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Hospital Practice (1995) Feb 2010The definition of septic shock includes sepsis-induced hypotension despite adequate fluid resuscitation, along with the presence of organ perfusion abnormalities, and... (Review)
Review
The definition of septic shock includes sepsis-induced hypotension despite adequate fluid resuscitation, along with the presence of organ perfusion abnormalities, and ultimately cell dysfunction. To restore adequate organ perfusion and cell homeostasis, cardiac output should be restored with volume infusion plus vasopressor agents as indicated. Appropriate arterial pressure for each individual patient and proper arterial oxygen content are key elements to restoring perfusion. Tissue perfusion can be monitored by markers of organ and mitochondrial function, namely urine output, level of consciousness, peripheral skin perfusion, central or mixed venous oxygen saturation, and lactate. The hemodynamic effects of the different vasopressor agents depend on the relative affinity to adrenergic receptors. Those with predominant alpha-agonist activity produce more vasoconstriction (inoconstrictors) while those with predominant beta-agonist stimulation increase cardiac performance (inodilators). The debate about whether one vasopressor agent is superior to another is still ongoing. The Surviving Sepsis Campaign guidelines refer to either norepinephrine or dopamine as the first-choice vasopressor agent to correct hypotension in septic shock. However, recent data from observational and controlled trials have challenged these recommendations concerning different adrenergic agents. As a result, our view on the prescription of vasopressors has changed from a probably oversimplified "one-size-fits-all" approach to a multimodal approach in vasopressor selection.
Topics: Adrenergic Agents; Algorithms; Blood Flow Velocity; Blood Pressure; Cardiotonic Agents; Decision Trees; Dobutamine; Dopamine; Epinephrine; Fluid Therapy; Humans; Lypressin; Monitoring, Physiologic; Norepinephrine; Patient Selection; Practice Guidelines as Topic; Resuscitation; Shock, Septic; Terlipressin; Treatment Outcome; Vasoconstrictor Agents; Vasopressins
PubMed: 20469626
DOI: 10.3810/hp.2010.02.280 -
The Annals of Pharmacotherapy Apr 2013To describe the evidence for serotonergic and adrenergic drug interactions with linezolid and discuss clinical management strategies. (Review)
Review
OBJECTIVE
To describe the evidence for serotonergic and adrenergic drug interactions with linezolid and discuss clinical management strategies.
DATA SOURCES
A literature search of PubMed (1947-November 2012), MEDLINE (1946-November 2012), EMBASE (1974-November 2012), and International Pharmaceutical Abstracts (1970-November 2012) was conducted using the terms linezolid, drug interaction, serotonin syndrome, serotonin toxicity, sympathomimetic, serotonergic agents, and adrenergic agents. Citations of retrieved articles were also reviewed.
STUDY SELECTION AND DATA EXTRACTION
English-language articles describing coadministration of serotonergic or adrenergic agents with linezolid to humans were included. Studies published only in abstract form were excluded.
DATA SYNTHESIS
One prospective study, 6 retrospective studies, and 24 case reports were identified describing a serotonergic or adrenergic drug interaction. Incidence of serotonin syndrome in patients on linezolid and serotonergic agents ranged between 0.24% and 4%. Serotonergic agents determined to have probable (according to the Horn Drug Interaction Probability Scale) linezolid interactions in case reports included meperidine, citalopram, escitalopram, fluoxetine, paroxetine, sertraline, duloxetine, and venlafaxine. Serotonergic agent dose and duration of coadministration with linezolid did not appear to influence the occurrence of serotonin syndrome. Adrenergic medication coadministration was associated with a possible drug interaction as determined by the Horn Drug Interaction Probability Scale but did not appear to result in clinically significant drug interactions with linezolid.
CONCLUSIONS
Linezolid-associated serotonergic drug interactions occur more commonly than adrenergic interactions. Serotonergic interactions considered probable according to the Horn Drug Interaction Probability Scale do not appear to correlate with drug dosage; time of onset ranges from <1 to 20 days, and effect resolves in <1 to 5 days after discontinuation of offending agents. If coadministration of linezolid and a serotonergic agent cannot be avoided, clinicians should be aware of the symptoms and management of serotonergic toxicity; close monitoring is recommended and additional serotonergic agents should not be used. While adrenergic drug interactions with linezolid are less common in clinical practice, monitoring for signs of hypertension remains important.
Topics: Acetamides; Adrenergic Agents; Drug Interactions; Humans; Linezolid; Oxazolidinones; Prospective Studies; Retrospective Studies; Serotonin Agents; Serotonin Syndrome
PubMed: 23548646
DOI: 10.1345/aph.1R604 -
Handbook of Experimental Pharmacology 2007Adrenergic and cholinergic signalling contributes significantly to the endogenous antinociceptive system. Exogenous alpha 2 adrenergic agonists have a well-established... (Review)
Review
Adrenergic and cholinergic signalling contributes significantly to the endogenous antinociceptive system. Exogenous alpha 2 adrenergic agonists have a well-established analgesic profile; however, recent investigations suggest that this class of agents is underused, and herein we highlight the potential for both current application and future development of these agents. Nicotinic and muscarinic cholinergic ligands represent a novel class of agents with much promise for the management of problematic pain. In this chapter we review advances in both preclinical and clinical arenas and highlight potential avenues for further research.
Topics: Adrenergic Agents; Adrenergic alpha-Agonists; Animals; Cholinergic Agents; Humans; Pain; Receptors, Adrenergic, alpha-2
PubMed: 17087126
DOI: 10.1007/978-3-540-33823-9_9 -
The Journal of Clinical Investigation Jan 2024The ability to fight or flee from a threat relies on an acute adrenergic surge that augments cardiac output, which is dependent on increased cardiac contractility and...
The ability to fight or flee from a threat relies on an acute adrenergic surge that augments cardiac output, which is dependent on increased cardiac contractility and heart rate. This cardiac response depends on β-adrenergic-initiated reversal of the small RGK G protein Rad-mediated inhibition of voltage-gated calcium channels (CaV) acting through the Cavβ subunit. Here, we investigate how Rad couples phosphorylation to augmented Ca2+ influx and increased cardiac contraction. We show that reversal required phosphorylation of Ser272 and Ser300 within Rad's polybasic, hydrophobic C-terminal domain (CTD). Phosphorylation of Ser25 and Ser38 in Rad's N-terminal domain (NTD) alone was ineffective. Phosphorylation of Ser272 and Ser300 or the addition of 4 Asp residues to the CTD reduced Rad's association with the negatively charged, cytoplasmic plasmalemmal surface and with CaVβ, even in the absence of CaVα, measured here by FRET. Addition of a posttranslationally prenylated CAAX motif to Rad's C-terminus, which constitutively tethers Rad to the membrane, prevented the physiological and biochemical effects of both phosphorylation and Asp substitution. Thus, dissociation of Rad from the sarcolemma, and consequently from CaVβ, is sufficient for sympathetic upregulation of Ca2+ currents.
Topics: Humans; Adrenergic Agents; Calcium; Calcium Channels, L-Type; Myocytes, Cardiac; Monomeric GTP-Binding Proteins; Arrhythmias, Cardiac
PubMed: 38227371
DOI: 10.1172/JCI176943 -
Journal of Cardiovascular Pharmacology... Jun 2003The primary goal of cardiopulmonary resuscitation is to reestablish blood flow to vital organs until spontaneous circulation is restored. Adrenergic vasopressor agents... (Review)
Review
The primary goal of cardiopulmonary resuscitation is to reestablish blood flow to vital organs until spontaneous circulation is restored. Adrenergic vasopressor agents produce systemic vasoconstriction. This increases aortic diastolic pressure, and consequently, coronary and cerebral perfusion pressures. The pharmacologic responses to the adrenergic agents are mediated by a group of receptors that are classified as alpha (alpha), including alpha1 and alpha2, and beta (beta), including beta1 and beta2. Epinephrine, which has each of these adrenergic actions, has been the preferred adrenergic agent for the management of cardiac arrest for almost 40 years. Its primary efficacy is due to its alpha-adrenergic vasopressor effects. This contrasts with its beta-adrenergic actions, which are inotropic, chronotropic, and vasodilator. Accordingly, beta-adrenergic actions prompt increases in myocardial oxygen consumption, ectopic ventricular arrhythmias, and transient hypoxemia due to pulmonary arteriovenous shunting. This may account for the failure to demonstrate that epinephrine improves ultimate outcomes in human victims of cardiac arrest. Major interest has more recently been focused on selective alpha-adrenergic agonists. Both alpha1-agonists and alpha2-agonists are peripheral vasopressors. However, rapid desensitization of alpha1-adrenergic receptors occurs during cardiopulmonary resuscitation. Moreover, alpha1-adrenergic receptors are present in the myocardium, and beta1-agonists, like beta-adrenergic agonists, increase myocardial oxygen consumption. If they cross the blood-brain barrier, alpha2-adrenoceptor agonists also have centrally acting vasodilator effects. In the absence of central nervous system access, alpha2-adrenergic agonists have selective peripheral vasoconstrictor effects. Under experimental conditions of cardiopulmonary resuscitation, selective alpha2-agonists, which do not gain entrance into the brain, produce only systemic vasoconstriction. Experimentally, these selective alpha2-agonists are as effective as epinephrine for initial cardiac resuscitation and have the additional advantage of minimizing myocardial oxygen consumption during the global myocardial ischemia of cardiac arrest. Accordingly, myocardial ischemic injury during cardiopulmonary resuscitation is minimized, and postresuscitation myocardial function is preserved with improved survival.
Topics: Adrenergic alpha-Agonists; Adrenergic beta-Agonists; Animals; Brain Ischemia; Cardiopulmonary Resuscitation; Epinephrine; Heart Arrest; Humans; Vasoconstrictor Agents; Vasopressins
PubMed: 12808484
DOI: 10.1177/107424840300800204 -
Pharmacological Reports : PR 2013α1-Adrenergic receptors (α1-ARs) are important players in peripheral and central nervous system (CNS) regulation and function and in mediating various behavioral... (Review)
Review
α1-Adrenergic receptors (α1-ARs) are important players in peripheral and central nervous system (CNS) regulation and function and in mediating various behavioral responses. The α1-AR family consists of three subtypes, α1A, α1B and α1D, which differ in their subcellular distribution, efficacy in evoking intracellular signals and transcriptional profiles. All three α1-AR subtypes are present at relatively high densities throughout the CNS, but the contributions of the individual subtypes to various central functions are currently unclear. Because of the lack of specific ligands, functionally characterizing the α1-ARs and discriminating between the three subtypes are difficult. To date, studies using genetically engineered mice have provided some information on subtype-related functions of the CNS α1-ARs. In this mini-review, we discuss several CNS processes where the α1-ARs role has been delineated with pharmacological tools and by studies using mutated mice strains that infer specific α1-AR subtype functions through evaluation of behavioral phenotypes.
Topics: Adrenergic Agents; Animals; Animals, Genetically Modified; Central Nervous System; Humans; Mice; Receptors, Adrenergic, alpha-1
PubMed: 24552996
DOI: 10.1016/s1734-1140(13)71509-3 -
Annual Review of Pharmacology 1965
Review
Topics: Adrenergic Agents; Adrenergic Antagonists; Neurons; Pharmacology; Sympatholytics
PubMed: 14287879
DOI: 10.1146/annurev.pa.05.040165.001151 -
Lancet (London, England) Nov 1964
Topics: Adrenergic Antagonists; Adrenergic beta-Antagonists; Asthma; Humans; Pharmacology; Propranolol; Respiratory Function Tests; Statistics as Topic; Sympatholytics
PubMed: 14207902
DOI: 10.1016/s0140-6736(64)92617-0 -
Archives of Razi Institute Jul 2021Central dopaminergic (DAergic) and adrenergic systems have a prominent role in appetite regulation; however, their interaction(s) have not been studied in neonatal layer...
Central dopaminergic (DAergic) and adrenergic systems have a prominent role in appetite regulation; however, their interaction(s) have not been studied in neonatal layer chickens.Therefore, the current study aimed to determine the interaction of central DAergic and noradrenergic systems in food intake regulation in neonatal layer chickens. In the first experiment, chickens received the intracerebroventricular (ICV) injection of a control solution, prazosin (i.e., α1 adrenergic receptor antagonist; 10 nmol), dopamine (DA; 40 nmol), and prazosin plus DA. The second to fifth experiments were similar to the first experiment except that the birds were injected with yohimbine (i.e., α2 receptor antagonist; 13 nmol), metoprolol (i.e., β1 adrenergic receptor antagonist; 24 nmol), ICI 118,551 (i.e., β2 adrenergic receptor antagonist; 5 nmol), and SR59230R (i.e., β3 adrenergic receptor antagonist; 20 nmol) instead of prazosin. In the sixth experiment, the chickens received ICV injection with the control solution and noradrenaline (NA; 75, 150, and 300 nmol). In the seventh experiment, the birds were injected with the control solution, SCH23390 (i.e., D1 DAergic receptor antagonist; 5 nmol), NA (300 nmol), and SCH23390 plus NA In the eighth experiment, the control solution, AMI-193 (i.e., D2 DAergic receptor antagonist; 5 nmol), NA (300 nmol), and AMI-193 plus NA were injected. Then, cumulative food intake was recorded at 30, 60, and 120 min after the injection. According to the obtained results, the ICV injection of DA (40 nmol) significantly decreased food intake in comparison to that reported for the control group (p <0.05). The co-injection of yohimbine plus DA significantly amplified DA-induced hypophagia in the neonatal chickens (p <0.05). In addition, the co-administration of ICI 118,551 plus DA significantly inhibited the hypophagic effect of DA in the neonatal chickens (p <0.05). Furthermore, NA (75, 150, and 300 nmol) significantly reduced food intake in a dose-dependent manner (p <0.05). The co-injection of SCH23390 plus NA decreased the hypophagic effect of NA in the neonatal chickens, compared to that reported for the control group (p <0.05). The co-injection of AMI-193 plus NA diminished NA-induced hypophagia, compared to that reported for the control group (p <0.05). The aforementioned results suggested that there is an interconnection between central DAergic and noradrenergic systems through α2/β2 adrenergic and D1/D2 DAergic receptors in food intake regulation in neonatal chicks.
Topics: Adrenergic Agents; Animals; Animals, Newborn; Chickens; Dopamine; Eating; Feeding Behavior
PubMed: 34223733
DOI: 10.22092/ari.2020.341240.1425 -
Clinical Pharmacy Jun 1987Glaucoma is described, and the chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of betaxolol and levobunolol... (Clinical Trial)
Clinical Trial Comparative Study Review
Glaucoma is described, and the chemistry, pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of betaxolol and levobunolol in comparison with timolol are reviewed. Betaxolol and levobunolol are two beta-adrenergic blocking agents being marketed as ophthalmic solutions for treatment of primary open-angle glaucoma (POAG) and ocular hypertension (OHT). Betaxolol is a relatively cardioselective beta-adrenergic blocker, while levobunolol is a nonselective beta-adrenergic blocking agent. Double-blind comparative trials have suggested that betaxolol has an equal to slightly lower efficacy and levobunolol has equal efficacy in reducing intraocular pressure (IOP) compared with timolol, the first ophthalmic beta blocker. A mean reduction in intraocular pressure of 15-35% occurs with both betaxolol and levobunolol and is reported to be maintained with prolonged use. Betaxolol is associated with a higher (25%) incidence of local ocular adverse reactions than timolol. However, betaxolol produces less systemic beta 2- and possibly beta 1-adrenergic receptor blockade than either timolol or levobunolol. Betaxolol may be relatively safer to use in patients with reactive airway disease than either timolol or levobunolol. Levobunolol causes a similar to greater incidence of local ocular adverse reactions and similar systemic beta blockade compared with timolol. Levobunolol may possibly be longer acting than timolol, allowing more patients to be controlled by once-daily dosing. Betaxolol and levobunolol appear to be similar to timolol in controlling IOP in patients with POAG and OHT; additional experience with these agents is needed to assess the advantages and disadvantages of each agent.
Topics: Adrenergic beta-Antagonists; Betaxolol; Cardiovascular System; Clinical Trials as Topic; Glaucoma; Humans; Intraocular Pressure; Levobunolol; Propanolamines
PubMed: 2891463
DOI: No ID Found