Intravenous adrenaline infusion causes vasoconstriction close to an intramuscular microdialysis catheter in humans

2010 ◽  
Vol 30 (6) ◽  
pp. 399-405 ◽  
Author(s):  
Torbjörn Vedung ◽  
Lennart Jorfeldt ◽  
Jan Henriksson
1991 ◽  
Vol 81 (5) ◽  
pp. 635-644 ◽  
Author(s):  
Alan A. Connacher ◽  
William M. Bennet ◽  
Roland T. Jung ◽  
Dennis M. Bier ◽  
Christopher C. T. Smith ◽  
...  

1. Energy expenditure, plasma glucose and palmitate kinetics and leg glycerol release were determined simultaneously both before and during adrenaline infusion in lean and obese human subjects. Seven lean subjects (mean 96.5% of ideal body weight) were studied in the post-absorptive state and also during mixed nutrient liquid feeding, eight obese subjects (mean 165% of ideal body weight) were studied in the post-absorptive state and six obese subjects (mean 174% of ideal body weight) were studied during feeding. 2. Resting energy expenditure was higher in the obese subjects, but the thermic response to adrenaline, both in absolute and percentage terms, was similar in lean and obese subjects. Plasma adrenaline concentrations attained (3 nmol/l) were comparable in all groups and the infusion had no differential effects on the plasma insulin concentration. Before adrenaline infusion the plasma glucose flux was higher in the obese than in the lean subjects in the fed state only (45.8 ± 3.8 versus 36.6 ± 1.0 mmol/h, P <0.05); it increased to the same extent in both groups with the adrenaline infusion. 3. Before the adrenaline infusion plasma palmitate flux was higher in the obese than in the lean subjects (by 51%, P <0.01, in the post-absorptive state and by 78%, P <0.05, in the fed state). However, there was no significant change during adrenaline infusion in the obese subjects (from 13.5 ± 1.00 to 15.0 ± 1.84 mmol/h, not significant, in the post-absorptive state and from 14.4 ± 2.13 to 15.7 ± 1.74 mmol/h, not significant, in the fed state), whereas there were increases in the lean subjects (from 8.93 ± 1.10 to 11.2 ± 1.19 mmol/h, P <0.05, in the post-absorptive state, and from 8.06 ± 1.19 to 9.86 ± 0.93 mmol/h, P <0.05, in the fed state). 4. Before adrenaline infusion the palmitate oxidation rate was also higher in the obese than in the lean subjects (1.86 ± 0.14 versus 1.22 ± .09 mmol/h, P <0.01, in the post-absorptive state and 1,73 ± 0.25 versus 1.12 ± 0.12 mmol/h, P <0.05, in the fed state). However, in response to adrenaline the fractional oxidation rate (% of flux) increased less in the obese than in the lean subjects, especially in the post-absorptive state (from 13.8 ± 1.02 to 14.9 ± 1.39%, not significant, versus from 13.7 ± 0.98 to 19.3 ± 1.92%, P <0.05). These effects were independent of feeding. Leg glycerol release increased more in the lean subjects with adrenaline infusion, although increases in the plasma glycerol concentration did not differ between the groups. 5. These results suggest that in obese subjects plasma inter-organ transport of fatty acids and the subsequent fractional oxidation responses favour storage of triacylglycerol. These factors may be important determinants for the development and maintenance of the obese state.


1970 ◽  
Vol 23 (4) ◽  
pp. 903 ◽  
Author(s):  
JM Bassett

Intravenous infusion of 1� 5 mg adrenaline over 30 min into adult Merino wethers (50 kg body weight), increased glucose, lactate, and free fatty acid (FFA) concentrations in plasma much more than did a single rapid intravenous injection of the same amount. There was no increase in plasma insulin concentration during adrenaline infusion or after adrenaline injection.


2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Sanjib Kumar Sharma ◽  
Emilie Alirol ◽  
Anup Ghimire ◽  
Suman Shrestha ◽  
Rupesh Jha ◽  
...  

Diagnosing and treating acute severe and recurrent antivenom-related anaphylaxis (ARA) is challenging and reported experience is limited. Herein, we describe our experience of severe ARA in patients with neurotoxic snakebite envenoming in Nepal. Patients were enrolled in a randomised, double-blind trial of high vs. low dose antivenom, given by intravenous (IV) push, followed by infusion. Training in ARA management emphasised stopping antivenom and giving intramuscular (IM) adrenaline, IV hydrocortisone, and IV chlorphenamine at the first sign/s of ARA. Later, IV adrenaline infusion (IVAI) was introduced for patients with antecedent ARA requiring additional antivenom infusions. Preantivenom subcutaneous adrenaline (SCAd) was introduced in the second study year (2012). Of 155 envenomed patients who received ≥ 1 antivenom dose, 13 (8.4%), three children (aged 5−11 years) and 10 adults (18−52 years), developed clinical features consistent with severe ARA, including six with overlapping signs of severe envenoming. Four and nine patients received low and high dose antivenom, respectively, and six had received SCAd. Principal signs of severe ARA were dyspnoea alone (n=5 patients), dyspnoea with wheezing (n=3), hypotension (n=3), shock (n=3), restlessness (n=3), respiratory/cardiorespiratory arrest (n=7), and early (n=1) and late laryngeal oedema (n=1); rash was associated with severe ARA in 10 patients. Four patients were given IVAI. Of the 8 (5.1%) deaths, three occurred in transit to hospital. Severe ARA was common and recurrent and had overlapping signs with severe neurotoxic envenoming. Optimising the management of ARA at different healthy system levels needs more research. This trial is registered withNCT01284855.


2018 ◽  
Vol 46 (6) ◽  
pp. 566-571 ◽  
Author(s):  
P. H. M. Sadleir ◽  
R. C. Clarke ◽  
B. S. L. Lim ◽  
P. R. Platt

We describe a case of severe left ventricular outflow tract obstruction (LVOTO) with severe mitral incompetence due to systolic anterior motion of the anterior mitral leaflet (SAM) that was recognised thanks to the immediate availability of transoesophageal echocardiography during the resuscitation of anaphylactic shock. The patient rapidly responded to cessation of the epinephrine (adrenaline) infusion and intravascular volume expansion with intravenous crystalloid. The absence of risk factors for developing SAM/LVOTO serve as a warning to clinicians to consider this diagnosis in all cases of epinephrine non-responsive anaphylactic shock.


1990 ◽  
Vol 17 (4) ◽  
pp. 257-261 ◽  
Author(s):  
Anthony W. Bachmann ◽  
Richard D. Gordon ◽  
Ross A.D. Bathgate ◽  
Robyn E. Thompson
Keyword(s):  

1975 ◽  
Vol 53 (1) ◽  
pp. 124-128 ◽  
Author(s):  
Suzanne Rousseau-Migneron ◽  
Jacques LeBlanc ◽  
Louise Lafrance ◽  
Florent Depocas

Following a subcutaneous injection of adrenaline (300 μg/kg), blood-glucose levels were lower in rats treated chronically with adrenaline (300 μg/kg twice a day for 28 days) than in control rats during at least 2.5 h after the injection. To explain this difference of response, the turnover rate of glucose was measured in control and adrenaline-treated rats during adrenaline infusion (0.75 μg/kg−1 min−1), with [U-14C]glucose as tracer. It was found that the rate of appearance of glucose was greater in the control than in the adrenaline-treated group after a 120-min infusion of adrenaline. The rate of disappearance of glucose in the treated rats increased during the first 60 min of infusion and stayed at this elevated level for a subsequent 2 h, whereas in the control rats, it remained unchanged at the beginning of adrenaline infusion and significantly increased only during the second and third hours of infusion. In addition, the metabolic-clearance rate of glucose was not modified by adrenaline in the treated group, but in the control group, the initial clearance rate was significantly less than in the treated group, and decreased during the first hour of adrenaline infusion even though blood glucose reached values of 244 mg/100 ml. From these data, it is suggested that rats adapt to a chronic exogenous supply of adrenaline by a reduced increase in glucose production in response to adrenaline infusion and a better glucose utilization, which possibly indicates a decrease in the inhibitory effect of adrenaline on insulin secretion.


1974 ◽  
Vol 2 (1) ◽  
pp. 58-68 ◽  
Author(s):  
V. I. Callanan ◽  
G. A. Harrison

Four cases are described of the use of prolonged and/or high doses of adrenaline in the treatment of the low cardiac output syndrome following cardiac surgery. Adrenaline was chosen because it produced a more favourable effect on central cardiovascular haemodynamics and myocardial metabolism when compared with isoprenaline, while its detrimental effects on renal function were less marked than those found when using noradrenaline. The renal insufficiency encountered was reversed in those cases without previous renal disease. Tachyphylaxis was demonstrated and weaning was achieved by gradual withdrawal of the vasopressor with concomitant blood volume expansion. Two cases with predominant right ventricular failure developed gross ascites and peripheral oedema, making control of fluid balance difficult. These problems are discussed with a summary of the relevant pharmacology of isoprenaline, noradrenaline, adrenaline and glucagon. The conclusions reached regarding the use and management of adrenaline infusion are given.


2006 ◽  
Vol 58 (suppl_4) ◽  
pp. ONS-313-ONS-321 ◽  
Author(s):  
Robin Bhatia ◽  
Parastoo Hashemi ◽  
Ashfaq Razzaq ◽  
Mark C. Parkin ◽  
Sarah E. Hopwood ◽  
...  

Abstract Objective: To introduce rapid-sampling microdialysis for the early detection of adverse metabolic changes in tissue at risk during aneurysm surgery. Methods: A microdialysis catheter was inserted under direct vision into at-risk cortex at the start of surgery. This monitoring was sustained throughout the course of the operation, during which intraoperative events, for example, temporary arterial occlusion or lobe retraction, were precisely documented. A continuous online flow of dialysate was fed into a mobile bedside glucose and lactate analyser. This comprises flow-injection dual-assay enzyme-based biosensors capable of determining values of metabolites every 30 seconds. Results: Eight patients underwent clipping or wrapping of intracranial aneurysms and were monitored. Time between events and detection: 9 minutes. Mean change in metabolite value ± standard deviation: temporal lobe retraction lactate, +656 ± 562 µmol/L (n = 7, P&lt; 0.05); glucose, -123 ± 138 µmol/L (n = 6, P = 0.08). Glucose intravenous bolus infusion glucose, +512 ± 244 µmol/L (n = 5, P&lt; 0.01); peak at mean time after bolus, 16 minutes. Temporary proximal clip lactate, +731 ± 346 µmol/L (n = 6, P&lt; 0.01); glucose, -139 ± 96 µmol/L (n = 5, P&lt; 0.05); mean clip time, 8.6 minutes. Conclusion: The technique detects changes 9 minutes after intraoperative events occur (limited only by probe-to-sensor tubing length and dialysate flow rate). This provides reliable information to the surgeon and anesthetist promptly. It is a useful method for monitoring glucose and lactate in dialysate, particularly when rapid, transient changes in brain analyte levels need to be determined and the alternative offline methodology would be inadequate.


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