Amrinone
Aminopyridines
Cardiotonic Agents
Milrinone
Effects of single administration of a phosphodiesterase III inhibitor during cardiopulmonary bypass: comparison of milrinone and amrinone. (1/66)
The effects of phosphodiesterase III (PDE III) inhibitors administered after aortic declamping during cardiopulmonary bypass (CPB) for open heart surgery were investigated. Ten patients (group M) were administered milrinone (50 microg/kg) after aortic declamping during CPB, 10 patients were administered amrinone (1 mg/kg) at the same time during their surgery (group A), and 10 patients served as controls with no drug administered (group C). Soon after bolus infusion of the PDE III inhibitor, perfusion pressure dropped significantly in groups M and A. However, after release of CPB and at the end of surgery, there was no difference in aortic pressure between the 3 groups. There were also no differences between the groups in heart rate, pulmonary artery pressure, and pulmonary capillary wedge pressure. After weaning from CPB, the cardiac index was high and systemic vascular resistance index was low in groups M and A. There were no significant differences in the need for additional catecholamines and time for rewarming between groups. No adverse reactions were observed. A single administration of a PDE III inhibitor during CPB was useful for post-CPB management of patients undergoing open heart surgery. Amrinone reduced perfusion pressures more than milrinone, but cardiac indices and aortic pressures after weaning from CPB showed no differences between group M and group A patients. (+info)Effects of amrinone on ischaemia-reperfusion injury in cirrhotic patients undergoing hepatectomy: a comparative study with prostaglandin E1. (2/66)
The effects of amrinone, a selective phosphodiesterase III inhibitor, on liver ischaemia reperfusion injury have not yet been clarified. Forty-five patients with hepatocellular carcinoma who underwent partial liver resection using Pringle's manoeuvre were studied. Patients were divided into three groups: those given amrinone, those given prostaglandin E1 (PGE1) and those not treated (controls). An indocyanine green (ICG) clearance test was performed before the operation and three times during surgery: just before induction of liver ischaemia, just after liver resection and 60 min after reperfusion. Blood lactate and base excess were measured at the same times. Systolic and diastolic arterial pressure, heart rate, cardiac index and oesophageal temperature were monitored. Aminotransferase levels were recorded the day before surgery, 1 h after operation and on the first and third postoperative days. These data were compared between groups. The ICG elimination rate, lactate and base excess in the amrinone group differed significantly from those in controls during the observation period (P = 0.03, P = 0.04 and P = 0.03, respectively). The differences between the PGE1 and control groups were not significant. There were no significant differences between the groups in perioperative vital signs, cardiac index or postoperative aminotransferase. Amrinone enhanced intraoperative ICG elimination in cirrhotic patients who underwent liver resection. (+info)Effects of the specific phosphodiesterase inhibitors on alloxan-induced diabetic rabbit cavernous tissue in vitro. (3/66)
An experimental study was done to examine a potential role of phosphodiesterase (PDE) inhibitors in the treatment of diabetic erectile dysfunction. Relaxant effect of specific PDE inhibitors were measured in strips of corpus cavernosum smooth muscle taken from control and diabetic groups. Diabetes mellitus was induced in New Zealand white rabbits using alloxan. Penises excised from diabetic rabbits 8 weeks after the induction of diabetes mellitus. In the organ bath strips from control and diabetic rabbit corpus cavernosum were precontracted and increasing doses of several PDE inhibitors were added. In the precontracted rabbit cavernous tissue, sulmazole and zaprinast specific PDE V inhibitors were equally potent and efficacious in vitro but amrinone, a specific PDE III inhibitor, exhibits low relaxant effects. All PDE inhibitors tested showed a similar relaxation effect on corpus cavernosum smooth muscle from control and 8-week diabetic rabbits. The present study provides the possibility of using selective PDE III and V inhibitors in the treatment of diabetic impotence. (+info)Lack of role for nitric oxide in cholinergic modulation of myocardial contractility in vivo. (4/66)
Despite intensive investigation, the role of nitric oxide (NO) in cholinergic modulation of myocardial contractility remains unresolved. The left anterior descending coronary artery of 34 anesthetized, open-chest dogs was perfused via an extracorporeal circuit. Segmental shortening (SS) was measured with ultrasonic crystals and coronary blood flow (CBF) was measured with an ultrasonic flow transducer. An intracoronary infusion of ACh (20 microg/min) was performed, with CBF held constant, under baseline and during dobutamine, CaCl(2), or amrinone at doses increasing SS by approximately 50% (10 microg/min, 15 mg/min, and 300 microg/min ic, respectively). ACh-induced responses during dobutamine were also assessed following treatment with the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME; 300 microg/min ic for 15 min). The effects of sodium nitroprusside (SNP; 80 microg/min ic), an exogenous NO donor, bradykinin (2.5 microg/min ic), a nonmuscarinic releaser of endothelial NO, and bilateral vagal stimulation (before and after L-NAME) were evaluated during dobutamine. ACh had no effect on SS under baseline or during CaCl(2), but it decreased SS during dobutamine or amrinone (-23 +/- 4% and -30 +/- 5%, respectively). Vagal stimulation also reduced SS during dobutamine. L-NAME did not alter the ACh- or vagal-induced decreases in SS during dobutamine. Neither SNP nor bradykinin affected SS during dobutamine. In conclusion, ACh and vagal stimulation have a negative inotropic effect during stimulation of the beta-adrenergic receptors that is independent of NO. The persistence of this effect during amrinone suggests that a mechanism downstream from adenylate cyclase is involved. (+info)In contrast to forskolin and 3-isobutyl-1-methylxanthine, amrinone stimulates the cardiac voltage-sensitive release mechanism without increasing calcium-induced calcium release. (5/66)
The objective of this study was to determine whether the voltage-sensitive release mechanism (VSRM) can be stimulated independently from Ca(2+)-induced Ca(2+) release (CICR) by drugs that elevate intracellular cAMP. Contractions were measured in voltage-clamped guinea pig ventricular myocytes at 37 degrees C. Na(+) current was blocked. We compared effects of agents that elevate cAMP through activation of adenylyl cyclase (1 microM forskolin), nonspecific inhibition of phosphodiesterases (PDEs) [100 microM 3-isobutyl-1-methylxanthine (IBMX)], and selective inhibition of PDE III (100-500 microM amrinone) on contractions initiated by the VSRM and CICR. Forskolin and IBMX significantly increased peak Ca(2+) current and CICR. In addition, these agents also markedly increased contractions elicited by test steps from -65 to -40 mV, which activate the VSRM. However, because these steps also induced inward current in the presence of forskolin or IBMX, CICR could not be excluded. In contrast, amrinone caused a large, concentration-dependent increase in VSRM contractions but had no effect on CICR contractions or Ca(2+) current. Sarcoplasmic reticulum Ca(2+), assessed by rapid application of caffeine (10 mM), was increased only modestly by all three drugs. Normalization of contractions to caffeine contractures indicated that amrinone increased fractional release by the VSRM, but not CICR. Forskolin and IBMX increased fractional release elicited by steps to -40 mV. Increases in CICR induced by forskolin and IBMX were proportional to caffeine contractures. Thus, positive inotropic effects of cAMP on VSRM contractions may be compartmentalized separately from effects on Ca(2+) current and CICR. (+info)Amrinone can accelerate the cooling rate of core temperature during deliberate mild hypothermia for neurosurgical procedures. (6/66)
We investigated the effects of i.v. amrinone on intraoperative changes of core temperature during deliberate mild hypothermia for neurosurgery. The patients in a control group (n=10) did not receive amrinone and patients in the amrinone group (n=10) received amrinone 5 microg kg(-1) min(-1) after a loading dose of 1.0 mg kg(-1). Anaesthesia was maintained with nitrous oxide in oxygen, propofol and fentanyl. After the induction of anaesthesia, patients were cooled and tympanic membrane temperature was maintained at 34.5 degrees C. After completion of the main surgical procedures, patients were rewarmed in the operating room. Tympanic membrane temperatures between 30 and 90 min after cooling were significantly lower in the amrinone group than in the control group. During cooling, the times taken to cool to 35 degrees C and to the lowest temperature were significantly shorter in the amrinone group than in the control group. These results suggest that i.v. amrinone can accelerate the cooling rate of core temperature during deliberate mild hypothermia for neurosurgical procedures. (+info)High-dose amrinone is required to accelerate rewarming from deliberate mild intraoperative hypothermia for neurosurgical procedures. (7/66)
BACKGROUND: Since the time available to provide the cooling and rewarming is limited during deliberate mild hypothermia, the technique to accelerate the cooling and rewarming rate of core temperature has been studied. Amrinone has been reported to accelerate the cooling rate but not the rewarming rate of core temperature during deliberate mild hypothermia. The failure of amrinone effect on the rewarming rate might be due to an insufficient dose of amrinone during hypothermic conditions. The authors therefore tested whether higher doses of amrinone can accelerate the rewarming rate of core temperature during deliberate mild hypothermia for neurosurgery. METHODS: After institutional approval and informed consent, 30 patients were randomly assigned to one of three groups. Patients in the control group (n = 10) did not receive amrinone; patients in the AMR 15 group (n = 10) received 15 microg x kg(-1) x min(-1) amrinone with a 1.0-mg/kg loading dose of amrinone at the beginning of cooling; and patients in the ReAMR group (n = 10) received 5 microg x kg(-1) x min(-1) amrinone with 1.0-mg/kg loading and reloading doses of amrinone at the beginning of cooling and rewarming, respectively. Administration of amrinone was started just after the induction of cooling and continued until the end of anesthesia. Anesthesia was maintained with nitrous oxide in oxygen, propofol, and fentanyl. After induction of anesthesia, patients were cooled, and tympanic membrane temperature was maintained at 34.5 degrees C. After completion of the main surgical procedures, patients were actively rewarmed and extubated in the operating room. RESULTS: The cooling and rewarming rates of core temperature were both significantly faster in both amrinone groups than in the control group. During the cooling and rewarming periods, forearm minus fingertip temperature gradient was significantly smaller in both amrinone groups than in the control group. During the rewarming period, heart rate and mean arterial pressure in the AMR 15 group were significantly faster and lower, respectively, than in the control group. Systemic vascular resistance in the AMR 15 group was smaller than in the control group throughout the study; on the other hand, only the value after the start of rewarming in the ReAMR group was smaller than in the control group. CONCLUSIONS: Amrinone at an infusion rate of 15 or 5 microg x kg(-1) x min(-1) with a reloading at the beginning of rewarming accelerated the rewarming rate of core temperature during deliberate mild hypothermia. This suggests that high-dose amrinone is required to accelerate rewarming from deliberate mild intraoperative hypothermia for neurosurgical procedures. (+info)Differential effects of amrinone and milrinone upon myocardial inflammatory signaling. (8/66)
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. (+info)Amrinone is a pharmacological agent, specifically a positive inotrope, that is used in the treatment of heart failure. It works by increasing the force of heart muscle contractions and improving cardiac output. Amrinone belongs to a class of drugs called phosphodiesterase inhibitors, which increase cyclic AMP levels in the heart, leading to increased contractility.
Here is the medical definition of 'Amrinone':
Amrinone: A synthetic cardiac drug that acts as a positive inotrope and vasodilator. It works by increasing the force of heart muscle contractions and reducing afterload, which improves cardiac output. Amrinone inhibits phosphodiesterase III, leading to increased intracellular cyclic AMP levels and enhanced calcium sensitivity in myocardial cells. It is used in the treatment of congestive heart failure and is administered intravenously.
Aminopyridines are a group of organic compounds that contain an amino group (-NH2) attached to a pyridine ring, which is a six-membered aromatic heterocycle containing one nitrogen atom. Aminopyridines have various pharmacological properties and are used in the treatment of several medical conditions.
The most commonly used aminopyridines in medicine include:
1. 4-Aminopyridine (also known as Fampridine): It is a potassium channel blocker that is used to improve walking ability in patients with multiple sclerosis (MS) and other neurological disorders. It works by increasing the conduction of nerve impulses in demyelinated nerves, thereby improving muscle strength and coordination.
2. 3,4-Diaminopyridine: It is a potassium channel blocker that is used to treat Lambert-Eaton myasthenic syndrome (LEMS), a rare autoimmune disorder characterized by muscle weakness. It works by increasing the release of acetylcholine from nerve endings, thereby improving muscle strength and function.
3. 2-Aminopyridine: It is an experimental drug that has been studied for its potential use in treating various neurological disorders, including MS, Parkinson's disease, and stroke. It works by increasing the release of neurotransmitters from nerve endings, thereby improving neuronal communication.
Like all medications, aminopyridines can have side effects, including gastrointestinal symptoms, headache, dizziness, and in rare cases, seizures. It is important to use these drugs under the supervision of a healthcare provider and follow their dosage instructions carefully.
Cardiotonic agents are a type of medication that have a positive inotropic effect on the heart, meaning they help to improve the contractility and strength of heart muscle contractions. These medications are often used to treat heart failure, as they can help to improve the efficiency of the heart's pumping ability and increase cardiac output.
Cardiotonic agents work by increasing the levels of calcium ions inside heart muscle cells during each heartbeat, which in turn enhances the force of contraction. Some common examples of cardiotonic agents include digitalis glycosides (such as digoxin), which are derived from the foxglove plant, and synthetic medications such as dobutamine and milrinone.
While cardiotonic agents can be effective in improving heart function, they can also have potentially serious side effects, including arrhythmias, electrolyte imbalances, and digestive symptoms. As a result, they are typically used under close medical supervision and their dosages may need to be carefully monitored to minimize the risk of adverse effects.
Milrinone is a type of medication known as an inotrope and vasodilator. It works by increasing the force of heart muscle contractions and relaxing the blood vessels, which leads to improved pumping ability of the heart and increased blood flow. Milrinone is primarily used in the treatment of heart failure, either in the hospital setting or after discharge, to improve symptoms and help the heart work more efficiently. It is given intravenously (through an IV) and its effects are closely monitored by healthcare professionals due to the potential for serious side effects such as irregular heart rhythms.
Rewarming, in a medical context, refers to the process of gradually increasing the body temperature of a person who is experiencing hypothermia. Hypothermia is a condition in which the core body temperature drops below 95°F (35°C), which can be caused by exposure to cold environments or certain medical conditions.
Rewarming can be accomplished through various methods, including:
1. Passive rewarming: This involves removing wet clothing and covering the person with warm blankets to allow their body to naturally increase its temperature.
2. Active external rewarming: This involves using warming devices such as heating pads or warm water bottles to apply heat to the skin surface.
3. Active core rewarming: This involves using more invasive methods, such as warmed intravenous fluids, warm air insufflation, or extracorporeal membrane oxygenation (ECMO) with a heat exchanger, to directly warm the internal organs and blood.
The choice of rewarming method depends on the severity of hypothermia, the presence of other medical conditions, and the resources available. It is important to monitor the person's vital signs and core temperature during rewarming to avoid complications such as rewarming shock or arrhythmias.
Phosphodiesterase inhibitors (PDE inhibitors) are a class of drugs that work by blocking the action of phosphodiesterase enzymes, which are responsible for breaking down cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), two crucial intracellular signaling molecules.
By inhibiting these enzymes, PDE inhibitors increase the concentration of cAMP and cGMP in the cells, leading to a variety of effects depending on the specific type of PDE enzyme that is inhibited. These drugs have been used in the treatment of various medical conditions such as erectile dysfunction, pulmonary arterial hypertension, and heart failure.
Examples of PDE inhibitors include sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra) for erectile dysfunction, and iloprost, treprostinil, and sildenafil for pulmonary arterial hypertension. It's important to note that different PDE inhibitors have varying levels of selectivity for specific PDE isoforms, which can result in different therapeutic effects and side effect profiles.
Amrinone
PDE3 inhibitor
Antihypotensive agent
List of MeSH codes (D03)
ATC code C01
List of MeSH codes (D02)
List of drugs: Am
Inotrope
Peter Wilmshurst
Phosphodiesterase inhibitor
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Error - wikidoc
Milrinone2
- Pharmacokinetics of the bipyridines amrinone and milrinone. (derangedphysiology.com)
- Positive inotropic and vasodilating effects of amrinone and milrinone in isolated canine heart. (ac.ir)
Congestive heart f1
- Amrinone also has beneficial effects during diastole in the left ventricle, including relaxation, compliance and filling in patients with congestive heart failure. (wikipedia.org)
Inamrinone2
- Amrinone, also known as inamrinone, and sold as Inocor, is a pyridine phosphodiesterase 3 inhibitor. (wikipedia.org)
- Formerly known as amrinone, inamrinone is a phosphodiesterase inhibitor with positive inotropic and vasodilator activity. (medscape.com)
Dobutamine1
- More recently, dopamine, dobutamine, and amrinone have been used to provide necessary inotropic support for the failing heart. (justia.com)
Inotropic2
- The positive inotropic effect of amrinone is mediated by the selective enhancement of high-gain CICR, which contributes to the contraction of myocytes by phosphorylation through cAMP dependent protein kinase A (PKA) and Ca2+ calmodulin kinase pathways. (wikipedia.org)
- Both inotropic and lusitropic effects justify the use of amrinone to treat heart failure. (wikipedia.org)
Cardiac2
- Amrinone decreases the pulmonary capillary wedge pressure while increasing cardiac output, as it functions as an arterial vasodilator and increases venous capacitance while decreasing venous return. (wikipedia.org)
- An IV administration of amrinone has been shown to increase cardiac output (CO) and stroke volume (SV), while concurrently reducing the filling pressure of the left ventricle and decreasing the resistance in the peripheral vasculature. (wikipedia.org)
Effects1
- Effects of Amrinone on Regional Myocardial Function and Oxygen Balance in Stunned Myocardium in Dogs. (ekja.org)
Agents1
- For this, the in vitro activity of four non-dihydropyridine agents (amrinone, fendiline, mibefradil, and lidoflazine) was tested against different Leishmania species and their cytotoxicity to mammalian cells was evaluated. (hindawi.com)
Heart2
- Amrinone has been shown to increase the contractions initiated in the heart by high-gain calcium induced calcium release (CICR). (wikipedia.org)
- Early studies in patients with heart failure showed that amrinone produced short-term hemodynamic improvement, but had limited long-term clinical benefit. (wikipedia.org)
Milrinone2
- PDE type III inhibitors like amrinone and milrinone are indicated for heart failure. (egpat.com)
- shows that Viagra Is able to amrinone and milrinone, and plays aspecific illnesses or of medical treatment for certain illnesses. (marshanorman.com)
Pulmonary3
- Amrinone decreases the pulmonary capillary wedge pressure while increasing cardiac output, as it functions as an arterial vasodilator and increases venous capacitance while decreasing venous return. (wikipedia.org)
- A decrease in pulmonary arterial diastolic pressure was observed after oral amrinone administration in three patients. (psu.edu)
- Effects of amrinone on pulmonary hemodynamics and pulmonary gas exchange in highland piglets]. (bvsalud.org)
Cardiovascular depression2
- A comparison of amrinone and glucagon therapy for cardiovascular depression associated with propranolol toxicity in a canine model. (nih.gov)
- A comparison of combined amrinone and glucagon therapy to glucagon alone for cardiovascular depression associated with propranolol toxicity in a canine model. (nih.gov)
Heart failure1
- Early studies in patients with heart failure showed that amrinone produced short-term hemodynamic improvement, but had limited long-term clinical benefit. (wikipedia.org)
Consumption1
- There is a net decrease in myocardial wall tension, and O2 consumption when using amrinone. (wikipedia.org)
Produces1
- An increase in cAMP with the administration of amrinone in vascular smooth muscle produces vasodilation by facilitating calcium uptake by the sarcoplasmic reticulum (a special type of smooth ER) and decreasing the calcium available for contraction. (wikipedia.org)