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 163 records · Page 9Linked to original sources
PubMed1991

Amrinone reverses cardiac depression and augments coronary vasodilation with isoflurane in the isolated heart.

Amrinone is a positive inotropic and vasodilatory agent and may be administered during anesthesia with isoflurane. The authors' aims were 1) to examine if amrinone produces coronary artery vasodilation through an increase in metabolic demand or through a direct vasodilatory effect or through both and 2) to test if amrinone attenuates cardiac depression and enhances coronary artery vasodilation produced with exposure to isoflurane. The effects of these drugs were examined in 11 isolated perfused guinea pig hearts. Variables measured were: heart rate (HR), atrioventricular conduction time (AVCT), isovolumetric peak left ventricular pressure (LVP), coronary flow, percent O2 extraction, myocardial O2 consumption (MVO2), and the ratio of O2 delivery (DO2) to MVO2. Each heart was exposed for 10-min periods to 10, 50, 100, and 500 microM amrinone alone, and to 0.5 or 1% isoflurane before, during, and after amrinone. Initial control values were: heart rate 216 +/- 5 beats per min; AVCT 56 +/- 1 ms; peak LVP 86 +/- 3 mmHg; coronary flow 6.3 +/- 0.3 ml.min-1.g-1 (11.4 +/- 0.7 ml.min-1.g-1 with adenosine bolus), percent O2 extraction 52 +/- 3%; DO2 107 +/- 3 microliters.min-1.g-1; MVO2 56 +/- 4 microliters.min-1.g-1; and DO2/MVO2 1.75 +/- 0.08. Amrinone 500 microM alone increased (P less than 0.05) heart rate by 9%, LVP by 13%, coronary flow by 18%, and MVO2 by 23%; AVCT decreased by 3%.(ABSTRACT TRUNCATED AT 250 WORDS)

Amrinone↗
PubMed1992

The effect of amrinone on recovery from severe bupivacaine intoxication in pigs.

Cardiovascular collapse following intravascular bupivacaine may be resistant to treatment. The effect of amrinone on recovery from bupivacaine-induced severe cardiovascular depression was evaluated in 20 pigs (13-26 kg) in a placebo-controlled randomized double-blind study. Under 0.7% isoflurane anesthesia at FIO2 0.21, 0.5% bupivacaine 2 mg.kg-1.min-1 was infused until mean arterial pressure was 40% of the baseline. Cardiac output and heart rate decreased 75% and 50% from the baseline, respectively. The total dose of bupivacaine was 17 +/- 6 (SD) mg.kg-1 in the control and 19 +/- 5 mg.kg-1 in the amrinone group, resulting in mean plasma concentrations of 42 +/- 6 and 53 +/- 19 micrograms.ml-1, respectively. A bolus of amrinone 4 mg.kg-1 (n = 10) was given immediately after cardiovascular depression, followed by an infusion of 0.6 mg.kg-1.min-1. The control animals received corresponding volumes of physiologic saline (n = 10). After cardiovascular depression, the lungs were ventilated with FIO2 1.0 without anaesthetics or sympathomimetic support. Electric activity of the heart ceased in all control animals in 3.9 +/- 2 min after cardiovascular depression despite atropine and external cardiac compression. All animals in the control group and 5 of 10 animals in the amrinone group were given atropine (P less than 0.01). The animals receiving amrinone survived without cardiac compression (P less than 0.0001). During bupivacaine infusion, all animals developed burst suppression in the electroencephalogram. At the time of cardiovascular depression, in 8 of 10 control and in 6 of 10 amrinone animals, the electroencephalogram was isoelectric.(ABSTRACT TRUNCATED AT 250 WORDS)

Amrinone↗
PubMed1995

Amrinone is superior to epinephrine in reversing bupivacaine-induced cardiovascular depression in sevoflurane-anesthetized dogs.

BACKGROUND: Bupivacaine-induced cardiovascular depression is known to be difficult to treat, and the efficacy of epinephrine for treatment of bupivacaine-induced cardiovascular depression is in doubt. We compared the efficacy of amrinone with that of epinephrine for the treatment of bupivacaine-induced cardiovascular depression in anesthetized dogs. METHODS: In dogs receiving 1.5-2% sevoflurane anesthesia, 0.5% bupivacaine was infused at a rate of 0.5 mg.kg-1.min-1 intravenously until mean arterial blood pressure decreased to 40 mmHg or less. In the amrinone group (n = 9), amrinone (4 mg.kg-1, intravenously) was given immediately after cardiovascular depression, followed by intravenous infusion at a rate of 0.1 mg.kg-1.min-1. In the epinephrine group (n = 9), epinephrine (0.01 mg.kg-1, intravenously) was given as a bolus, and the same dose was given again as required. RESULTS: All nine dogs that received amrinone survived. Of the nine dogs that received epinephrine, five survived; fatal cardiovascular depression developed in the four remaining animals (P < 0.05). Only one animal in the amrinone group showed tachyrhythmia with wide QRS complexes during resuscitation, whereas all nine animals in the epinephrine group showed tachyrhythmia with wide QRS complexes during resuscitation. CONCLUSIONS: Amrinone is superior to epinephrine for the treatment of bupivacaine-induced cardiovascular depression in sevoflurane-anesthetized dogs.

Amrinone↗
PubMedDate not supplied

Responses to amrinone in isolated cardiac muscles from cat, rabbit, and guinea pig.

Amrinone (10(-5)-10(-2) M) produced a positive inotropic response in several electrically stimulated, isolated cardiac muscle preparations. The order of potencies for amrinone in the tissues studied was: cat papillary muscle greater than rabbit papillary muscle greater than muscle strips from rabbit left atria = guinea pig papillary muscle greater than guinea pig left atria. Amrinone also restored contractility to cat and rabbit papillary muscles which had been partially depolarized with 20 mM K+. The beta-adrenergic antagonists timolol and propranolol partially inhibited these responses in rabbit but not cat papillary muscles. Reserpine pretreatment did not influence the responses to amrinone in any of the preparations studied. In conclusion, (a) the cat papillary muscle was the most sensitive preparation to the inotropic effect of amrinone, and (b) in the rabbit papillary muscle, beta-adrenoceptors contribute to the amrinone response but are not solely responsible for the enhanced inotropy.

Aminopyridines↗
PubMed1992

Amrinone as an inotrope in managing hypermetabolic surgical stress.

Dobutamine is the standard inotrope used as cardiac support for hyperdynamic hypermetabolic patients following acute surgical stress. Amrinone has been utilized in medical patients with heart failure, but its use in hyperdynamic patients to our knowledge has never been reported. We now report the results of a trial of amrinone versus dobutamine in this setting. Over a 3-month period, we compared 28 trials of dobutamine and 27 trials of amrinone in 47 patients. Attempts were made to achieve non-flow-dependent oxygen consumption. Values are expressed as pre/post inotrope. Student's two-tailed t test was used for evaluation. [table: see text] Patients treated initially with dobutamine were slightly younger (mean, 46 vs. 57 years). They required slightly higher doses of dobutamine (mean, 12.9 vs. 12.2 micrograms/kg/min) and a slightly longer treatment period (mean, 11.3 vs. 9.8 hours) to achieve the desired effect. Of the 47 trials with dobutamine, six (13%) failed to achieve non-flow-dependent oxygen consumption. All then responded somewhat to amrinone. The failure rate for amrinone was 10%. No patient developed hypotension when treated with either drug. Amrinone is an effective inotrope useful in the cardiovascular support of hyperdynamic patients following surgical stress. Hypotension is not a problem with adequate intravascular volume loading. It should become part of the standard drug regimen in the surgical ICU.

Adolescent↗
PubMed1994

Amrinone suppresses the synthesis of tumor necrosis factor-alpha in human mononuclear cells.

Tumor necrosis factor-alpha (TNF) exerts a wide spectrum of biological activities and contributes to the pathophysiology of septic shock. Elevated circulating levels of TNF have also been reported in patients with severe chronic heart failure. We studied the effect of amrinone, a class III cyclic nucleotide phosphodiesterase inhibitor used in the treatment of acute heart failure, on the synthesis of TNF in vitro. Peripheral blood mononuclear cells from healthy volunteers or cells of a permanent monoblast cell line were stimulated for 20 h with bacterial lipopolysaccharide and different doses of amrinone. TNF production is suppressed in a dose-dependent manner to a minimum of 9% of controls with 1000 microM of amrinone, reaching half-maximal inhibition at 80 microM amrinone. This effect appears to be mediated via cAMP, which accumulated nearly twofold in the presence of amrinone. Suppression of TNF synthesis by therapeutically administered phosphodiesterase inhibitors such as amrinone may contribute to their beneficial effect in the treatment of heart failure.

Amrinone↗
PubMed1996

Amrinone reverses bupivacaine-induced regional myocardial dysfunction.

Amrinone has been shown to have therapeutic effects on bupivacaine-induced cardiovascular toxicity, but its exact effects on the heart are not well understood. This study evaluated the regional myocardial effect of amrinone on bupivacaine-induced cardiovascular toxicity in in situ beating hearts in 10 dogs using a selective coronary perfusion and sonomicrometry. In the control group, bupivacaine was administered into the left anterior descending coronary artery (LAD) for 15 min at four steps: baseline, step 1, step 2 and step 3, (calculated LAD plasma concentrations; 0, 5, 5 and 10 mu g center dot ml-1, respectively). In the amrinone group, amrinone (5 mu g center dot ml-1) was simultaneously infused at steps 2 and 3 in addition to bupivacaine infusions. Regional myocardial function of the LAD supplied area was evaluated by analysis of the left ventricular pressure-segment length loop. In the control group, systolic shortening decreased from the baseline (10.5 +/- 1.3%, mean +/- SEM) to step 3 (0.1 +/- 1.3%), and post-systolic shortening increased from the baseline (18.0 +/- 3.7%) to step 3 (52.3 +/- 5.5%) dose-dependently. In contrast, with amrinone infusion at steps 2 and 3, both variables returned to near baseline values. These results indicate that amrinone reverses bupivacaine-induced regional myocardial dysfunction.

Amrinone↗
PubMed1983

Effects of amrinone on the transmembrane action potential of rabbit sinus node pacemaker cells.

Effects of amrinone on the membrane action potential and spontaneous activity were investigated in sinus node pacemaker cells of rabbit heart by use of microelectrode techniques. Amrinone (1 X 10(-4) M to 6 X 10(-6) M) caused a shortening of cycle length of spontaneous firing (SPCL) accompanied by an increase in the maximum upstroke velocity at phase O (Vmax) and amplitude of action potential (AAP), while it did not affect the maximum diastolic potential (MDP). All the effects of amrinone on sinus node pacemaker cells were markedly attenuated or abolished in a low calcium medium (Ca+ 0.1 mM or 0.3 mM) or in the presence of the slow channel blocking agent, verapamil (5 X 10(-7) M, 2 X 10(-6) M). The effects of amrinone were not antagonized by the beta-adrenoceptor blocking agent, pindolol (2 X 10(-7) M). These results indicate that amrinone has an intrinsic effect on sinus node pacemaker cells, increasing their spontaneous firing activity. It is also assumed that the effects of amrinone on sinus node cells are probably mediated by an augmentation of the slow calcium and/or sodium inward current through the cell membrane.

Action Potentials↗
PubMed1996

Amrinone as an antidote in experimental verapamil overdose.

OBJECTIVE: To evaluate the effect of amrinone as a treatment for the hemodynamic effects of verapamil overdose in a canine model. METHODS: This nonblind interventional study was performed in an established canine model of verapamil toxicity, without concurrent control animals. Pentobarbital-anesthetized and instrumented dogs (n = 8) were maintained and observed for 60 minutes or until death. The animals were overdosed with verapamil, 15 mg/ kg IV, over 30 minutes. Hemodynamic parameters, including cardiac index (CI), heart rate (HR), and mean arterial pressure (MAP), were monitored. Completion of the verapamil infusion represented the defined point of toxicity; at that point, all the animals received an amrinone bolus of 2 mg/kg IV over 2 minutes followed by an amrinone drip at 10 micrograms/kg/min. The hemodynamic values at the defined point of toxicity were compared with those obtained postinitiation of the amrinone infusion. RESULTS: Two animals died before the 60-minute observation period elapsed. Baseline CI was 5.6 L/min/m2. Following verapamil-induced toxicity, mean CI was 2.2 L/min/m2. After administration of amrinone, a significant (p < 0.05) increase in CI was observed at 30 minutes (CI = 3.6 L/min/m2), 45 minutes (CI = 4.2 L/ min/m2), and 60 minutes (CI = 4.2 L/min/m2). There was no statistically significant difference noted for MAP or HR compared with "point of toxicity" values. CONCLUSION: Amrinone appears to reverse the depressed cardiac index associated with verapamil overdose in a canine model while having no significant effect on the hypotension or bradycardia.

Amrinone↗
PubMed1985

Effects of amrinone on the contractile behaviour of frog striated muscle fibres.

The effects of amrinone (0.005-2.1 mM) were studied on isolated single muscle fibres of the frog (0.6-4.3 degrees C). In the concentrations used amrinone potentiated the isometric twitch, increased the initial rate of force development and prolonged the time to peak twitch force and the time from peak force to half relaxation. There was a moderate but statistically significant (P less than 0.001) enhancement of the maximum tetanic force and a marked slowing of the relaxation phase of the tetanus. Amrinone depressed the velocity of unloaded shortening by 33 +/- 2% (mean +/- SE, n = 6) and reduced the curvature of the force-velocity relation leading to an increase of a/Po in Hill's (1938) hyperbolic equation. In accordance with the effects of amrinone on the force-velocity relation, there was a decrease in the rate of redevelopment of force after the fibre was released to zero tension during the tetanus plateau. The evidence suggests that the drug affects the contractile properties of frog muscle fibres by two different mechanisms: (I) amrinone affects the excitation-contraction coupling causing enhanced calcium release in response to membrane excitation and (2) amrinone exerts a direct effect on the kinetics of turnover of the myosin cross-bridges. The latter aspect of the drug effect was evaluated in terms of A.F. Huxley's (1957) cross-bridge model by means of a computer program.

Aminopyridines↗
PubMed1995

Amrinone prevents muscle protein wasting during chronic sepsis.

The time course for the effects of sepsis on rates of protein synthesis, RNA contents, and translational efficiencies was measured in mixed muscles of rat hindlimb perfused in vitro 3, 5, and 10 days after induction of sepsis. Furthermore, the effect of daily injections of amrinone (5 mg.kg-1.day-1) on muscle protein synthesis was investigated. On day 3 of sepsis, decreased rates of protein synthesis in muscle from untreated septic animals or septic rats treated with amrinone resulted from a reduced food intake. When food intake became normalized to control after 5 days, rates of protein synthesis in untreated septic rats remained depressed. Treatment of septic animals with amrinone for 5 days prevented the sepsis-induced inhibition of protein synthesis by abolishing the inhibition of peptide-chain initiation and restoring translational efficiency to control values. In contrast, amrinone treatment of control rats for 5 days did not cause an accretion of muscle protein or augment protein synthesis. Ten days after induction of sepsis, there were no differences in rates of protein synthesis, RNA content, or translational efficiency in septic animals compared with control or amrinone-treated septic rats. Thus, amrinone prevented the sepsis-induced abnormalities in skeletal muscle protein synthesis.

Abscess↗
PubMed1994

Effects of amrinone and dobutamine on PGF2 alpha-induced pulmonary hypertension in dogs.

The hemodynamic benefits and pulmonary vascular selectivity of amrinone, dobutamine and amrinone + dobutamine were assessed in a canine model of vasoconstrictive pulmonary hypertension. Dogs were equipped with central and peripheral catheters and with an electromagnetic flow probe placed around the ascending aorta for the measurement of cardiac function. Through a laparotomy, an arteriovenous fistula was created between the abdominal aorta and the inferior vena cava. Gradual opening of this fistula, which permitted construction of pressure-flow curves (mean pulmonary artery pressure over the cardiac index, PAP/CI), was utilized to identify the pulmonary vascular effects of amrinone and dobutamine. PGF2 alpha, prostaglandin derivative, induced stable pulmonary hypertension along with significant reduction in CI. The resultant pulmonary hypertension translated into a significant increase in both the slope and pressure intercept of the PAP/CI curve. The bipyridine derivative, amrinone, did not reverse the CI reduction observed with PGF2 alpha: both mean arterial pressure and PAP were decreased as was the intercept of the PAP/CI curve. Dobutamine, a beta-agonist, reversed the CI decline elicited by PGF2 alpha but the elevated pulmonary pressure remained unaffected; dobutamine reduced the slope of the PAP/CI curve. When combined, amrinone and dobutamine demonstrated additive beneficial hemodynamic effects and improved lung perfusion. Their additive effects were also indicated by data on the PAP/CI curve: both the slope and the pressure intercept were significantly reduced. These results suggest that amrinone and dobutamine interact at different sites of the pulmonary vasculature and that their association might be beneficial in vasoconstrictive pulmonary hypertension although no significant pulmonary vascular selectivity could be observed.

Amrinone↗
PubMed1985

Long-term oral administration of amrinone for congestive heart failure: lack of efficacy in a multicenter controlled trial.

A number of uncontrolled studies have indicated that oral administration of amrinone, a phosphodiesterase inhibitor with potent positive inotropic effects in experimental preparations, may be beneficial in patients with chronic congestive heart failure. The present multicenter trial was designed to prospectively evaluate clinical response and change in exercise tolerance during 12 weeks of amrinone therapy in a double-blind, placebo-controlled protocol. Ninety-nine patients with NYHA functional class 3 or 4 congestive heart failure on digitalis and diuretics, of whom 31 were also receiving captopril, were enrolled. After baseline clinical assessment and determination of exercise tolerance, radionuclide left ventricular ejection fraction, and roentgenographic cardiothoracic ratio, patients were randomly assigned to receive amrinone or placebo, beginning at 1.5 mg/kg tid and increasing to a maximum dosage of 200 mg tid. After 12 weeks of therapy or at the last blinded evaluation in patients who did not complete this protocol, there were no significant differences from baseline values between treatment with amrinone or placebo with regard to symptoms, NYHA functional class, left ventricular ejection fraction, cardiothoracic ratio, frequency and severity of ventricular ectopy, or mortality. Exercise tolerance improved significantly from baseline by 37 +/- 10% (mean 163 sec) in patients on amrinone and 35 +/- 11% (mean 149 sec) in patients on placebo, but there was no significant difference between treatments. Adverse reactions were significantly more frequent and more severe on amrinone, occurring in 83% of patients and necessitating withdrawal in 34%.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1997

Amrinone versus dobutamine in cardiac surgical patients with severe pulmonary hypertension after cardiopulmonary bypass: a prospective, randomized double-blinded trial.

We compared the relative effects of dobutamine (5 micrograms/kg/min) and amrinone (1.0 mg/kg bolus followed by 10 micrograms/kg/min) on right and left ventricular function and pulmonary arterial pressures during weaning from cardiopulmonary bypass in patients with a mean preoperative pulmonary pressure > 30 mmHg. Twenty patients scheduled for mitral valve replacement were studied in a prospective, randomized, double-blind trial. Patients receiving amrinone had a greater increase in cardiac index (CI) of 1.38 (+/-0.95) litre/min/m2 at separation vs 0.69 (+/-0.63) litre/min/m2 in the dobutamine group (P < 0.05). The amrinone group also had a greater increase in right ventricular ejection fraction (0.15 +/- 0.08 at separation from cardiopulmonary bypass versus an increase of 0.04 +/- 0.11 in those receiving dobutamine; P < 0.005). Amrinone produced a larger decrease in pulmonary artery wedge pressure 8.0 (+/-4.4) mmHg vs 0.75 (+/-6.6) mmHg at separation; pulmonary artery systolic and diastolic pressures also were reduced more in the amrinone group. There were no differences in heart rate, mean arterial pressure, central venous pressure and right ventricular stroke work index between patient groups. In the doses chosen, the use of amrinone compared to dobutamine was associated with a reduction in pulmonary arterial pressures and an increase in cardiac index and right ventricular ejection fraction after separation from bypass in patients with severe preoperative pulmonary hypertension.

Amrinone↗
PubMed1986

Involvement of cyclic AMP in vasodilatation by amrinone: a comparative study with 3-isobutyl-methyl-xanthine (IBMX).

We investigated the effect of amrinone, a non-glycosidic, non-adrenergic cardiotonic drug, on rabbit aortic strips and vascular smooth muscle cells cultured from rabbit aorta. Amrinone relaxed the strips precontracted by KCl, norepinephrine, serotonin or STA2 in a dose-dependent manner, and it shifted the dose-response curves downward. A similar mode of relaxation was noted with IBMX, an inhibitor of cyclic AMP phosphodiesterase (cAMPPDE). Although propranolol did not affect the relaxation induced by amrinone, W-7, a calmodulin antagonist, slightly potentiated and IBMX attenuated the response. In intact smooth muscle cells in culture, amrinone increased basal levels of cAMP and markedly potentiated cAMP accumulation in response to 10(-6) M isoproterenol. The effect on cAMP accumulation mimicked that of IBMX but the effects were not additive. Inhibition of cAMPPDE was also demonstrated in a cell-free system, IC50 values for amrinone and IBMX being 2.1 X 10(-5) M and 1.2 X 10(-6) M, respectively, using a preparation of cAMPPDE partially purified from the cells by DEAE cellulose chromatography. Amrinone seems to exert a direct effect on vascular smooth muscle cells by potently inhibiting cAMPPDE. This inhibition would to some extent explain the vasodilatory property.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Vasodilator mechanisms of action of amrinone do not involve the opening of either ATP-sensitive or Ca(2+)-activated K+ channels.

Amrinone is more coronary vasodilatory than positive inotropic compared with other newer phosphodiesterase inhibitors. In order to explore possible involvements of ATP-sensitive K+ (KATP) and large-conductance Ca(2+)-activated K+ (KCa) channels in the vasodilator effect of amrinone, we investigated whether amrinone-induced vasodilation would be antagonized by glibenclamide, a blocker of KATP channels, or by charybdotoxin or tetraethylammonium, blockers of KCa channels. In isolated, blood-perfused canine papillary muscle preparations, the amrinone-induced increase in blood flow was not affected by glibenclamide given to support dogs. In canine large coronary arteries contracted with high (25 mM) KCl, amrinone-induced relaxation was not affected by glibenclamide, charybdotoxin and tetraethylammonium. These results suggest that the vasodilator mechanisms of amrinone do not involve the opening of either KATP or KCa channels.

Adenosine Triphosphate↗
PubMed2002

Differential effects of amrinone and milrinone upon myocardial inflammatory signaling.

BACKGROUND: Mounting evidence links systemic and local inflammatory cytokine production to myocardial dysfunction and injury occurring during ischemia-reperfusion, cardiopulmonary bypass, and heart failure. Phosphodiesterase inhibitors (PDEIs), used frequently in these states, can modulate inflammatory signaling. The mechanisms for these effects are unclear. We therefore examined the effects of 2 commonly used PDEIs, amrinone and milrinone, on cardiac cell inflammatory responses. METHODS AND RESULTS: Primary rat cardiomyocyte cultures were treated with endotoxin (LPS) or tumor necrosis factor-alpha (TNF-alpha), alone or in the presence of clinically relevant concentrations of amrinone or milrinone. Regulation of nuclear factor-kappa B (NFkappaB), nitric oxide synthase and cyclooxygenase isoforms, and cytokine production were assessed by electrophoretic mobility shift assays, Western immunoblotting, and enzyme-linked immunoassays, respectively. Both LPS and TNF-alpha induced significant NFkappaB activation, cyclooxygenase-2 (COX-2) expression, and inducible NO synthase (iNOS) and cytokine production; with the exception of COX-2 expression, all were significantly reduced by amrinone, beginning at concentrations of 10 to 50 micro mol/L. In contrast, milrinone increased nuclear NFkappaB translocation, iNOS and COX-2 expression, and cardiomyocyte production of interleukin-1beta. Cell-permeable cAMP increased inflammatory gene expression, whereas cell-permeable cGMP had no effect, indicating that the effects of amrinone were not due to phosphodiesterase inhibition. Similar results were seen in macrophages and coronary vascular endothelial cells. CONCLUSIONS: Both amrinone and milrinone have significant effects on cardiac inflammatory signaling. Overall, amrinone reduces activation of the key transcription factor NFkappaB and limits the production of pro-inflammatory cytokines, whereas milrinone does not.

Amrinone↗
PubMed2002

[Randomized controlled trial for the effect of amrinone and aprotinin on expression leukocyte adhesion molecule in patients with prosthetic valve replacement during perioperative period].

OBJECTIVE: To explore the effect of amrinone and aprotinin on expression of leukocyte adhesion molecule in patients with prosthetic valve replacement during perioperative period. METHODS: Thirty-two patients undergoing valve replacement were randomized to control group, the first aprotinin group, the second aprotinin group, and amrinone combined with aprotinin group; each group consisted of eight cases. In the first aprotinin group, 3 x 10(6) units of aprotinin was added to the priming solution of the extracorporeal circulation (ECC). In the second aprotinin group, 3 x 10(6) units of aprotinin was added to the priming solution of ECC, which was combined with 1 x 10(6) units of aprotinin for intravenous bolus. In the amrinone combined with aprotinin group, 3 x 10(6) units aprotinin was added to the priming solution of the ECC and amrinone began with a bolus of 1 mg/kg followed by a maintenance intrusion of 8 micrograms/kg.min. The control group received an equivalence without aprotinin. Venous blood samples were drawn before the operation, at the end of the ECC, 1 hour after the end of the ECC, and one day after the operation, respectively. Flow cytometry was used to demonstrate the expression of leukocyte adhesion molecule CD11b/CD18. RESULTS: Before ECC, there were no differences of the levels of CD11b+/CD18+ in all groups (P > 0.05). One hour after the ECC, the level of CD11b+/CD18+ in group B was lower than that in group A, the level of CD11b+/CD18+ in group C was lower than that in group B, and the level of CD11b+/CD18+ in group D was higher than that in group C, but no significant difference between groups was noted (P > 0.05). CONCLUSION: Although amrinone and aprotinin have anti-inflammatory activity, the pump prime which was added aprotinin alone or aprotinin combined with amrinone might fail in preventing the expression of leukocyte adhesion molecule CD11b/CD18 completely in patients with prosthetic valve replacement during ECC perioperative period.

Adult↗