bigjosh said:
Composition : Arginine hydrochloride 200 mg/mL, sodium glucuronate 50 mg/mL.
Some things I dug up about the active ingredients:
J Invest Surg 2001 Sep-Oct;14(5):267-73 Related Articles, Links
Exogenous and endogenous nitric oxide but not iNOS inhibition improves function and survival of ischemically injured livers.
Rivera-Chavez FA, Toledo-Pereyra LH, Dean RE, Crouch L, Ward PA.
Department of Surgery, Michigan State University, East Lansing, USA.
The role of nitric oxide (NO) in liver ischemia/reperfusion (I/R) injury remains controversial and few works have shed more information regarding the effect of exogenous (EX) and/or endogenous NO (EN) under conditions of I/R of the liver. We investigated the role of exogenous and endogenous NO and inducible nitric oxide synthase (iNOS) inhibition in liver function, neutrophil infiltration, and animal survival after liver I/R. Sprague-Dawley rats were subjected to total hepatic ischemia for 90 min using an extracorporeal porto-systemic shunt. The animals were divided into five groups, including the sham porto-systemic shunt with no ischemia, the control ischemic group, the L-arginine-treated group, the sodium nitroprusside (SNP or NaNP)-treated group, and the L-N6-(1-iminoethyl) lysine hydrochloride (L-NIL) (selective iNOS inhibitor)-treated group. The animal survival was followed for 7 days. Liver injury tests, tissue myeloperoxidase (MPO), and histology were analyzed at 6 h postreperfusion.
L-Arginine- and sodium nitroprusside-treated groups demonstrated significant improvement in 7 days survival in comparison to the control (20%) (p < .05). The best overall survival was obtained with SNP (70%), followed by survival in the L-arginine treated group (60%). The iNOS inhibitor group (40%) did not show any statistical significance when compared to the control group (p > .05).
Liver injury tests and histology scores in the SNP- and L-arginine-treated groups showed significant improvement when compared to the control group (p < .01 and p < .05, respectively). The iNOS group demonstrated only a slight improvement in these parameters. The liver MPO (as a measurement of neutrophil migration into the liver parenchyma) was significantly decreased only in the SNP and L-arginine groups (p < .05) but not in the iNOS group (p > .5). We conclude that NO exogenous donors and substrates for the endogenous pathway are beneficial for the liver after severe I/R and could be important therapeutic targets to prevent damage following this phenomenon
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This study doesn't talk about the liver, but it could be another benefit:
Int J Sport Nutr 1999 Sep;9(3):241-50 Related Articles, Links
The effect of a carbohydrate--arginine supplement on postexercise carbohydrate metabolism.
Yaspelkis BB 3rd, Ivy JL.
Department of Kinesiology and Health Education, University of Texas, Austin, TX 78712, USA.
The effect of a carbohydrate-arginine supplement on postexercise muscle glycogen storage was investigated. Twelve well-trained cyclists rode for 2 hr on two separate occasions to deplete their muscle glycogen stores. At 0, 1, 2, and 3 hr after each exercise bout, the subjects ingested either a carbohydrate (CHO) supplement (1 g carbohydrate/kg body weight) or a carbohydrate-arginine (CHO/AA) supplement (1 g carbohydrate/kg body mass and 0.08 g arginine-hydrochloride/kg body weight). No difference in rate of glycogen storage was found between the CHO/AA and CHO treatments, although significance was approached. There were also no differences in plasma glucose, insulin, or blood lactate responses between treatments.
Postexercise carbohydrate oxidation during the CHO/AA treatment was significantly reduced compared to the CHO treatment. These results suggest that the addition of arginine to a CHO supplement reduces the rate of CHO oxidation postexercise and therefore may increase the availability of glucose for muscle glycogen storage during recovery.
Publication Types:
Clinical Trial
Controlled Clinical Trial
PMID: 10477360 [PubMed - indexed for MEDLINE]
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A reason to take only the recommened dose:
J Toxicol Clin Toxicol 1997;35(6):621-5 Related Articles, Links
A fatal overdose of arginine hydrochloride.
Gerard JM, Luisiri A.
St. Louis University, School of Medicine, St. Louis University Health Sciences Center, Missouri, USA.
CASE REPORT: Arginine hydrochloride is used both diagnostically to test for growth hormone deficiency and therapeutically for treatment of metabolic alkalosis. We describe a 21-month-old girl who developed cardiopulmonary arrest following an accidental overdose of arginine hydrochloride. The patient developed acute metabolic acidosis and transient, but severe, hyponatremia. Thirty-six hours after successful resuscitation, she developed fatal central pontine and extrapontine myelinolysis.
Unlike previous reports of arginine-toxicity, our patient showed no evidence of hyperkalemia. This case illustrates a previously unreported mechanism of arginine hydrochloride toxicity.
PMID: 9365430 [PubMed - indexed for MEDLINE]
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Another possible benefit:
J Endocrinol Invest 1997 Sep;20(8):488-92 Related Articles, Links
Comparison among the effects of arginine, a nitric oxide precursor, isosorbide dinitrate and molsidomine, two nitric oxide donors, on hormonal secretions and blood pressure in man.
Maccario M, Oleandri SE, Procopio M, Grottoli S, Avogadri E, Camanni F, Ghigo E.
Dipartimento di Medicina Interna, Universita di Torino, Italy.
Arginine has well-known stimulatory effects on GH, PRL and insulin secretion in man but the mechanisms underlying these effects are still unclear. More recently, it has been demonstrated that arginine is the precursor of nitric oxide (NO) which mediates its vasodilatatory effect. Thus, it has been hypothesized that NO could also mediate the hormonal effects of arginine. To clarify this point, in seven normal young volunteers (7 normal male subjects, age 26-35 yr) we compared the effects of arginine hydrochloride (ARG, 0.5 g/kg iv over 30 min) on GH, PRL, insulin and glucose levels as well as on blood pressure, with those of isosorbide dinitrate (ISDN, 5 mg po) and molsidomine (MOLS, 4 mg po), two NO donors which possess well-known vasodilatatory effects.
ARG infusion elicited a clear-cut GH increase (peak vs baseline 17.6 +/- 4.7 vs 2.7 +/- 0.8 (g/L, p < 0.01), PRL (20.6 +/- 2.8 vs 6.9 +/- 0.5 (g/L, p < 0.01) and insulin levels (31.4 +/- 5.7 vs 4.5 +/- 2.1 (U/L, p < 0.01) while induced a biphasic variation of plasma glucose levels with early increase (p < 0.01), followed by late decrease below basal values (p < 0.01). On the other hand, blood pressure was decreased by ARG (nadir vs baseline; systolic: 103 +/- 6 vs 112 +/- 3, p < 0.02 and diastolic 61 +/- 4 vs 72 +/- 2 mmHg, p < 0.02, respectively). ISDN and MOLS did not modify basal GH, PRL and insulin as well as glucose levels while induced a clear reduction in blood pressure (ISDN: nadir vs baseline; systolic: 94 +/- 4 vs 112 +/- 2, p < 0.02; diastolic 69 +/- 3 vs 80 +/- 2, p < 0.02; MOLS: systolic: 94 +/- 3 vs 113 +/- 2 p < 0.02; diastolic 63 +/- 4 vs 72 +/- 2, p < 0.02). The lowering effect of both ISDN and MOLS on both systolic and diastolic blood pressure levels was higher than that induced by ARG. The effect of the latter was, in turn, significantly different from that of placebo on diastolic levels only. In conclusion, our present date are against the hypothesis that NO mediates the stimulatory effects of arginine on GH, PRL and insulin secretion. On the other hand, our findings agree with the hypothesis that ARG has NO-mediated vasodilatatory effect able to decrease blood pressure in man.
Publication Types:
Clinical Trial
PMID: 9364253 [PubMed - indexed for MEDLINE]