Find information on thousands of medical conditions and prescription drugs.

Levophed

Norepinephrine (INN) or noradrenaline (BAN) is a catecholamine and a phenethylamine with chemical formula C₈H₁₁NO₃. It is released from the adrenal glands as a hormone into the blood, but it is also a neurotransmitter in the nervous system where it is released from noradrenergic neurons during synaptic transmission. As a stress hormone, it affects parts of the human brain where attention and impulsivity are controlled. more...

Home

Lamisil

Lantus

Lariam

Larotid

Lasix

Lescol

Leucine

Levitra

Levora

Levoxyl

Levulan

Lexapro

Lexiva

Librium

Lidopen

Lipidil

Lipitor

Lithane

Lodine

Lomotil

Lortab

Lotrel

Lovenox

LSD

Lupron

Luvox

Luxiq

Theophylline

Along with epinephrine, this compound effects the fight-or-flight response, activating the sympathetic nervous system to directly increase heart rate, release energy from fat, and increase muscle readiness.

The host of physiological changes activated by a stressful event are unleashed in part by activation of a nucleus in the brain stem called the locus ceruleus. This nucleus is the origin of most norepinephrine pathways in the brain. Neurons using norepinephrine as their neurotransmitter project bilaterally from the locus ceruleus along distinct pathways to the cerebral cortex, limbic system, and the spinal cord, among other projections.

At synapses it acts on both alpha and beta adrenoreceptors.

Antidepressants

Changes in the norepinephrine system are implicated in depression. Serotonin-norepinephrine reuptake inhibitors (SNRIs) treat depression by increasing the amount of serotonin and norepinephrine available to postsynaptic cells in the brain. There is some recent evidence showing that the norepinephrine transporter also normally transports some dopamine as well, implying that SNRIs may also increase dopamine transmission. This is because SNRIs work by preventing the serotonin and norepinephrine transporter from taking their respective neurotransmitters back to their storage vesicles for later use. If the norepinephrine transporter normally recycles some dopamine too, then SNRIs will also enhance dopaminergic transmission. Therefore, the antidepressant effects associated with increasing norepinephrine levels may also be partly or largely due to the concurrent increase in dopamine (particularly in the prefrontal cortex).

Some other antidepressants (for example some tricyclic antidepressants (TCAs)) affect norepinephrine as well, in some cases without affecting other neurotransmitters (at least not directly).

Role in attention

Norepinephrine, along with dopamine, has come to be recognized as playing a large role in attention and focus. In response, Eli Lilly Pharmaceuticals has released Strattera (atomoxetine), a selective norephinephrine reuptake inhibitor, for the treatment of ADHD in adults and children. Strattera is unique in medications specifically indicated for ADHD, as, unlike the psychostimulants (methylphenidate, dextroamphetamine, Adderall (a racemic mixture of amphetamine salts)), it affects norephinephrine, rather than dopamine. As a result, Strattera has a very low abuse potential and can act 24 hours-per-day. (It should be noted that some antidepressants, including SNRIs, have been used off-label for treatment of ADHD.)

Clinical use

Norepinephrine (commonly referred to by the brand name Levophed) is also a powerful medicine used in critically-ill patients as a vasopressor. It is given intravenously and acts on both alpha-1 and beta-1 adrenergic receptors to cause vasoconstriction. Norepinephrine is mainly used to treat patients in septic shock.

Read more at Wikipedia.org

• [List your site here Free!]

Impact Of Tumor Necrosis Factor Gene Polymorphisms On Outcomes Of Coronary Artery Bypass Graft Surgery - TNF - CABG - Abstract
From CHEST, 10/1/00 by Yende Sachin

Sachin Yende, MBBS(*); Michael Quasney, MD PhD; Sarah Lambert, RN; Qing Zhang, BS and Richard Wunderink, MD FCCP. Methodist Lebonheur Healthcare, Memphis, TN and Methodist Lebonheur Healthcare and University of Tennessee, Memphis, TN.

PURPOSE: During CABG, exposure of blood to bypass circuit, products of complement system, ischemia-reperfusion injury and endotoxin re]eased from the gastrointestinal tract stimulate release of TNF[Alpha]. TNF[Alpha] itself is known to stimulate pro-inflammatory and anti-inflammatory cytokines;and plays a crucial role in the post CABG inflammatory cascade. The G[right arrow]--A transitions at the -308 site within the TNFa gene (TNFa-308) and at the +250 site within the TNF[Beta] gene (TNF[Beta]+250) is associated with increased TNF [Alpha] production. We therefore studied effects of these polymorphisms on outcomes of CABG.

METHODS: This was a prospective observational study. All patients undergoing conventional and off-pump CABG (OPCAB) were enrolled. Patients were weaned by standardized respiratory protocol and assessed at 8, 24 and 48 hours for failure to wean. Duration of inotropes (dopamine, dobutamine, levophed, amrinone, milrinone and epinephrine) and need for blood products (packed red cells, fresh frozen plasma, cryoprecipitate or platelets) within the first 48 hours were recorded. Patients homozygous for A allele (AA) at TNF[Alpha]-308 or TNF[Beta]+250 loci were compared to patients who were heterozygous for A allele (GA) or homozygous for G allele (GG). Pre-collected blood was used for gene analysis using polymerase chain reaction and restriction enzyme digestion. Primary endpoints include duration of mechanical ventilation, need for inotrope support and blood product transfusion within 48 hours after surgery. Secondary end-points include length of stay, need for discharge to rehabilition facility and 30 day mortality.

RESULTS: 247 patients were enrolled. 40.8% and 8.6% of patients failed to wean at 8 and 24 hours respectively. AA at both loci were more likely to wean at 8 and 24 hours (table). Kaplan Meier curves were plotted to study time to wean. AA at TNF[Alpha]-308, TNF[Beta]+250 or either of these loci weaned faster compared to GA/GG at these sites (p values 0.047, 0.02 and 0.005 respectively). AA at either loci had decreased length of stay and need for discharge to rehabilitation facility. The polymorphisms did not affect need for inotrope support, blood product transfusions or 30 day mortality. The effect of gene polymorphism on mechanical ventilation was seen only amongst patients undergoing conventional CABG (table). The positive, negative predictive values and odds ratio of the gene polymorphism to predict weaning was 99%, 8% and 10 respectively.

CONCLUSION: Patients AA at TNF[Beta]+250 or TNF[Alpha]-308 loci are associated with shorter duration of mechanical ventilation, length of ICU and hospital stay and less likely to require rehabilitation after CABG.

CLINICAL IMPLICATIONS: This is the first study to demonstrate effect of specific genotypes on outcomes of surgery. Pre-operative genotyping will improve risk stratification of patients and help surgeons choose optimal surgical technique (OPCAB versus conventional). Genotyping may equal spirometry as screening tool to predict risk of prolonged mechanical ventilation.

GRANT SUPPORT: This study was funded by the Methodist Lebonheur Healthcare and Crippled Children's Foundation.

Return to Levophed

Home

Contact

Resources

Exchange Links

ebay