Improvement of arginine hydrochloride based antibody lyophilisates

2020 ◽  
Vol 589 ◽  
pp. 119859
Author(s):  
Ivonne Seifert ◽  
Wolfgang Friess
2021 ◽  
pp. 159101992110251
Author(s):  
Jennifer Ayers-Ringler ◽  
Praveen Kolumam Parameswaran ◽  
Zenith Khashim ◽  
Daying Dai ◽  
Yong-Hong Ding ◽  
...  

Background Flow diverters (FDs) are an effective treatment for intracranial aneurysms, though not free from hemorrhagic complications. A previous study demonstrated increased vascular contractility after FD-implantation as a potential mechanism of distal complications. Our study aimed to investigate whether L-arginine medication affects vascular contractility following FD deployment in a rabbit model. Methods FDs were implanted in the aorta of normal rabbits (+FD, n = 10), with sham-operated aorta as controls (n = 5). L-Arginine was given in the drinking water (2.25% L-arginine hydrochloride) of half of the +FD animals (+FD/+Arg). Force contraction vascular contractility studies were performed on the aortic rings proximal and distal to the FD using an organ bath. Total eNOS, eNOS(pS1177), eNOS(pT495), COX-2, and S100A4 were quantified by western analysis on total protein lysates from aortic segments, normalizing to GAPDH. Results Mean vascular contractility was 53% higher in distal relative to proximal aortic segments (P = 0.0038) in +FD animals, but were not significantly different in +FD/+Arg animals, or in sham-operated controls. The +FD animals expressed significantly reduced levels of eNOS(pS1177) than sham-operated controls (P = 0.0335), while both the +FD and +FD/+Arg groups had reduced levels of eNOS(pT495) relative to sham-operated controls (P = 0.0331 and P = 0.0311, respectively). Conclusion These results suggest that L-arginine medication reduces distal vascular contractility after FD treatment via nitric oxide production and thus might mitigate risk for downstream complications.


2002 ◽  
Vol 30 (Supplement) ◽  
pp. A151
Author(s):  
Lakshmi Yella ◽  
Yizhak Kupfer ◽  
Chanaka Seneviratne ◽  
Sidney Tessler

1991 ◽  
Vol 81 (5) ◽  
pp. 695-700 ◽  
Author(s):  
Alison Calver ◽  
Joe Collier ◽  
Patrick Vallance

1. l-Arginine is the physiological precursor for the formation of endothelium-derived nitric oxide. The synthesis of nitric oxide is stereospecific: d-arginine is not a substrate for nitric oxide synthase. It is possible that the provision of excess l-arginine substrate might increase the vascular synthesis of nitric oxide. We have examined this possibility by studying the effects of local infusion of l-and d-arginine in the forearm resistance bed and the superficial dorsal hand veins of healthy subjects. 2. Drugs were either infused locally into a vein on the back of the hand and then the vein diameter was measured using a linear displacement technique, or into the brachial artery and then the forearm blood flow was measured by venous occlusion plethysmography. 3. In the superficial hand veins, l- and d-arginine free base and l- and d-arginine hydrochloride (all four preparations at a dose of 5 μmol/min) all caused a significant increase in venous diameter. The responses of the l-and d-enantiomers did not differ significantly from one another. 4. In the forearm resistance bed, l- and d-arginine free base and l-arginine hydrochloride were without effect at doses of 10 and 40 μmol/min. However, at doses of 160 μmol/min all three preparations of arginine caused a significant increase in forearm blood flow compared with control values. The responses to the three preparations of arginine did not differ significantly from one another. 5. These results show that arginine in high dose is a vasodilator in both human resistance vessels and superficial veins in vivo. The response to arginine was not stereospecific: both the l- and d-enantiomers had the same effect. The dilator effect of high-dose arginine showed neither arterio-nor veno-selectivity. 6. This suggests that the hypotensive effect of systemic infusions of l-arginine in man is mediated by peripheral vasodilatation. It is not possible to ascribe the actions of arginine supplementation in this study to activation of the l-arginine/nitric oxide pathway through the provision of excess substrate.


2020 ◽  
Author(s):  
Nathalie Ollivier ◽  
Vangelis Agouridas ◽  
Benoît Snella ◽  
Rémi Desmet ◽  
Hervé Drobecq ◽  
...  

Hydrazone and oxime peptide ligations are catalyzed by arginine. The catalysis is assisted intramolecularly by the side-chain guanidinium group. Hydrazone ligation in the presence of arginine proceeds efficiently in phosphate buffer at neutral pH but is particularly powerful in bicarbonate/CO<sub>2</sub> buffer. In addition to acting as a catalyst, arginine prevents the aggregation of proteins during ligation. With its dual properties as nucleophilic catalyst and protein aggregation inhibitor, arginine hydrochloride is a useful addition to the hydrazone/oxime ligation toolbox.<br>


2002 ◽  
Vol 33 (8) ◽  
pp. 625-630 ◽  
Author(s):  
R. J. C. Lima ◽  
P. T. C. Freire ◽  
J. M. Sasaki ◽  
F. E. A. Melo ◽  
J. Mendes Filho

PEDIATRICS ◽  
1976 ◽  
Vol 57 (1) ◽  
pp. 166-166
Author(s):  
Hans-Joachim Dietzsch

In answer to the questions of Solonions and Cotton concerning our recent study on the use of arginine hydrochloride inhalations in cystic fibrosis patients,1 we wonder whether these authors misunderstood us. The fate of these children with cystic fibrosis depends on the quality of the inhalation treatment. This means if you replace a good mucolytic drug with a better one you step by step approach the ideal mucolytic solution. As a result of many years' experience we have learned that N-acetylcysteine is an effective and well tolerated mucolytic drug (Dietzsch, H-J, et al: Dtsch Gesundheitsw 28:842, 1973).


1984 ◽  
Vol 105 (3) ◽  
pp. 407-410 ◽  
Author(s):  
Jeffrey L. Barron ◽  
Leslie J. Klaff ◽  
Naomi S. Levitt ◽  
Nicholas Ling ◽  
Robert P. Millar

Abstract. Potassium, aldosterone and insulin responses to arginine infusion were compared in 5 normal men during infusions of somatostatin-14 (SS-14), somatostatin-28 (SS-28) and a control infusion. SS-14 and SS-28 were infused continuously at a rate of 8.6 pmol/min/kg and arginine (0.5 g/kg) was infused from 30–60 min. Following the control infusion with arginine hydrochloride, serum aldosterone and potassium levels increased slightly. The rise in potassium appears to be due to an exchange of cellular potassium for the proton from the arginine hydrochloride. SS-14 had no significant effect on serum potassium or aldosterone but an equimolar dose of SS-28 significantly enhanced the rise in potassium and aldosterone. SS-28 completely inhibited the arginine-stimulated insulin increase while SS-14 only partially inhibited the insulin increase. Since insulin opposes the increase in serum potassium by stimulating cellular uptake of this cation, the enhanced rise in serum potassium in response to arginine hydrochloride during the SS-28 infusion is likely due to the potent insulin suppressing effect of SS-28. The rise in serum aldosterone is directly related to the degree of elevation of serum potassium. These findings caution against the infusion of SS-28 during an arginine stimulation test.


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