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Norepinephrine

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10381. Pharmacological characterization of isolated human prostate. (Abstract)

transducers. Specimens were subjected to agonist induced contractions, the first always being norepinephrine (NE). Specimens were pretreated with antagonist (adrenergic, cholinergic, nonadrenergic noncholinergic or none if control), followed by contraction with a second agonist (NE or other). Contractile tensions were recorded on a polygraph and then statistically analyzed.The order of highest to lowest agonist induced tensile forces was NE, dopamine, acetylcholine, bethanechol, histamine and serotonin

2003 Journal of Urology

10382. A review of the physiology and pharmacology of peripheral (vaginal and clitoral) female genital arousal in the animal model. (Abstract)

culture, genital strip organ bath and in vivo animal model studies.Nitric oxide (NO) appears to be a key pathway mediating clitoral smooth muscle relaxation. In the vagina NO appeared to have a more controversial role in mediating vaginal muscularis smooth muscle relaxation. Vasoactive intestinal polypeptide induced vaginal smooth muscle relaxation. Functional alpha-adrenergic receptors were expressed in the clitoris and vagina, and mediated norepinephrine induced genital smooth muscle contraction

2003 Journal of Urology

10383. 5-hydroxytryptamine and thromboxane A2 as physiologic mediators of human umbilical artery closure. (Abstract)

II, bradykinin, endothelin-1, histamine, norepinephrine, phenylephrine, and U46619 (a thromboxane A(2) mimetic).Only 5-hydroxytryptamine, bradykinin, endothelin-1, histamine, and U46619 produced appreciable maximal contractions. Furthermore, although the contractile force generated by these agonists was diminished in normal oxygen conditions, this reduction affected responses to 5-hydroxytryptamine and U46619 least.5-Hydroxytryptamine and U46619 demonstrated the characteristics most likely

2003 Journal of the Society for Gynecologic Investigation

10384. Mechanistic investigation of the adrenergic induction of ventral prostate hyperplasia in mice. (Abstract)

Mechanistic investigation of the adrenergic induction of ventral prostate hyperplasia in mice. The norepinephrine (NE) analog phenylephrine has previously been shown to induce atypical prostate hyperplasia in rats. The objective of the present study was to provide further insight into the mechanism of phenylephrine-induced prostate growth.Adult male C57/BL6 mice were given daily subcutaneous injection of phenylephrine, isoproterenol, or phenylephrine in combination with BMY7378, cyclazosin

2003 Prostate

10385. The vascular endothelin system is not overactive in normotensive hemodialysis patients. (Full text)

The vascular endothelin system is not overactive in normotensive hemodialysis patients. The hemodynamic significance of elevated endothelin-1 (ET) plasma levels in hemodialysis (HD) patients is unknown. Therefore, we studied the role of ET in the regulation of vascular tone in normotensive HD patients and matched healthy controls (C).The forearm blood flow (FBF) responses to adenosine, norepinephrine, the ET-A receptor antagonist BQ-123 (40 nmol/min), the ET-B receptor antagonist BQ-788 (1 (...) and 50 nmol/min), and ET (5 pmol/min) were measured. Results are percent of baseline change +/- SEM (baseline = 100%).Responses to adenosine and norepinephrine were both unchanged in HD. In HD, BQ-123 increased FBF less than in C (133 +/- 9 vs. 178 +/- 27%; P = 0.02). BQ-788 failed to change FBF in C but decreased FBF to 83 +/- 4% in HD. Compared to BQ-123 alone, BQ-123 plus BQ-788 (50 nmol/min) caused an additional increase of FBF (234 +/- 32%, P < 0.001) in C, but not in HD (139 +/- 14

2002 Kidney International PubMed abstract

10386. Sympathetic control of the circulation in hypertension: lessons from autonomic disorders. (Abstract)

outflow, and enhanced norepinephrine release (or decrease reuptake) from sympathetic nerve terminals. Whether genetic polymorphisms of adrenoreceptors are associated with essential hypertension is an area of active research.Increased sympathetic activity can contribute to sustained hypertension not only because of its hemodynamic effects (increased cardiac output and vascular resistance), but also by altering renal and water handling by the kidney, and by inducing cardiac and vascular remodeling

2003 Current Opinion in Nephrology and Hypertension

10387. Effect of botulinum toxin A on the autonomic nervous system of the rat lower urinary tract. (Abstract)

Effect of botulinum toxin A on the autonomic nervous system of the rat lower urinary tract. The magnitude and duration of the effects of botulinum toxin A on acetylcholine (ACh) and norepinephrine release from the bladder and urethra of rats were measured using a radiochemical method.Saline (sham treatment) or botulinum toxin A was injected into the bladder (50 microl.) or urethra (30 microl.) in separate groups of animals. The release of 3H-norepinephrine or 14C-choline was measured at 2 time (...) points after injection (5 or 30 days).The fractional release of ACh in botulinum toxin A treated animals was significantly inhibited at higher frequencies of electrical field stimulation (20 Hz.) but not at lower frequencies (2 Hz.) 5 days after injection. However, ACh release recovered to sham injected values 30 days after toxin injection. No significant differences in the fractional release of norepinephrine from sham injected or botulinum toxin A bladders were observed. In contrast, norepinephrine

2003 Journal of Urology

10388. Hemodynamic response to lower body negative pressure in hemodialysis patients. (Abstract)

continuously after cannulation of the right jugular vein. Stroke volume index was measured at each step echocardiographically. At the end of each level of LBNP, blood samples were obtained to measure norepinephrine (NE), epinephrine (E), and atrial natriuretic peptide (ANP) levels.At baseline, CVP (12 +/- 5 and 16 +/- 7 mm Hg), heart rate (72 +/- 9 and 70 +/- 13 beats/min), cardiac index (2.3 +/- 0.6 and 2.5 +/- 0.9 L/min), NE (median, 341 pg/mL [range,198 to 789 pg/mL] and 365 pg/mL [range, 177 to 675 pg

2003 American Journal of Kidney Diseases

10389. Role of the alpha2-adrenoceptors on the pulmonary circulation in the ovine fetus. (Full text)

Role of the alpha2-adrenoceptors on the pulmonary circulation in the ovine fetus. Recent in vitro studies reported that nitric oxide release and pulmonary vasorelaxation can be mediated by endothelial alpha2-adrenoceptor activation. As norepinephrine (alpha1-,alpha2-, and beta1-adrenoceptor agonist) was found to induce pulmonary vasodilation in the ovine fetus, we hypothesized that alpha2-adrenoceptors may modulate basal pulmonary vascular tone and mediate the vascular effect of norepinephrine (...) during fetal life. To determine the role of alpha2-adrenoceptors and the mechanisms of norepinephrine-mediated vasodilation in the fetal pulmonary circulation, we tested, in chronically prepared late-gestation fetal lambs, the hemodynamic response to 1). yohimbine (alpha2 antagonist); 2). UK 14304 (alpha2 agonist) with and without l-nitro-arginine (nitric oxide synthase inhibitor); and 3). norepinephrine infusion with and without yohimbine. We found that yohimbine increased mean pulmonary artery

2003 Pediatric Research PubMed abstract

10390. Early reversal of pediatric-neonatal septic shock by community physicians is associated with improved outcome. (Abstract)

increased odds of mortality (2.29 [1.19-4.44]). Nonsurvivors, compared with survivors, were treated with more inotropic therapies (dopamine/dobutamine [42% vs 20%] and epinephrine/norepinephrine [42% vs 6%]) but not increased fluid therapy (median volume; 32.9 mL/kg vs 20.0 mL/kg). Resuscitation practice was consistent with ACCM-PALS Guidelines in only 27 (30%) patients; however, when practice was in agreement with guideline recommendations, a lower mortality was observed (8% vs 38%).Early recognition

2003 Pediatrics

10391. Effect of maternal smoking on fetal catecholamine concentrations at birth. (Full text)

was collected at delivery for arterial pH and catecholamine concentrations. Cord blood was obtained from 51 subjects, including 21 smokers and 30 nonsmokers. Median epinephrine concentrations [304 pg/mL versus 597 pg/mL (Mann-Whitney U = 170; p = 0.006)] and median norepinephrine concentrations [3148 pg/mL versus 6558 pg/mL (Mann-Whitney U = 191; p = 0.006)] were significantly lower in smokers compared with nonsmokers, respectively. After controlling for gestational age, route of delivery, and arterial pH (...) , log-transformed epinephrine concentrations between smokers and nonsmokers were statistically significant (p = 0.03), with a similar trend for log-transformed norepinephrine concentrations (p = 0.07). Analyses of the data using cotinine <20 ng/mL to classify nonsmokers also showed differences in epinephrine concentrations between groups (p = 0.02). These results are consistent with results from animal studies showing that catecholamine concentrations may be affected by prenatal nicotine exposure

2003 Pediatric Research PubMed abstract

10392. Catecholamine response to exercise in children with attention deficit hyperactivity disorder. (Full text)

in children with ADHD. To test this, we recruited 10 treatment-naïve children with newly diagnosed ADHD and 8 age-matched controls (all male) and measured CA response to an exercise test in which the work was scaled to each subject's physical capability. After exercise, epinephrine and norepinephrine increased in both control and ADHD subjects (p = 0.006 and p = 0.002, respectively), but the responses were substantially blunted in the ADHD group (p = 0.018) even though the work performed did not differ

2003 Pediatric Research PubMed abstract

10393. Multifactorial analysis of the aetiology of craniomandibular dysfunction in children. (Abstract)

parafunctions were recorded by the same investigator in an interview. Emotional stress was measured through urinary catecholamines including epinephrine, norepinephrine and dopamine, detected in a 24-h urine sample, using high performance liquid chromatography. A questionnaire was distributed to the parents to collect information regarding socioeconomic factors and the history of dentofacial injuries. A logistic multiple regression was carried out to estimate the partial effect of each aetiologic factor

2002 International Journal of Paediatric Dentistry

10394. Plasma levels of catechols and metanephrines in neurogenic orthostatic hypotension. (Abstract)

Plasma levels of catechols and metanephrines in neurogenic orthostatic hypotension. Neurogenic orthostatic hypotension (NOH) usually results from deficient release of the sympathetic neurotransmitter norepinephrine (NE) when the patient stands up. In pure autonomic failure (PAF) and PD with NOH, sympathetic denervation can explain this deficiency, whereas in multiple-system atrophy (MSA), deficient baroreflex regulation of sympathetic traffic to intact terminals probably causes the NOH. From

2003 Neurology

10395. Neurotransmitter specificity of sympathetic denervation in Parkinson's disease. (Abstract)

Neurotransmitter specificity of sympathetic denervation in Parkinson's disease. In PD, orthostatic hypotension reflects sympathetic noradrenergic denervation. The authors assessed sympathetic cholinergic innervation by the quantitative sudomotor axon reflex test (QSART) in 12 patients who had sympathetic neurocirculatory failure, markedly decreased cardiac 6-[18F] fluorodopamine-derived radioactivity, and subnormal plasma norepinephrine increments during standing. All 12 had normal QSART

2003 Neurology

10396. beta 2-Adrenoceptor regulation of CGRP release from capsaicin-sensitive neurons. (Abstract)

(iCGRP) release from capsaicin-sensitive nociceptive neurons via in vitro superfusion of bovine dental pulp. Either norepinephrine or epinephrine inhibited capsaicin-evoked iCGRP. The norepinephrine effect was blocked by the selective beta(2)-adrenoceptor antagonist, ICI 118,551, but not by pre-treatment with the selective beta(1)-adrenoceptor antagonist, atenolol. In addition, application of albuterol, a selective beta(2)-adrenoceptor agonist, significantly blocked capsaicin-evoked release of iCGRP

2003 Journal of Dental Research

10397. Intrinsic regulation of CGRP release by dental pulp sympathetic fibers. (Abstract)

Intrinsic regulation of CGRP release by dental pulp sympathetic fibers. Neurotransmission from sympathetic and peptidergic afferent fibers participates in the regulation of pulpal blood flow (PBF) via opposing effects. In this study, we directly tested the hypothesis that activation of pulpal sympathetic terminals inhibits exocytosis of immunoreactive calcitonin gene-related peptide (iCGRP) from peptidergic afferents innervating bovine dental pulp. The results demonstrate that norepinephrine

2003 Journal of Dental Research

10398. Hemodynamic response to coupled plasmafiltration-adsorption in human septic shock. (Abstract)

-1,867] dynes x s/cm(5); [ p<0.001]), PO2/FIO2 ratio (204+/-87 [CI 95%; 185-223] vs. 238+/-82 [CI 95%; 220-256]; [ p<0.001]), significantly improved during 100 global treatments (pre- vs. post-treatment values). Intra-thoracic blood volume and extra-vascular lung water did not change across treatments. Vasopressor requirement was reduced: norepinephrine decrease from an infusion rate of 0.13+/-0.07 (CI 95%; 0.06-0.16) to 0 gamma/kg/min after a mean of 5.3+/-2.7 sessions. C reactive protein (CRP

2003 Intensive Care Medicine

10399. A canine study of immunotherapy in scorpion envenomation. (Abstract)

) to 5775 dyn sec(-1 )m(5), P<0.05 for all). Heart rate, cardiac output, and stroke volume decreased. There was a 40-fold increase in epinephrine and norepinephrine plasma concentrations. Circulating NPY and ANP dosages increased too. PAOP and MAP decreased thereafter to reach baseline levels. Simultaneous administration of SAV with venom totally offset the hallmarks of scorpion envenomation. Delayed administration of SAV at any dosage failed to alter the features of scorpion envenomation.While

2003 Intensive Care Medicine

10400. Cyclooxygenase-2 and inducible nitric oxide synthase in omental arteries harvested from patients with severe liver diseases: immuno-localization and influence on vascular tone. (Abstract)

responses to norepinephrine and the thromboxane A(2) analog, U46619, were not significantly different between patients with severe liver dysfunction and controls. Exposure to either the NO-synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), the cyclooxygenase inhibitor, indomethacin, or their combination did not significantly modify contractions of agonists in controls and CH patients. In FHF, the specific COX-2 inhibitor, N-(2-cyclohexyloxy-4-nitrophenyl) methanesulfonamide (1 micro m/l

2003 Intensive Care Medicine

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