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View Full Version : Hepargine another vet sup i found, could it be good for liver detox?



bigjosh
12-13-2002, 02:55 AM
I always take milk thistle and ala on cycle to help my liver out, but am always looking for more things. Here is a legal veterinary liver product I found (profile shown below). I do not know much of any of the medical jargon on the profile, but I'm posting it to see if anyone knows if it would be a good adjunct to a cycle that is liver toxic such as one consisting of anadrol, dbol, or winny. For all I know this could have no use for such, but if anyone understands the jargon and has any thoughts and/or ideas on weather it's use could be beneficial w/ AS please post. Any info is greatly appreciated, after all we are all here to learn. The profile is below:

Hepargine 25% 50ml

Composition : Arginine hydrochloride 200 mg/mL, sodium glucuronate 50 mg/mL.

Actions : Arginine and sodium glucuronate supplementation. Arginine is an essential amino acid involved in ammonia detoxification processes in the liver and kidneys; its action is complemented and enhanced by sodium glucuronate. The primary role is to assist liver recovery from toxaemia, and as supportive therapy in horses recovering from hard work or disease.

Indications : Recovery after hard work and exercise, severe stress and liver depression caused by toxaemia or disease.

Contraindications : Use in severe hepatic damage.

Warnings : Intramuscular injection in some horses and dogs may cause tissue reaction and soreness; oral or slow intravenous administration under veterinary supervision is preferred.

Dosage and Administration : Horses, dogs. 1 mL/10 kg bodyweight daily for 2 to 3 days.

Presentation : Injection (multidose vial): 50 mL.

rooster1
12-13-2002, 11:01 AM
:) For a chemical guru.Inquring minds want to know.....:D

WeirdAl
12-13-2002, 10:39 PM
sounds interesting. bump!

chewin iron
12-13-2002, 10:47 PM
yes....would like to know a little also.......could you mix it with your injections also?????

Badgermoon
12-13-2002, 10:48 PM
This sounds promising, but I know little about drugs and how they might react in a human body. might have a different result than in an animal... like giving you a toungue like a dog and a dick like a horse. All you'd need to add is to drill a hole in the top of your head so you can breathe like a dolfin and violla' babe magnate!

(oh god I need help) :D

jaywooly
12-17-2002, 01:47 PM
I wouldn't mind a dick like a horse.

bigjosh
04-20-2003, 12:22 AM
BUMP

does anyone think this product would help as a detox when using toxic AS?

bigjosh
04-20-2003, 12:23 AM
pic of it; it only costs ten bucks. If it may work I might get some...

scorpio
04-20-2003, 12:54 AM
Might have some info. I'm going on vacation, give me a few days to check up on my references.

bigjosh
04-20-2003, 12:58 AM
cool thanks scropio, and have fun on your vacation!

scorpio
04-20-2003, 01:01 AM
Yeah, I'll try. Got a pool to sit next to and I'll check it out for ya, if I can't figure it out i've got a few freinds in the know...

Harvey Balboner
04-20-2003, 01:11 AM
Very interesting.

bigjosh
06-01-2003, 02:03 PM
maybe it does work; I see it for sale at http://killdevill.com/page4.html as a liver detoxifier.

Anyone else know?

I'm thinking of running some anadrol in my next cycle and am gonna take ala, milk thistle, and cranberry to help with liver and kidneys and if hepargine helps I will add it too....

footballcat
06-01-2003, 02:27 PM
hmm ttt

machine99
06-01-2003, 04:23 PM
Originally posted by bigjosh
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

------------------------------

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]

----------------------------------

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]

---------------------------------------

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]

machine99
06-01-2003, 04:34 PM
J Pediatr Endocrinol Metab 1996 Sep-Oct;9(5):523-31 Related Articles, Links


Effects of phenylalanine, histidine, and leucine on basal and GHRH-stimulated GH secretion and on PRL, insulin, and glucose levels in short children. Comparison with the effects of arginine.

Bellone J, Valetto MR, Aimaretti G, Segni M, Volta C, Cardimale G, Baffoni C, Pasquino AM, Bernasconi S, Bartolotta E, Mucci M, Ghigo E.

Department of Internal Medicine, University of Turin, Italy.

Of the amino acids arginine is the most potent GH secretagogue in man. It potentiates the GH response to GHRH, exerts a weaker PRL-releasing effect, stimulates insulin and glucagon and induces a biphasic glucose variation. The potency and effects of other amino acids on pituitary and pancreatic hormones need to be clarified. In 43 children with normal short stature (5.3-14.0 yr; 30 M and 13 F) the effects of the infusion of phenylalanine (Phe, 0.08 g/kg), histidine (His, 0.1 g/kg), and leucine (Leu, 0.08 g/kg) on basal and GHRH-stimulated GH secretion and on PRL, insulin and glucose levels were studied and compared with those of arginine at high (hArg, 0.5 g/kg) or low dose (lArg, 0.2 g/kg). Phe increased basal (p < 0.05) but not GHRH-stimulated GH levels, induced PRL and insulin rises (p < 0.03 and p < 0.03), and did not change glycemia. Though a trend toward an increase in basal GH levels was found after His, His and Leu did not significantly modify either basal or GHRH-induced GH secretion nor basal PRL, insulin and glucose levels. Both hArg and lArg increased basal (p < 0.0001 and p < 0.05, respectively) and GHRH-stimulated GH levels (p < 0.006 and p < 0.006). hArg increased both PRL (p < 0.002) and insulin levels (p < 0.005) more (p < 0.0005 and p < 0.004) than lArg (p < 0.005 and p < 0.005), while glucose levels showed a similar increase followed by a similar decrease. We conclude that in childhood: a) Phe significantly increases GH secretion but, differently from Arg, does not potentiate the response to GHRH, suggesting different mechanisms of action of these amino acids; b) differently from His and Leu, Phe is a PRL and insulin secretagogue but is less potent than Arg; c) Arg has the highest stimulatory effect on pituitary and pancreatic hormones.

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Could be helpful to take with hgh

J Clin Endocrinol Metab 2000 Oct;85(10):3604-8 Related Articles, Links


Arginine counteracts the inhibitory effect of recombinant human insulin-like growth factor I on the somatotroph responsiveness to growth hormone-releasing hormone in humans.

Gianotti L, Maccario M, Lanfranco F, Ramunni J, Di Vito L, Grottoli S, Muller EE, Ghigo E, Arvat E.

Department of Internal Medicine, University of Turin, Italy.

Insulin-like growth factor I (IGF-I) exerts a negative feedback effect on GH secretion via either direct actions at the pituitary level or indirect ones at the hypothalamic level, through stimulation of somatostatin (SS) and/or inhibition of GHRH release. In fact, recombinant human IGF-I (rhIGF-I) in humans inhibits spontaneous GH secretion as well as the GH response to GHRH and even more to GH/GH-releasing peptides, whose main action is on the hypothalamus, antagonizing SS and enhancing GHRH activity. The aim of the present study was to further clarify in humans the mechanisms underlying IGF-I-induced inhibition of somatotroph secretion. In six normal young volunteers (all women; mean +/- SEM: age, 28.3+/-1.2 yr; body mass index, 21.3+/-1.2 kg/m2) we studied the GH response to GHRH (1 microg/kg, iv, at 0 min), both alone and combined with arginine (ARG; 0.5 g/kg, iv, from 0-30 min), which probably acts via inhibition of hypothalamic SS release, after pretreatment with rhIGF-I (20 microg/kg, sc, at -180 min) or placebo. rhIGF-I increased circulating IGF-I levels (peak at -60 vs. -180 min: 54.9+/-3.9 vs. 35.9+/-3.3 mmol/L; P < 0.05) to a reproducible extent, and these levels remained stable and within the normal range until 90 min. The mean GH concentration over 3 h (from -180 to 0 min) before ARG and/or GHRH was not modified by placebo or rhIGF-I. After placebo, the GH response to GHRH (peak, 23.6+/-2.9 microg/L) was strikingly enhanced (P < 0.05) by ARG coadministration (69.6+/-9.9 microg/L). rhIGF-I blunted the GH response to GHRH (13.1+/-4.5 microg/L; P < 0.05), whereas that to GHRH plus ARG was not modified (59.5+/-8.9 microg/L), although it occurred with some delay. Mean glucose and insulin concentrations were not modified by either placebo or rhIGF-I. In conclusion, ARG counteracts the inhibitory effect of rhIGF-I on somatotroph responsiveness to GHRH in humans. These findings suggest that the acute inhibitory effect of rhIGF-I on the GH response to GHRH takes place on the hypothalamus, possibly via enhancement of SS release, and that ARG overrides this action.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 11061509 [PubMed - indexed for MEDLINE]


PMID: 8961128 [PubMed - indexed for MEDLINE]

machine99
06-02-2003, 10:39 AM
oh so know one else posts any studies or nothing. That's great I see how it is, let Machine post all the studies he's crazy.... Sometimes I don't know why I bother. :( :cry:

Serious didn't find much on that particular sodium yet, but I will... The effects of the amino acid seem to be worth a try though especially IM injections