive surgery.

Administration, Topical↗
PubMed1990

Hemodynamic effects of amrinone in children after cardiac surgery.

The hemodynamic effects of amrinone were assessed in seven children following cardiac surgery. Amrinone was administered as a bolus of 1 mg kg-1 body wt., followed by continuous infusion at 10 micrograms kg-1 min-1 for 1 h and two stepwise increases to 20 and 40 micrograms kg-1 min-1 for 30 min each. Hemodynamic data were obtained and plasma concentrations of amrinone measured 1 h after the bolus dose and immediately before each increment of the infusion rate. Amrinone levels ranged from 0.7 to 2.3 mg l-1. Administration of amrinone lowered systemic vascular resistance from 20.0 +/- 4.3 to 16.5 +/- 4.6 mmHg l-1 min-1 m-2 (p less than 0.05) and reduced mean arterial pressure from 71.7 +/- 9.5 to 62.6 +/- 13.5 mmHg (p less than 0.05) at the highest infusion rate, confirming the known vasodilative effect of the drug. However, these effects did not result in a statistically significant increase in stroke volume (35.0 +/- 7.5 to 35.5 +/- 7.0 ml m-2, NS) or cardiac index (3.10 +/- 0.50 to 3.20 +/- 0.40 l min-1 m-2). One additional patient, in whom a higher loading dose was tried in order to achieve a higher plasma concentration, developed systemic hypotension. A correlation was established between the plasma concentrations of amrinone and the percentage decrease in systemic resistance (r = 0.70, p less than 0.05). These results suggest that in children after open heart surgery, amrinone acts primarily as a systemic vasodilator, with questionable inotropic effect. Accordingly, its use should be restricted to children with severe cardiac failure and documented highly elevated afterload.

Adolescent↗
PubMed2002

Effects of amrinone on bilateral renal ischemia/reperfusion injury.

Renal ischemia/reperfusion injury could arise as a consequence of clinical conditions such as renal transplantation, shock, cardiac arrest, hemorrhage and renal artery surgery. In this experimental study, we aimed to determine the preventive effects of amrinone on bilateral renal ischemia/reperfusion injury in rats. A total of 60 Wistar-albino rats were divided into six groups ( n=10). Midline laparotomies were made under ketamine anesthesia. In the sham, amrinone1 and amrinone2 without ischemia (AWI1 and AWI2) groups saline, 5 and 10 mg/kg of amrinone was infused, respectively. In the ischemia, ischemia plus amrinone1 (IPA1) and ischemia plus amrinone2 (IPA2) groups, saline and 5 and 10 mg/kg of amrinone was infused, respectively, at the beginning of reperfusion, subsequent to 45 min of bilateral renal artery occlusion. Following 6 h of reperfusion, blood was drawn to study serum BUN and creatinine and a bilateral nephrectomy was done to determine tissue malonyldialdehyde ( MDA) and myeloperoxidase (MPO) levels. The results were analysed by Mann-Whitney U-test. The parameters studied were statistically higher in the ischemia group compared with the other groups ( P<0.05 for each comparison), indicating renal I/R injury. These parameters were lower in the amrinone without ischemia groups (AWI1 and AWI2) than in the sham group, however there were no significant differences between the groups ( P>0.05, for each comparison). The treatment groups IPA1 and IPA2 had statistically similar results compared with the sham group, showing the preventive effect of amrinone on renal I/R injury at the given doses. We conclude that amrinone prevented experimental renal ischemia/reperfusion injury in rats, independently of the administered doses. This preventive effect of the agent could depend on its effect of regulating the microcirculation, in decreasing intracellular calcium and in preventing neutrophil activation. We propose that this preventive effect of amrinone - which has gained clinical application especially in cases of cardiac insufficiency - could also be exploited in clinical conditions related with renal ischemia/reperfusion.

Amrinone↗
PubMed1984

Amrinone: acute electrophysiologic and hemodynamic effects in patients with congestive heart failure.

Amrinone is an effective inotropic agent, but its electrophysiologic effects in humans have not been previously determined. Fifteen patients with congestive heart failure (CHF) New York Heart Association functional class II to IV, underwent an electrophysiologic study after withdrawal of all other cardioactive drugs before and after 10 to 20 micrograms/kg/min of intravenous amrinone (doses that increased cardiac index and decreased pulmonary capillary wedge pressure and systemic vascular resistance, p less than 0.002). Amrinone caused no change in PR, QRS, QTc, AH or HV intervals or maximal corrected sinus node recovery time and had no significant effect on the ventricular effective refractory periods. Amrinone decreased the atrial effective refractory period from 256 +/- 40 to 240 +/- 38 ms (p = 0.015), and the atrioventricular (AV) nodal functional refractory period from 374 +/- 65 to 356 +/- 64 ms (p less than 0.05), and enhanced maximal 1:1 AV nodal conduction from 371 +/- 46 to 334 +/- 47 ms (p = 0.006). Nine patients had baseline HV prolongation; this was not affected by amrinone. The frequency of inducible ventricular tachycardia was not significantly affected by amrinone. Holter recordings (24 to 48 hours) were obtained from 10 patients before and after acute oral amrinone dosing (75 to 150 mg every 8 hours). There was no change in the number of ventricular premature contractions per 24 hours (2,197 +/- 3,305 vs 2,616 +/- 2,436) or number of runs of ventricular tachycardia per 24 hours (10 +/- 12 vs 12 +/- 13); however, the number of ventricular couplets per 24 hours increased from 22 +/- 34 to 52 +/- 55 (p = 0.054).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗