Stabilité d’un mélange de vitamines B1/B6 dans une solution saline de perfusion

2017 ◽  
Vol 52 (4) ◽  
pp. 380-381
Author(s):  
Jean-baptiste Pain ◽  
Lionel Tortolano ◽  
Amélie Gaudin
Keyword(s):  
1987 ◽  
Author(s):  
P Pabón ◽  
V Vicente ◽  
I Alberca ◽  
C Martin Luengo ◽  
A Lopez Borrasca

Infarct size, estimated by electrocardiographic changes (the QRS Scoring System, developed by Wagner et al, Circulation 65,342, 1982) and enzymatic analysis (creatinine kinase, CK) was studied in 45 patients with no history of previous infarcts. 25 received an intravenous dose of DDAVP (0.3 ug/kg) and 20 received a placebo solution (saline). The time between the onset of symptoms and DDVAP administration was less than 12 hours. The results showed no significant differences between the two groups in maximal or acumulative activity of creatinine kinase (CKr) or the QRS score peak. However, in patients with a mean evolution time of less than 1 hour, the CK peak was significantly lower in the DDAVP group than in the placebo group (p<0.05). Furthermore the percent of maximal increase in the QRS score was lower in the DDAVP group than in the patients receiving the placebo (p=0.1). On admission, the fibrinolytic activity of euglobulin fractions (measured by fibrin plates) was higher in the patients in both groups than in a group of healthy subjects (n=40). Also, DDAVP significantly increased fibrinolyric activity whereas no changes were found in patients receiving the placebo. The mean CKr value was lower in patients with an increase in fibrinolysis than in those who showed no changes in it. Finally, in the DDAVP group the QRS score peak was strongly dependent on the initial QRS score and, regarding this, our results suggest that small infarcts on admission may represent a potential indication for DDAVP therapy.


1985 ◽  
Vol 69 (2) ◽  
pp. 215-222 ◽  
Author(s):  
I. W. Fellows ◽  
T. Bennett ◽  
I. A. Macdonald

1. On three separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline, 50 ng min−1 kg−1 (high A), adrenaline, 10 ng min−1 kg−1 (low A) or sodium chloride solution (saline :154 mmol of NaCl/1) plus ascorbic acid, 1 mg/ml (control), over 30 min. 2. Venous adrenaline concentrations of 2.19 ± 0.15 nmol/l, 0.73 ± 0.08 nmol/l and 0.15 ± 0.03 nmol/l were achieved during the high A, low A and control infusions respectively. 3. Heart rate rose significantly by 19 ± 3 beats/min (high A) and by 6 ± 1 beats/min (low A). Heart rate remained significantly elevated 30 min after cessation of the high A infusion, despite venous plasma adrenaline concentration having fallen to control levels. 4. The diastolic blood pressure fell during the high A and low A infusions, but the systolic blood pressure rose only during the high A infusion. 5. Vasodilatation occurred in the calf vascular bed during both high A and low A infusions. The changes in hand blood flow and hand vascular resistance were not statistically significant, although there was a tendency to vasoconstriction during the infusion of adrenaline. 6. Metabolic rate rose significantly by 23.5 ± 1.8% (high A) and by 11.8 ± 1.6% (low A). Metabolic rate remained elevated between 15 and 30 min after termination of the high A infusion. There was an initial transient increase in respiratory exchange ratio (RER) during the adrenaline infusions. During the later stages of the adrenaline infusions and after their cessation, RER fell, probably reflecting increased fat oxidation. 7. Blood glucose, glycerol and lactate concentrations all rose significantly during the high A infusion, but only the blood glycerol concentration rose during the low A infusion. Plasma potassium concentration fell during and after the high A infusion but only after cessation of the low A infusion. 8. When adrenaline was infused intravenously at rates that elevated the plasma adrenaline concentration within the physiological range, peripheral circulatory effects were observed similar to those previously described for larger doses of adrenaline. The persistent tachycardia noted after stopping the high A infusion may, at least in part, have been a consequence of the concomitantly elevated metabolic rate.


1975 ◽  
Vol 49 (5) ◽  
pp. 459-463 ◽  
Author(s):  
N. Papanicolaou ◽  
M. Safar ◽  
A. Hornych ◽  
F. Fontaliran ◽  
Y. Weiss ◽  
...  

1. Renal venous prostaglandin concentrations (PGA, PGE and PGF) were determined, together with renal plasma flow, urinary output and blood pressure changes, before and after infusion of sodium chloride solution (saline) in four normotensive and three hypertensive subjects. 2. No changes in blood pressure and in glomerular filtration rate were observed. 3. Saline infusion induced a significant increase in renal venous PGA and PGE, and also in total and non-cortical renal plasma flow and urinary output. There was an insignificant increase in renal venous PGF. 4. These findings show that prostaglandin release after saline infusion is associated with changes in renal blood flow and suggest that the natriuretic and diuretic effect of saline could be the result of prostaglandin release.


1985 ◽  
Vol 68 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Anne Allistone ◽  
J. G. Collier ◽  
R. N. Davidson ◽  
R. W. Fuller ◽  
P. S. Richardson

1. Ten healthy subjects received, on separate occasions, intravenous infusions of 0.9% NaCl solution (saline) and of sodium cromoglycate given in a double-blind cross-over fashion. 2. After 20 min of infusion the specific airway conductance (sGaw) of each subject was measured in a body plethysmograph. The subject then breathed first a low (1-20 p.p.m.) and then a higher (4-40 p.p.m.) concentration of sulphur dioxide (SO2) for 2 min while the infusion continued. Measurements of sGaw were repeated after each inhalation of SO2. 3. Sodium cromoglycate infusion did not affect the sGaw measured before challenge with SO2. 4. During the infusion of sodium cromoglycate, the falls in sGaw in response to both concentrations of SO2 were significantly less than those which occurred during saline infusion. 5. Plasma concentrations of sodium cromoglycate were found to be 209 ± 22 nmol/l at the end of the drug infusion. This is about one-hundredth of lowest dose required to stabilize mast cells in vitro. 6. We conclude that sodium cromoglycate acted by a mechanism which did not involve mast cells. Other possible modes of action are discussed.


1986 ◽  
Vol 71 (2) ◽  
pp. 151-155 ◽  
Author(s):  
J. V. Anderson ◽  
J. Donckier ◽  
W. J. McKenna ◽  
S. R. Bloom

1. We studied plasma atrial natriuretic peptide (ANP) concentrations in seven normal subjects after the acute intravenous infusion of sodium chloride/potassium chloride solution (saline). 2. Three separate infusions of 6, 12 and 18 ml of saline/kg body weight each significantly increased the circulating concentration of ANP without changes of plasma osmolality or electrolyte concentrations. 3. The mean maximal rise of the plasma ANP concentration after the three saline infusions was significantly correlated (r = 0.74, P < 0.001) with, but occurred 10–30 min later than, the maximal atrial pressure rise. 4. These observations are in accord with the hypotheses that: (a) ANP is a circulating natriuretic factor; (b) atrial distension is an important stimulus to ANP release in man.


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