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1 amol, formoterol, fenoterol, clenbuterol, or adrenaline).
2 ds, 83% antihistamines, and 9% intramuscular adrenaline.
3  were corticoids and antihistamines, but not adrenaline.
4 ed their autoinjector needed another dose of adrenaline.
5 to survive polymyxin B following addition of adrenaline.
6 ng with the first purification of a hormone, adrenaline.
7 on and increases in plasma noradrenaline and adrenaline.
8 ted neurogenic contractions and responses to adrenaline.
9 duct always responded best to stimulation by adrenaline.
10 ses modified the response to inhaled racemic adrenaline.
11 menoptera sting anaphylaxis is intramuscular adrenaline.
12 erenol, a beta-adrenergic agonist similar to adrenaline.
13 e or by a counter-regulatory hormone such as adrenaline.
14 sponsible for conversion of noradrenaline to adrenaline.
15 s relieved by the intramuscular injection of adrenaline.
16  an explanatory meeting on auto-injection of adrenaline.
17 tered three cases of accidental injection of adrenaline.
18 27.6% of insect anaphylaxis received on-site adrenaline.
19 ulla (RVLM), which results in the release of adrenaline.
20  short-acting bronchodilators, and nebulized adrenaline.
21 e treatment for anaphylaxis is intramuscular adrenaline.
22 nol, and the low-affinity endogenous agonist adrenaline.
23                                  Infusion of adrenaline (1 mug kg(-1) min(-1) ) increased minute vent
24                  Hypoxaemia increased plasma adrenaline (26-fold) and noradrenaline (5-fold) in shams
25 d by hyperoxia (noradrenaline 50.7 +/- 5.2%, adrenaline 62.6 +/- 3.3%, cortisol 63.2 +/- 2.1%, growth
26                     67% of patients received adrenaline, 85% oral antihistamines, and 89% received IV
27 ferential ratio of noradrenaline (NA) versus adrenaline (A) release secreted in response to various p
28 lyst for oxidation of ascorbic acid (AA) and adrenaline (AD).
29 vidence of a relationship between successful adrenaline administration and risk estimation.
30               Primary outcome was successful adrenaline administration at six weeks, assessed by an i
31        A survey with regard to the timing of adrenaline administration for anaphylaxis was conducted
32 drenaline self-injector (ASJ), and timing of adrenaline administration for anaphylaxis.
33                                              Adrenaline administration is a top priority treatment fo
34 did not necessarily understand the timing of adrenaline administration.
35 a transient or stable BP increase induced by adrenaline administration.
36  design is a major determinant of successful adrenaline administration.
37                 There were no differences in adrenaline (ADR) at rest or with heavy exercise, but the
38                       Noradrenaline (NA) and adrenaline (ADR) effluxes were monitored from ex vivo ad
39 by the catecholamines isoprenaline (Iso) and adrenaline (Adr) is regulated by V(M).
40 ial environment mediated by activation of an adrenaline/ADRB2/PKA/BAD antiapoptotic signaling pathway
41 iotensin-converting enzyme (ACE) inhibitors, adrenaline, allergic myocardial infarction, anaphylaxis,
42 tyltransferase, the synthesizing enzymes for adrenaline and acetylcholine, respectively.
43 on and elicit cardiorespiratory stimulation, adrenaline and adrenocorticotropic hormone (ACTH) releas
44 used extralobular duct was used to show that adrenaline and carbachol stimulated the duct through the
45 R showed reduced survival in the presence of adrenaline and complete restoration of growth upon addit
46 s were accompanied by increased fetal plasma adrenaline and cortisol, and reduced plasma insulin leve
47                 Salmonella are able to sense adrenaline and downregulate the antimicrobial peptide re
48 l principal cell line (DC2) and increased by adrenaline and forskolin.
49 ted to govern activity of PP1 in response to adrenaline and insulin.
50 cluding training updates for self-injectable adrenaline and nasal spray use.
51 ne concentration was restored, whilst plasma adrenaline and neuropeptide Y (NPY) concentrations were
52                                              Adrenaline and noradrenaline concentrations were lower i
53 ressure (radial artery catheter), and plasma adrenaline and noradrenaline concentrations were measure
54  manipulated plasma catecholamines (combined adrenaline and noradrenaline concentrations) to three le
55                                              Adrenaline and noradrenaline correlated with syndecan-1
56 vous system and secreting the catecholamines adrenaline and noradrenaline in the 'fight-or-flight' re
57 e and respond to the host NE stress hormones adrenaline and noradrenaline to modulate virulence.
58 -3 and the host neuroendocrine (NE) hormones adrenaline and noradrenaline were reported to display cr
59 Escherichia coli O157:H7, the catecholamines adrenaline and noradrenaline were shown to act synergist
60                   The second group comprised adrenaline and noradrenaline which displayed higher intr
61 sma concentrations of cortisol, vasopressin, adrenaline and noradrenaline, and falls in the fetal : m
62 fere with signaling from the stress hormones adrenaline and noradrenaline, have a lower incidence of
63  octopamine, the invertebrate counterpart of adrenaline and noradrenaline, in synaptic and behavioral
64                                              Adrenaline and noradrenaline, the main effectors of the
65 inding catecholamine agonist ligands such as adrenaline and noradrenaline.
66  contractions produced by nerve stimulation, adrenaline and NPY, but not ATP.
67 .45 +/- 1.59 ml h-1; P < 0.01 relative to Jv adrenaline and P < 0.005 relative to Jv dichlorobenzamil
68 erns by modulating neurotransmitters such as adrenaline and serotonin.
69  in the infants treated with inhaled racemic adrenaline and those treated with inhaled saline (P>0.1
70 rease in fetal plasma noradrenaline, but not adrenaline and vasopressin concentrations relative to sh
71 , in plasma concentrations of noradrenaline, adrenaline and vasopressin, and in the maternal-to-fetal
72 , L-NE is converted to L-epinephrine (L-Epi, adrenaline) and released as the primary neurotransmitter
73                          Subjective fatigue, adrenaline, and body temperature variations during two 7
74 istration of anesthetics such as tetracaine, adrenaline, and cocaine and lidocaine, epinephrine, and
75 3,4-hydroxyphenylalanine [l-dopa], dopamine, adrenaline, and noradrenaline) elevate FUS1 and RLM1 tra
76  base excess, platelet count and hemoglobin, adrenaline, and syndecan-1 were the only independent pre
77 atients used oral antihistamine, six inhaled adrenaline, and ten took no treatment.
78                    Hypoxia increased venous [adrenaline] and [noradrenaline] but not [dopamine] at a
79      Reports on accidental auto-injection of adrenaline are few.
80  assess the effectiveness of inhaled racemic adrenaline as compared with inhaled saline and the strat
81 mmediately following its first use, cases of adrenaline-associated sepsis were reported.
82 nged a second cohort of lambs with exogenous adrenaline at 21 dA.
83  in humans, but it is unclear if circulating adrenaline attenuates peripheral vasoconstriction during
84 opose indications for the prescription of an adrenaline auto-injector (AAI), and to discuss other for
85 h a written emergency management plan and an adrenaline auto-injector and educated to its use.
86                                 Provision of adrenaline auto-injector devices and education on how an
87 but only a minority received the recommended adrenaline auto-injector for self-administration at disc
88                                        If an adrenaline auto-injector is prescribed, education on whe
89  help later than 30 min after symptom onset, adrenaline auto-injector prescription is a necessity.
90 rs (<16 years) with food allergy, trained in adrenaline auto-injector use, were recruited from a hosp
91 plan, and, where appropriate, prescribing an adrenaline auto-injector.
92 mend that at-risk patients are provided with adrenaline auto-injectors (AAIs).
93          The low rate of doctors prescribing adrenaline auto-injectors in the ED setting underlines t
94     Our findings suggest that while handling adrenaline auto-injectors, we should keep in mind the po
95                                     However, adrenaline autoinjector activation has remained fairly s
96 ood allergic children who were prescribed an adrenaline autoinjector and to assess whether it was use
97 d and sport (at least for 2 h), and carry an adrenaline autoinjector at all times.
98                          Similarly, rates of adrenaline autoinjector usage in the school environment
99 rs require more effective guidance on proper adrenaline autoinjector use.
100                                           An adrenaline autoinjector was prescribed to 139 food aller
101                                           An adrenaline autoinjector was used by 41 (16.7%, 95% CI: 1
102 ood allergic children who were prescribed an adrenaline autoinjector were investigated.
103  should carry an emergency kit containing an adrenaline autoinjector, H1 -antihistamines, and cortico
104 s in quality of life compared to carrying an adrenaline autoinjector.
105 ious work has shown patients commonly misuse adrenaline autoinjectors (AAI).
106                  Patients already prescribed adrenaline autoinjectors (AAIs) for anaphylaxis were exa
107                                The number of adrenaline autoinjectors activated per 1000 students at
108 all year levels and the annual usage rate of adrenaline autoinjectors in the school setting relative
109           There has been a debate about when adrenaline autoinjectors should be prescribed and how ma
110 children/carers are unsure when to use their adrenaline autoinjectors, contributing to a low quality
111                                 Overall, the adrenaline-bound receptor structure is similar to the ot
112             It unravels a strong underuse of adrenaline by emergency physicians, not reflecting treat
113 mice that cannot synthesize noradrenaline or adrenaline by inactivating the gene that encodes dopamin
114  This is the first study to demonstrate that adrenaline can indirectly activate the PDC in skeletal m
115 ansport by the submandibular salivary gland (adrenaline, carbachol, isoprenaline and forskolin) mobil
116 rupted time series and - only in relation to adrenaline - case series investigating the effectiveness
117       In seven experiments, 0.5 microg min-1 adrenaline caused a significant (P < 0.0005) reduction i
118       In eight experiments, 0.5 microg min-1 adrenaline caused a significant (P < 0.005) reduction in
119 imilar interactions are seen with the hPheOH.adrenaline complex and Ser23.
120 t also significantly reduced baseline plasma adrenaline concentration (403 +/- 69 compared with 73 +/
121              This is not reflected in plasma adrenaline concentrations because of reduced plasma clea
122     A fall in fetal plasma noradrenaline and adrenaline concentrations occurred during betamethasone
123 ffect on heart rate (HR), plasma lactate and adrenaline concentrations or oxygen uptake at rest and d
124 uroglycopenic symptoms, and higher levels of adrenaline, cortisol, and growth hormone.
125 omotes prostate carcinogenesis in mice in an adrenaline-dependent manner.
126                            Noradrenaline and adrenaline dose-dependently suppressed the release of IL
127                                         Both adrenaline effects can be inhibited by the addition of t
128  room air and 40% O2: (1) during intravenous adrenaline (epinephrine) infusion at 320 ng kg(-1) min(-
129                                     Although adrenaline (epinephrine) is a cornerstone of initial ana
130           In contrast to SNS activity, tonic adrenaline (epinephrine) secretion from the adrenal medu
131 d show how the binding of an agonist ligand, adrenaline (epinephrine), causes conformational changes
132 t studies investigating the effectiveness of adrenaline (epinephrine), H1-antihistamines, systemic gl
133 ical conditions, willingness to always carry adrenaline, etc.), consideration may be given to allow t
134 ignaling induced by either thrombin, ADP, or adrenaline, examined by suppression of forskolin-stimula
135  participants received more than one dose of adrenaline, for nine of these a health professional gave
136 um route, site and dose of administration of adrenaline from trials studying people with a history of
137          The commonest reasons for not using adrenaline in anaphylaxis were 'thought adrenaline unnec
138 ntrinsic activity than the endogenous ligand adrenaline in cAMP accumulation, beta-arrestin-2 recruit
139           We sought to assess whether use of adrenaline in hemodynamically stable patients with anaph
140 64.4%), whereas when physicians administered adrenaline in patients, it resulted in circulatory (74.8
141 ns of vasopressin and noradrenaline, but not adrenaline in the fetus, and inversely related to the fe
142 ked by catecholaminergic challenge (caffeine/adrenaline) in S2814D(+/+) mice in vivo or programmed el
143                          Plasma caffeine and adrenaline increased after caf, but not after decaf.
144                 The results demonstrate that adrenaline increased glycogen phosphorylase activation a
145              Physiological concentrations of adrenaline increased the CO2 sensitivity of freshly diss
146 of epithelial sodium channels) abolished the adrenaline-induced absorption of lung liquid (mean Jv am
147 poral relationship, combined with a probable adrenaline-induced increase in metabolic rate (and there
148 5 x 10-5 M did not significantly inhibit the adrenaline-induced lung liquid absorption (Jv dichlorobe
149 ng times and are protected from collagen and adrenaline-induced thromboembolism.
150 = 10) before and during (1, 3, 7 and 15 min) adrenaline infusion (0.14 microg (kg body mass)(-1) min(
151     The PDC was activated following 7 min of adrenaline infusion (pre-infusion = 0.22 +/- 0.04 vs. 7
152  mg atropine), before and during intravenous adrenaline infusion at 80 ng kg(-1) min(-1) (ATR + 80 AD
153                                              Adrenaline infusion increased glycogen phosphorylase "a"
154     The present study examined the effect of adrenaline infusion on the activation status of glycogen
155  reaction and treated him with intramuscular adrenaline injection, corticosteroid and antihistamine i
156 of the myofibrillar ATPase that occurs after adrenaline intervention.
157 ggested that administration of intramuscular adrenaline into the middle of vastus lateralis muscle is
158                                              Adrenaline is a fundamental circulating hormone for bodi
159 eement that rapid intramuscular injection of adrenaline is life-saving and constitutes the first-line
160 te bronchiolitis in infants, inhaled racemic adrenaline is not more effective than inhaled saline.
161                    If promptly administered, adrenaline is potentially life-saving.
162                                     Although adrenaline is recommended as first line treatment for an
163                                Intramuscular adrenaline is the gold standard treatment for anaphylaxi
164                                              Adrenaline is used by only a minority of patients experi
165                                 Epinephrine (adrenaline) is a medication widely used in the pediatric
166 time, when patients injected themselves with adrenaline, it resulted in laryngeal (78.4%) and circula
167                                  Addition of adrenaline led to an induction of key metal transport sy
168                     Plasma noradrenaline and adrenaline levels rose rapidly with dramatic increases i
169     At a blood glucose of 3.8 mmol/L, plasma adrenaline levels were twice as high after caffeine than
170                      Through iron transport, adrenaline may affect the oxidative stress balance of th
171                                     However, adrenaline may also serve in favour of the host defences
172 that a failure or delay in administration of adrenaline may increase the risk of death.
173 th 0.31 +/- 0.04 and 0.34 +/- 0.01 hours for adrenaline-mediated beta-arrestin-2 recruitment and GFP-
174                      Physiological levels of adrenaline mimicked the effect of hypoglycaemia on venti
175              However, in granular ducts only adrenaline mobilized the entire IP3-sensitive pool where
176  adrenaline unnecessary' (54.4%) and 'unsure adrenaline necessary' (19.1%).
177    We conclude that, in fetal sheep, neither adrenaline nor cGMP stimulate lung liquid absorption by
178  blood gases, glucose and lactate and plasma adrenaline, noradrenaline and vasopressin concentration
179   Admission plasma levels of catecholamines (adrenaline, noradrenaline) and biomarkers reflecting end
180 rkers reflecting sympathoadrenal activation (adrenaline, noradrenaline), tissue/endothelial cell/glyc
181                              The addition of adrenaline, noradrenaline, hydrocortisone, or dexamethas
182       We wished to investigate the impact of adrenaline on the biology of Salmonella spp.
183             We have determined the effect of adrenaline on the transcriptome of the gut pathogen Salm
184    There were no differences in basal plasma adrenaline or cortisol concentrations between low and hi
185 -adrenergic receptors on the cell surface by adrenaline or noradrenaline leads to alterations in the
186 amine, the invertebrate homolog of mammalian adrenaline or noradrenaline, plays important roles in mo
187 g peripheral beta-adrenergic agonist akin to adrenaline, or saline.
188 quency (ln HF) power (P < 0.001) and reduced adrenaline (P < 0.001) and noradrenaline concentrations
189                                     Arterial adrenaline (P < 0.05) and venous noradrenaline (P < 0.05
190 ma, and prehospital fluids (100 pg/mL higher adrenaline predicted 2.75 ng/mL higher syndecan-1, P < 0
191 in management include injecting epinephrine (adrenaline) promptly, providing high-flow supplemental o
192                   These results suggest that adrenaline, rather than low glucose, is an adequate stim
193                  These findings suggest that adrenaline release can account for the ventilatory hyper
194                                      Indeed, adrenaline release in response to acute stress is substa
195 proximately 40%) were identified to regulate adrenaline release in response to glucoprivation.
196 oprivation in the PeH or in the RVLM elicits adrenaline release in vivo and 2) whether direct activat
197 d CO2 sensitivity is abolished by preventing adrenaline release or blocking its receptors.
198 had high plasma noradrenaline but attenuated adrenaline release with higher Injury Severity Score, im
199 t, autonomic pathways affecting glucagon and adrenaline release.
200  or orexin release in the RVLM modulates the adrenaline release.
201             Amiloride (10-4 M) inhibited the adrenaline response (Jv amiloride, +5.46 +/- 1.09 ml h-1
202    Leukocytosis strongly correlated with the adrenaline response to hypoglycemia.
203 ats), but did not alter the magnitude of the adrenaline response to restraint.
204  was determined to be 124.3 +/- 0.77% of the adrenaline response.
205 s whether they possessed registrations as an adrenaline self-injector (ASJ), and timing of adrenaline
206                                              Adrenaline sensing may provide an environmental cue for
207 ent signal transduction system is the likely adrenaline sensor mediating the antimicrobial peptide re
208  to local anaesthetic induced neurotoxicity: adrenaline significantly increases the neurotoxic effect
209                           The stress hormone adrenaline stimulates beta(2)-adrenoreceptors that are e
210 ld lower in the presence of isoprenaline and adrenaline than when salbutamol or terbutaline were pres
211  notable exception to this is the failure of adrenaline to have a direct effect on glycolysis.
212 ersely, it could be seen that the failure of adrenaline to maintain a constant glucose 6-phosphate co
213                               The ability of adrenaline to mobilize NEFA was 55 +/- 15% lower (P < 0.
214                We also tested the ability of adrenaline to mobilize non-esterified fatty acids (NEFAs
215  years and increased adrenomedullary output (adrenaline) to stress at 2.5 years.
216 eripheral beta-adrenergic agonist similar to adrenaline, to induce sensations of palpitation and dysp
217                                 Epinephrine (adrenaline) treatment is underused in health care and co
218 that in human cardiac muscle unstimulated by adrenaline, troponin I is phosphorylated on Ser24.
219 sing adrenaline in anaphylaxis were 'thought adrenaline unnecessary' (54.4%) and 'unsure adrenaline n
220                                              Adrenaline use in hemodynamically stable anaphylaxis pat
221                                              Adrenaline use in hemodynamically stable anaphylaxis pat
222 lled trial to evaluate ability to administer adrenaline using different AAI devices.
223               We assessed ability to deliver adrenaline using their AAI in a simulated anaphylaxis sc
224 ntrolled trial that compared inhaled racemic adrenaline versus saline.
225                                Intramuscular adrenaline was administered in 17 SRs, but only 65% of t
226 examethasone fetuses, the increase in plasma adrenaline was attenuated during H1 and the increase in
227         In another trial (120 min duration), adrenaline was infused (AI) at 0.1 microgram kg-1 min-1
228                  Treatment effect of inhaled adrenaline was not modified by virus type, load or coinf
229 thermore, no change in levels of circulating adrenaline was observed with L-NMMA.
230  the efficacy of the endogenous full agonist adrenaline was reduced by depolarization.
231 1 and r = 0.23, P < 0.001, respectively) but adrenaline was the only independent predictor of syndeca
232                                Intramuscular adrenaline was used after 0.01% of doses (one participan
233 onger hospital stay before death, and use of adrenaline were also significantly associated with poore
234 occurred upon addition of either glucagon or adrenaline were measured.
235                             Isoprenaline and adrenaline were more efficacious in functional studies,
236 erse effects of accidental auto-injection of adrenaline were not observed in these three cases.
237 ncentrations of ACTH, AVP, noradrenaline and adrenaline were observed during hypoxaemia in both group
238 reas the inhibitory or excitatory actions of adrenaline were prevented by alpha1 or alpha2 antagonist
239                    Adverse events induced by adrenaline were rare when the intramuscular route was us
240 ists such as adenosine diphosphate (ADP) and adrenaline were severely impaired.
241  consider how to best encourage the usage of adrenaline when clinically indicated in anaphylaxis.
242                Many natural agonists such as adrenaline, which activates the beta2-adrenoceptor (beta
243 ine (p < .001) but an attenuated increase in adrenaline with increasing Injury Severity Score and low
244 actorial design, we compared inhaled racemic adrenaline with inhaled saline and on-demand inhalation
245 boration of neuroendocrine hormones, such as adrenaline, with infectious disease.

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