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Norepinephrine

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10521. Lateral hypothalamic lesions and norepinephrine turnover in rats. Full Text available with Trip Pro

Lateral hypothalamic lesions and norepinephrine turnover in rats. Animals with lateral hypothalamic lesions lost significantly more weight in the 18 h following this lesion than did sham-operated animals or rats with cerebral cortical lesions deprived of food for the same time period. In the acutely fasted sham-operated animals the turnover of norepinephrine in interscapular brown adipose tissue, heart, and pancreas was slowed but in fasted rats with lateral hypothalamic lesions norepinephrine (...) turnover rates were three- to ninefold faster in all three organs. Exposure to the cold (4 degrees C) significantly increased norepinephrine turnover in the interscapular brown adipose tissue, heart, and pancreas of fasted sham-operated rats, but did not further increase the rate of turnover in lateral hypothalamic-lesioned rats. Rats with lesions in the cerebral cortex responded in a fashion similar to that of the sham-operated animals. Gastric erosions and microhemorrhagic gastric mucosa were

1983 Journal of Clinical Investigation

10522. Whole Body Clearance of Norepinephrine. THE SIGNIFICANCE OF ARTERIAL SAMPLING AND OF SURGICAL STRESS Full Text available with Trip Pro

Whole Body Clearance of Norepinephrine. THE SIGNIFICANCE OF ARTERIAL SAMPLING AND OF SURGICAL STRESS The whole body clearance of norepinephrine (NE) was measured in seven patients pre- and postoperatively. L[(3)H]NE was infused intravenously for 90 min and steady-state concentrations of L[(3)H]NE were measured at 75 and 90 min in both arterial and peripheral venous blood. Preoperatively, in the resting supine position, the clearance values based on arterial and venous sampling averaged 1.4

1983 Journal of Clinical Investigation

10523. Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response. Full Text available with Trip Pro

Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response. We have shown recently that norepinephrine stimulates muscle cell hypertrophy in primary cultures from the neonatal rat ventricle and that this stimulation is not blocked by the beta adrenergic antagonist propranolol. The present study was done to define the adrenergic specificity of the myocyte hypertrophic response to norepinephrine. 90% pure, single-cell cultures of nongrowing myocytes (...) were maintained in serum-free medium 199 with transferin and insulin. Myocyte size was quantitated 48 h after addition of adrenergic agents, by measuring cell volume, cell surface area, and cell protein. L-norepinephrine increased myocyte size to a maximum 150% of control; half-maximum effect was obtained at a concentration of 0.2 microM. This increase in cell size was inhibited by the nonselective alpha adrenergic antagonist phentolamine and by the alpha 1 adrenergic antagonists prazosin

1983 Journal of Clinical Investigation

10524. Effect of total hepatectomy and administration of branched-chain amino acids on regional norepinephrine, dopamine, and amino acids in rat brain. Full Text available with Trip Pro

Effect of total hepatectomy and administration of branched-chain amino acids on regional norepinephrine, dopamine, and amino acids in rat brain. In rats after total hepatectomy, the effect of infusing glucose alone or combined with branched-chain amino acids on amino acid concentrations in plasma and cerebral cortex and on catecholamine levels in eight different regions of the brain was studied. Infusion of branched-chain amino acids reduced the accumulation of tryptophan, phenylalanine (...) , and tyrosine in plasma, while in cerebral cortex, the concentrations of phenylalanine and tyrosine were normalized and that of tryptophan was reduced greatly. In rats with hepatectomy and glucose infusion alone, norepinephrine levels were decreased in seven of eight brain regions with the exception of striatum, while dopamine was reduced significantly in striatum only. Infusion of branched-chain amino acids resulted in higher norepinephrine in cortex, mesencephalon, and hypothalamus and higher striatal

1983 Annals of Surgery

10525. Cerebroventricular calcitonin gene-related peptide inhibits rat duodenal bicarbonate secretion by release of norepinephrine and vasopressin. Full Text available with Trip Pro

Cerebroventricular calcitonin gene-related peptide inhibits rat duodenal bicarbonate secretion by release of norepinephrine and vasopressin. Proximal duodenal bicarbonate secretion is an important factor in humans and animals protecting the mucosa against acid-peptic damage. This study examined the mechanisms responsible for the central nervous system regulation of duodenal bicarbonate secretion by calcitonin gene-related peptide (CGRP) in unrestrained rats. Cerebroventricular administration (...) with significant increases in plasma norepinephrine (NE) and vasopressin concentrations. The alpha adrenergic receptor antagonist, phentolamine, and the vasopressin V1 receptor antagonist, (1-deaminopenicillamine, 2-[O-methyl]Tyr, 8-Arg)-vasopressin, given intravenously reversed the central inhibitory effect of CGRP by approximately 50% each. Pretreatment of the animals with both phentolamine and the vasopressin antagonist completely abolished the central inhibitory effect of CGRP. Peripheral vasopressin

1990 Journal of Clinical Investigation

10526. Chronic norepinephrine elicits desensitization by uncoupling the beta-receptor. Full Text available with Trip Pro

Chronic norepinephrine elicits desensitization by uncoupling the beta-receptor. The goal of this study was to determine the mechanism of beta-adrenergic receptor desensitization after chronic elevation of circulating NE levels. Osmotic minipumps containing either NE or saline were implanted subcutaneously in dogs for 3-4 wk. Physiologic desensitization to isoproterenol was confirmed in conscious dogs, i.e., left ventricular dP/dt increased in response to isoproterenol (0.4 micrograms/kg per min

1989 Journal of Clinical Investigation

10527. Forearm beta adrenergic receptor-mediated vasodilation is impaired, without alteration of forearm norepinephrine spillover, in borderline hypertension. Full Text available with Trip Pro

Forearm beta adrenergic receptor-mediated vasodilation is impaired, without alteration of forearm norepinephrine spillover, in borderline hypertension. Impaired beta adrenoceptor-mediated vasodilation associated with enhanced sympathetic activity has been reported in established hypertension. We examined whether altered beta adrenoceptor-mediated vasodilation occurs early in the disease process, when structural vascular changes are likely to be less marked, by measurement of forearm blood flow (...) vascular resistance, was impaired in the BHT group so that flow at the highest dose of isoproterenol (400 ng/min) increased less (15.2 +/- 1.5 ml/100 ml per min) than in the NT group (24.4 +/- 2.4 ml/100 ml per minute) (P < 0.001). Although, systemic norepinephrine spillover was significantly greater in BHT, the difference in blood flow response to isoproterenol was not accounted for by increased local sympathetic activity since forearm norepinephrine spillover at baseline (BHT 1.0 +/- 0.4 ng/min vs

1995 Journal of Clinical Investigation

10528. Proadrenomedullin NH(2)-terminal 20 peptide, a new product of the adrenomedullin gene, inhibits norepinephrine overflow from nerve endings. Full Text available with Trip Pro

Proadrenomedullin NH(2)-terminal 20 peptide, a new product of the adrenomedullin gene, inhibits norepinephrine overflow from nerve endings. Proadrenomedullin NH(2)-terminal 20 peptide (PAMP) and adrenomedullin, which are derived from proadrenomedullin, exhibit remarkable hypotensive action. We investigated the effect of PAMP and adrenomedullin on peripheral sympathetic neutral transmission. Using perfused rat mesenteric arteries, PAMP (0, 1, 5, and 10 pmol/ml) decreased norepinephrine overflow (...) by periarterial electrical nerve stimulation in a dose-dependent fashion (0.244 +/- 0.043, 0.231 +/- 0.048, 0.195 +/- 0.061 and 0.168 +/- 0.051 ng/gram tissue weigh: NS, P < 0.05, and P < 0.02, respectively). In contrast to PAMP, adrenomedullin (1, 5, and 10 pmol/ml) did not change it. In contrast, vasoconstrictive response of mesenteric arteries to exogenous norepinephrine was significantly attenuated by 10 pmol/ml of adrenomedullin but not by the same dose of PAMP. Calcitonin gene-related peptide (8-37

1995 Journal of Clinical Investigation

10529. Anti-(14-3-3 protein) antibody inhibits stimulation of noradrenaline (norepinephrine) secretion by chromaffin-cell cytosolic proteins. Full Text available with Trip Pro

Anti-(14-3-3 protein) antibody inhibits stimulation of noradrenaline (norepinephrine) secretion by chromaffin-cell cytosolic proteins. Incubation of digitonin-permeabilized bovine chromaffin cells in the absence of Ca2+ results in a loss of both cytosolic proteins and Ca(2+)-dependent secretion. Addition of these leaked proteins prevents this loss of secretory activity. We have purified a protein from an extract of bovine adrenal medulla which can partially prevent this loss of Ca(2+)-dependent

1992 Biochemical Journal

10530. Sympathetic discharge to mesenteric organs and the liver. Evidence for substantial mesenteric organ norepinephrine spillover. Full Text available with Trip Pro

Sympathetic discharge to mesenteric organs and the liver. Evidence for substantial mesenteric organ norepinephrine spillover. This study using sampling of blood from the portal vein, in addition to arterial and hepatic sites, to estimate separately spillovers of norepinephrine from mesenteric organs and the liver in seven patients undergoing upper abdominal surgery. Conventional measurements in arterial and hepatic venous plasma provided a measure of net hepatomesenteric NE spillover (403 pmol

1996 Journal of Clinical Investigation

10531. Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose–response study Full Text available with Trip Pro

Inhaled nitric oxide in acute respiratory distress syndrome with and without septic shock requiring norepinephrine administration: a dose–response study BACKGROUND: The aim of this prospective study was to assess whether the presence of septic shock could influence the dose response to inhaled nitric oxide (NO) in NO-responding patients with adult respiratory distress syndrome (ARDS). RESULTS: Eight patients with ARDS and without septic shock (PaO2 = 95 +/- 16 mmHg, PEEP = 0, FiO2 = 1.0 (...) ), and eight patients with ARDS and septic shock (PaO2 = 88 +/- 11 mmHg, PEEP = 0, FiO2 = 1.0) receiving exclusively norepinephrine were studied. All responded to 15 ppm inhaled NO with an increase in PaO2 of at least 40 mmHg, at FiO2 1.0 and PEEP 10 cmH2O. Inspiratory intratracheal NO concentrations were recorded continuously using a fast response time chemiluminescence apparatus. Seven inspiratory NO concentrations were randomly administered: 0.15, 0.45, 1.5, 4.5, 15, 45 and 150 ppm. In both groups

1997 Critical Care Controlled trial quality: uncertain

10532. Elevated Plasma Norepinephrine After In Utero Exposure to Cocaine and Marijuana Full Text available with Trip Pro

Elevated Plasma Norepinephrine After In Utero Exposure to Cocaine and Marijuana To compare plasma catecholamine concentrations between cocaine-exposed and unexposed term newborns and to determine the relationship between plasma catecholamines and newborn behavior.Forty-six newborn infants participating in a prospective study of the neonatal and long-term effects of prenatal cocaine exposure were studied. Based on maternal self-report, maternal urine screening, and infant meconium analysis, 24 (...) infants were classified as cocaine-exposed and 22 as unexposed. Between 24 and 72 hours postpartum, plasma samples for norepinephrine (NE), epinephrine, dopamine, and dihydroxyphenylalanine analysis were obtained. The Neonatal Behavioral Assessment Scale was administered at 1 to 3 days of age and at 2 weeks of age by examiners masked to the drug exposure status of the newborns.The cocaine-exposed newborns had increased plasma NE concentrations when compared to the unexposed infants (geometric mean

1997 Pediatrics

10533. Nitric oxide, atrial natriuretic peptide, and cyclic GMP inhibit the growth-promoting effects of norepinephrine in cardiac myocytes and fibroblasts. Full Text available with Trip Pro

Nitric oxide, atrial natriuretic peptide, and cyclic GMP inhibit the growth-promoting effects of norepinephrine in cardiac myocytes and fibroblasts. This study tested the hypothesis that nitric oxide (NO) and atrial natriuretic peptide (ANP) can attenuate the effects of adrenergic agonists on the growth of cardiac myocytes and fibroblasts. In ventricular cells cultured from neonatal rat heart, ANP and the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP) caused concentration-dependent (...) decreases in the norepinephrine (NE)-stimulated incorporation of [3H]leucine in myocytes and [3H]thymidine in fibroblasts. In myocytes, the NO synthase inhibitor NG-monomethyl-L-arginine potentiated NE-stimulated [3H]leucine incorporation. In both cell types, ANP and SNAP increased intracellular cGMP levels, and their growth-suppressing effects were mimicked by the cGMP analogue 8-bromo-cGMP. Furthermore, in myocytes, 8-bromo-cGMP attenuated the alpha1-adrenergic receptor-stimulated increases in c-fos

1998 Journal of Clinical Investigation

10534. Inhibition of norepinephrine-induced cardiac hypertrophy in s100beta transgenic mice. Full Text available with Trip Pro

Inhibition of norepinephrine-induced cardiac hypertrophy in s100beta transgenic mice. We have recently reported that the Ca2+-binding protein S100beta was induced in rat heart after infarction and forced expression of S100beta in neonatal rat cardiac myocyte cultures inhibited alpha1-adrenergic induction of beta myosin heavy chain (MHC) and skeletal alpha-actin (skACT). We now extend this work by showing that S100beta is induced in hearts of human subjects after myocardial infarction (...) . Furthermore, to determine whether overexpression of S100beta was sufficient to inhibit in vivo hypertrophy, transgenic mice containing multiple copies of the human gene under the control of its own promoter, and CD1 control mice were treated with norepinephrine (NE) (1.5 mg/kg) or vehicle, intraperitoneally twice daily for 15 d. In CD1, NE produced an increase in left ventricular/body weight ratio, ventricular wall thickness, induction of skACT, atrial natriuretic factor, betaMHC, and downregulation

1998 Journal of Clinical Investigation

10535. Norepinephrine Modulates Myelopoiesis After Experimental Thermal Injury With Sepsis Full Text available with Trip Pro

Norepinephrine Modulates Myelopoiesis After Experimental Thermal Injury With Sepsis To determine whether thermal injury and sepsis cause an increase in bone marrow norepinephrine release and whether such a release influences bone marrow monocytopoiesis.The authors previously demonstrated enhanced bone marrow monocytopoiesis after burn with sepsis. They also showed that physiologic stress and bacterial challenge without injury could lead to a dynamic release of norepinephrine from the bone (...) marrow compartment. In this study, they sought to determine the potential cause-and-effect relationship of bone marrow norepinephrine release on increased monocytopoiesis after burn sepsis.Norepinephrine release from bone marrow was determined by traditional pulse-chase methods. Tissue and bone marrow norepinephrine content was ablated by chemical sympathectomy with 6-hydroxydopamine treatment. Clonogenic potential in response to colony-stimulating factors was determined in total nucleated bone

2001 Annals of Surgery

10536. The International Sepsis Forum's controversies in sepsis: my initial vasopressor agent in septic shock is norepinephrine rather than dopamine Full Text available with Trip Pro

The International Sepsis Forum's controversies in sepsis: my initial vasopressor agent in septic shock is norepinephrine rather than dopamine 12617728 2003 05 02 2018 11 13 1364-8535 7 1 2003 Feb Critical care (London, England) Crit Care The International Sepsis Forum's controversies in sepsis: my initial vasopressor agent in septic shock is norepinephrine rather than dopamine. 3-5 Sharma Vinay K VK Critical Care Section, Cooper Health System, Camden, New Jersey, USA. Dellinger R Phillip RP (...) SCCM. International Sepsis Forum eng Comparative Study Journal Article Research Support, Non-U.S. Gov't 2002 11 01 England Crit Care 9801902 1364-8535 0 Vasoconstrictor Agents 33X04XA5AT Lactic Acid VTD58H1Z2X Dopamine X4W3ENH1CV Norepinephrine IM Crit Care. 2003 Feb;7(1):6-8 12617729 Cardiac Output drug effects Cerebrovascular Circulation drug effects Dopamine pharmacology Glomerular Filtration Rate drug effects Guidelines as Topic Humans Hypothalamo-Hypophyseal System drug effects Lactic Acid

2002 Critical Care

10537. Mitral Cell β1 and 5-HT2A Receptor Colocalization and cAMP Coregulation: A New Model of Norepinephrine-Induced Learning in the Olfactory Bulb Full Text available with Trip Pro

Mitral Cell β1 and 5-HT2A Receptor Colocalization and cAMP Coregulation: A New Model of Norepinephrine-Induced Learning in the Olfactory Bulb In the present study we assess a new model for classical conditioning of odor preference learning in rat pups. In preference learning beta(1)-adrenoceptors activated by the locus coeruleus mediate the unconditioned stimulus, whereas olfactory nerve input mediates the conditioned stimulus, odor. Serotonin (5-HT) depletion prevents odor learning, with 5-HT

2003 Learning & Memory

10538. Norepinephrine exocytosis stimulated by alpha-latrotoxin requires both external and stored Ca2+ and is mediated by latrophilin, G proteins and phospholipase C. Full Text available with Trip Pro

Norepinephrine exocytosis stimulated by alpha-latrotoxin requires both external and stored Ca2+ and is mediated by latrophilin, G proteins and phospholipase C. alpha-latrotoxin (LTX) stimulates massive release of neurotransmitters by binding to a heptahelical transmembrane protein, latrophilin. Our experiments demonstrate that latrophilin is a G-protein-coupled receptor that specifically associates with heterotrimeric G proteins. The latrophilin-G protein complex is very stable in the presence (...) of GDP but dissociates when incubated with GTP, suggesting a functional interaction. As revealed by immunostaining, latrophilin interacts with G alpha q/11 and G alpha o but not with G alpha s, G alpha i or G alpha z, indicating that this receptor may couple to several G proteins but it is not promiscuous. The mechanisms underlying LTX-evoked norepinephrine secretion from rat brain nerve terminals were also studied. In the presence of extracellular Ca2+, LTX triggers vesicular exocytosis because

1999 Philosophical Transactions of the Royal Society B: Biological Sciences

10539. Norepinephrine prolongs tetracaine spinal anesthesia in surgical patients: a preliminary study. (Abstract)

Norepinephrine prolongs tetracaine spinal anesthesia in surgical patients: a preliminary study. We conducted a double-blinded examination of the effects of norepinephrine as a vasoconstrictor on the onset and duration of tetracaine spinal anesthesia in 80 surgical patients. The patients were randomly allocated to four groups (n = 20 in each group). Each patient received 10 mg of tetracaine in a volume of 2.0 mL which contained either 0 micrograms/mL, 5 micrograms/mL, 10 micrograms/mL, or 15 (...) micrograms/mL of norepinephrine. The onset of spinal anesthesia was determined by the time to reach Th-10 level as well as by the time required to obtain the highest level of sensory analgesia. The time for two-segment regression and full-motor recovery were defined as the duration of spinal anesthesia. The time to reach Th-10, the highest analgesia level, and the time to obtain the highest analgesia level did not differ among the groups. Two-segment regression was prolonged significantly by 175%, 103

1993 Anesthesia and analgesia Controlled trial quality: uncertain

10540. Plasma norepinephrine, plasma renin activity, and congestive heart failure. Relations to survival and the effects of therapy in V-HeFT II. The V-HeFT VA Cooperative Studies Group. (Abstract)

Plasma norepinephrine, plasma renin activity, and congestive heart failure. Relations to survival and the effects of therapy in V-HeFT II. The V-HeFT VA Cooperative Studies Group. Congestive heart failure is a clinical syndrome characterized by neuroendocrine activation. Measurements of plasma norepinephrine and plasma renin activity were performed in the Vasodilator-Heart Failure Trial II (V-HeFT II) to characterize the effect of therapy on neuroendocrine activation and to examine (...) the responses to therapy among patients with different degrees of activation.The baseline median plasma norepinephrine value (n = 743) was 490 pg/mL and the baseline median plasma renin activity (n = 737) was 6.9 ng.mL-1 x hr-1. Baseline plasma renin activity and plasma norepinephrine correlated poorly with each other (r = 0.12), implying that these two neuroendocrine systems are being activated by separate processes. By univariate analysis, the logarithms of the plasma norepinephrine (p < 0.0001

1993 Circulation Controlled trial quality: uncertain

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