PLCAR - Bulk Powder

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I ordered an extra 25 kilograms of PLCAR, in 100 gram containers.

I won't mark them up much to go to Nutra, but looking at around $25 per 100 grams.

Interest?

/FYI, standard preworkout dose is 1-2 grams - so about 50-75 days' worth.
 
bolt10

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Sounds good to me :)
 
strategicmove

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Great move. :)
 
Whacked

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NICE~!

(Quick question for dosing. How much teaspoon-wise is 1 gram? Thanks)
 
AdelV

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haha dammmm, put away 2-3 tubs for me...

any benefits from mega dosing or stick to 2-3g?
 
benj851

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PLCAR doesn’t stop after it’s created the perfect anabolic environment for Androsterone
and 11-Alpha. PLCAR is a powerful anti-oxidant that is clinically proven to enhance the
shuttling of fatty acids into muscle cellular mitochondria to be burned as a fuel source for
greater energy production in skeletal, cardiac, and smooth muscles during exercise.
This action alone prolongs an athlete’s energy levels and delays muscle fatigue onset for
superior result-generating workouts(2). PLCAR has also shown the ability to combat the
destructive effects on muscle tissue that low levels of oxygen induce when fatigue sets
in(15). Finally, Carnitines such as PLCAR have even proven to have promising, positive
effects on the human cardiovascular system!
.
.
.

Can anyone else tell me a little bit more feedback about what it is, and why it's so great since everyone seems to want it? just trying to learn a little
 
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Depending on what time they arrive here, Nutra will have stock by Next Friday.

Then again, they still haven't really accepted the product, so I am just assuming they will.
 
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Dsade sourcing Pclar 55 gallon drums! Awesome man I wanna pick up 2 or 3. Hoping I can time this order where I can get Pclar, A-yohombine, and strange ecstasy before they all sell out.
 
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Going out today...should be there Friday.
 
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So wait, what makes this so great???
PLCAR is a special esterified carnitine with a high affinity for cardiac and skeletal muscle tissue. It transports fatty acids directly into thes mitochondria to be used as fuel. The propionate ester is cleaved upon entry and coverted, without enrgy cost, into succinate which is a rate limiting KREBs intermediate - further enhancing energy production.

It has profound effects on the body.
 
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Here come some of the studies.

After VB-12, looking at a Coq10 strip as well. Looks like the Krillipid Balance will have some awesome synergy here:

1: Biofactors. 2008;32(1-4):135-44.Click here to read Links
Positive inotropic effect of coenzyme Q10, omega-3 fatty acids and propionyl-L-carnitine on papillary muscle force-frequency responses of BIO TO-2 cardiomyopathic Syrian hamsters.
Vargiu R, Littarru GP, Faa G, Mancinelli R.

Dipartimento di Scienze Applicate ai Biosistemi, Sezione di Fisiologia e Nutrizione Umana, Università di Cagliari, Cagliari, Italy.

The inability of heart muscle to generate ventricular pressure to adequately propel blood through the cardiovascular system is a primary defect associated with congestive heart failure (CHF). Force-frequency relationship (FFR) is one of the main cardiac defects associated with congestive heart failure. Thus FFR is a convenient methodological tool for evaluating the severity of muscle contractile dysfunction and the effectiveness of therapeutic agents. Papillary muscle isolated from BIO TO-2 cardiomyopathic Syrian hamsters (CMSHs), show a depressed FFR and represents an animal model of human idiopathic dilated cardiomyopathy. In the present study we investigated the effect of CoQ10, omega-3 fatty acids, propionyl-L-carnitine (PLC) and a combination of these 3 agents (formulation HS12607) on FFR in 8 month old BIO TO-2 CMSHs. Papillary muscles isolated from the anesthetized animals were placed in an incubation bath and attached to an isometric force transducer. A digital computer with an analog/digital interface allowed control of both muscle developed force and electrical stimulus parameters. Force-frequency response was evaluated, at Lmax, with increasing frequencies: 0.06, 0.12, 0.25, 0.5, 1, 2 and 4 Hz. HS12607-treatment produced a positive inotropic effect resulting in a significant enhancement (p < 0.05) of the peak force at the highest frequencies (1-4 Hz). In the range of frequency of 1-4 Hz also CoQ10 and omega-3 significantly (p < 0.05) attenuated the fractional decline in developed force. The significant improvement (p < 0.05) of the timing parameter peak rate of tension rise (+ T') and peak rate of tension fall (-T') indicating a faster rate of muscle contraction and relaxation respectively, found in CoQ10, omega-3 and PLC-treated CMSHs, may be due to the positive effects of these substances on sarcoplasmic reticulum functions. These findings suggest that naturally occurring CoQ10, omega-3 and PLC, particularly when administered together in a coformulation, might be a valid adjuvant to conventional therapy in dilated cardiomyopathy especially when considering that they are natural substances, devoid of side effects.
 
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1: Drugs R D. 2008;9(2):83-91.Links
ATP production and TCA activity are stimulated by propionyl-L-carnitine in the diabetic rat heart.
Broderick TL.

Department of Physiology, Midwestern University, Glendale, AZ 85308, USA. [email protected]

BACKGROUND AND OBJECTIVE: The beneficial effect of propionyl-L-carnitine (PLC) on cardiac function in diabetes mellitus is well documented. This study was designed to determine whether the improvement in cardiac function mediated by PLC in the diabetic rat heart is associated with an increase in ATP production and tricarboxylic acid (TCA) cycle activity. METHODS: Diabetes was induced by an intravenous injection of streptozotocin (60 mg/kg). Following diagnosis of diabetes, treatment was initiated by supplementing the drinking water with PLC at a concentration of 1 g/L for a period of 6 weeks. ATP production and TCA cycle activity were determined from oxidative rates of glucose and palmitate measured in isolated working hearts from control and diabetic animals. RESULTS: The effect of diabetes was associated with a decrease in heart function, expressed as rate-pressure product (RPP), and in rates of myocardial glucose oxidation. Rates of palmitate oxidation in diabetic hearts were similar to those of control hearts. In PLC-treated diabetic hearts, rates of both glucose and palmitate oxidation were increased and a significant improvement in RPP was observed. As a result, overall ATP production and TCA cycle activity from glucose and palmitate oxidation were increased in diabetic hearts. CONCLUSION: Our results indicate that the depression in RPP in the diabetic rat heart can be prevented with chronic PLC treatment. Increases in glucose and palmitate utilization with resultant increases in ATP production and TCA cycle activity may explain the benefit of PLC on diabetic rat heart function.
 
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Combined with NOxidant -

Free Radic Res. 2007 Aug;41(8):884-91.Click here to read Links
l-carnitine and its propionate: improvement of endothelial function in SHR through superoxide dismutase-dependent mechanisms.
de Sotomayor MA, Mingorance C, Rodriguez-Rodriguez R, Marhuenda E, Herrera MD.

Departamento de Farmacologia, Facultad de Farmacia, Universidad de Sevilla, Seville, Spain. [email protected]

To clarify the mechanism underlying the antioxidant properties of l-carnitine (LC) and propionyl-l-carnitine (PLC) on spontaneously hypertensive (SHR) and normotensive WKY, animals were treated with either PLC or LC (200 mg kg(- 1)). Aorta was dissected and contraction to (R)-( - )-phenylephrine (Phe) and relaxation to carbachol (CCh) were assessed in the presence or not of the NO synthase (NOS) inhibitor, l-NAME. [image omitted] production was evaluated by lucigenin-enhanced chemiluminescence and its participation on relaxation was observed after incubation with superoxide dismutase (SOD) plus catalase. Protein expressions of eNOS, Cu/Zn-SOD and Mn-SOD were studied by western blot. Both LC and PLC treatments improved endothelial function of SHR through increasing NO participation and decreasing [image omitted] probably involving higher Cu/Zn-SOD expression. PLC treatment augmented eNOS expression in SHR. Surprisingly, LC increased [image omitted] produced by aorta from WKY and thus diminished NO and damaged endothelial function. Conversely, PLC did not affect CCh-induced relaxation in WKY. These results demonstrate that LC and PLC prevent endothelial dysfunction in SHR through an antioxidant effect.
 
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Not going to elaborate at this time (another product coming down the road) but add in the VB-12 to this stack:

1: Haematologica. 2005 Dec;90(12 Suppl):ECR45.Click here to read Links
Two newborns with nutritional vitamin B12 deficiency: challenges in newborn screening for vitamin B12 deficiency.
Campbell CD, Ganesh J, Ficicioglu C.

The Children's Hospital of Philadelphia, Section of Metabolism, PA 19104, USA.

Vitamin B12 deficiency causes decreased Methionine Synthase and L-Methylmalonyl-CoA Mutase activity and results in accumulation of Homocysteine, Methylmalonic acid and Propionylcarnitine. Propionylcarnitine is included in tandem mass spectrometry-based newborn screening programs for detection of certain inborn errors of metabolism. We report two asymptomatic newborns with Vitamin B12 deficiency due to maternal deficiencies. One was detected incidentally at 3 weeks of age; the second on supplemental newborn screening based on elevated Propionylcarnitine at 2 days of age. This illustrates the potential for false negative results for Vitamin B12 deficiency screening by acylcarnitine profiling in newborn screening. Homocysteine and Methylmalonic acid may be better markers of Vitamin B12 deficiency. In conclusion, we suggest measuring Methylmalonic acid, Propionylcarnitine and Homocysteine levels in blood spots in expanded newborn screening in order to detect asymptomatic newborns with Vitamin B12 deficiency. Further studies are needed to establish the sensitivity of these three markers in screening for Vitamin B12 deficiency.
 
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1: Ann N Y Acad Sci. 2004 Nov;1033:79-91.Click here to read Links
Therapeutic effects of L-carnitine and propionyl-L-carnitine on cardiovascular diseases: a review.
Ferrari R, Merli E, Cicchitelli G, Mele D, Fucili A, Ceconi C.

Chair of Cardiology, University Hospital of Ferrara, Gussago (Brescia), Italy. [email protected]

Several experimental studies have shown that levocarnitine reduces myocardial injury after ischemia and reperfusion by counteracting the toxic effect of high levels of free fatty acids, which occur in ischemia, and by improving carbohydrate metabolism. In addition to increasing the rate of fatty acid transport into mitochondria, levocarnitine reduces the intramitochondrial ratio of acetyl-CoA to free CoA, thus stimulating the activity of pyruvate dehydrogenase and increasing the oxidation of pyruvate. Supplementation of the myocardium with levocarnitine results in an increased tissue carnitine content, a prevention of the loss of high-energy phosphate stores, ischemic injury, and improved heart recovery on reperfusion. Clinically, levocarnitine has been shown to have anti-ischemic properties. In small short-term studies, levocarnitine acts as an antianginal agent that reduces ST segment depression and left ventricular end-diastolic pressure. These short-term studies also show that levocarnitine releases the lactate of coronary artery disease patients subjected to either exercise testing or atrial pacing. These cardioprotective effects have been confirmed during aortocoronary bypass grafting and acute myocardial infarction. In a randomized multicenter trial performed on 472 patients, levocarnitine treatment (9 g/day by intravenous infusion for 5 initial days and 6 g/day orally for the next 12 months), when initiated early after acute myocardial infarction, attenuated left ventricular dilatation and prevented ventricular remodeling. In treated patients, there was a trend towards a reduction in the combined incidence of death and CHF after discharge. Levocarnitine could improve ischemia and reperfusion by (1) preventing the accumulation of long-chain acyl-CoA, which facilitates the production of free radicals by damaged mitochondria; (2) improving repair mechanisms for oxidative-induced damage to membrane phospholipids; (3) inhibiting malignancy arrhythmias because of accumulation within the myocardium of long-chain acyl-CoA; and (4) reducing the ischemia-induced apoptosis and the consequent remodeling of the left ventricle. Propionyl-L-carnitine is a carnitine derivative that has a high affinity for muscular carnitine transferase, and it increases cellular carnitine content, thereby allowing free fatty acid transport into the mitochondria. Moreover, propionyl-L-carnitine stimulates a better efficiency of the Krebs cycle during hypoxia by providing it with a very easily usable substrate, propionate, which is rapidly transformed into succinate without energy consumption (anaplerotic pathway). Alone, propionate cannot be administered to patients in view of its toxicity. The results of phase-2 studies in chronic heart failure patients showed that long-term oral treatment with propionyl-L-carnitine improves maximum exercise duration and maximum oxygen consumption over placebo and indicated a specific propionyl-L-carnitine effect on peripheral muscle metabolism. A multicenter trial on 537 patients showed that propionyl-L-carnitine improves exercise capacity in patients with heart failure, but preserved cardiac function.
 
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highly intriguing:

1: Curr Med Res Opin. 2004 Sep;20(9):1377-84.Click here to read Links
Preliminary observations on the use of propionyl-L-carnitine in combination with sildenafil in patients with erectile dysfunction and diabetes.
Gentile V, Vicini P, Prigiotti G, Koverech A, Di Silverio F.

Department of Urology U Bracci, University La Sapienza, Rome, Italy.

PURPOSE: To investigate the efficacy and tolerability of oral propionyl-L-carnitine (PLC) plus sildenafil in men with erectile dysfunction (ED) and diabetes unresponsive to sildenafil monotherapy. MATERIALS AND METHODS: Patients with medically documented ED of organic or mixed aetiology and diabetes (type 1 and 2) were randomised to receive oral PLC (2 g/day) plus sildenafil (50 mg twice weekly) (20 patients, Group 1) or sildenafil alone (20 patients, Group 2), in a double-blind, fixed-dose study. All patients had been previously treated unsuccessfully with a minimum of eight administrations of sildenafil. Efficacy was evaluated using the International Index of Erectile Function (IIEF) questionnaire: total score, subscores for questions 3 (Q3; achieving an erection) and 4 (Q4; maintaining an erection) and global efficacy question (GEQ: 'Has treatment improved your erections?'). Patients Event Logs were also used. RESULTS: After 24 weeks of treatment, mean scores for IIEF Q3 and Q4 had improved significantly in patients of Group 1 (4.25 +/- 0.63 and 3.95 +/- 1.0) compared with Group 2 (2.9 +/- 0.71 and 2.7 +/- 0.96) (p < 0.01). Moreover, the percentage of patients with improved erections (GEQ 68% vs. 23%) and successful intercourse attempts (76% vs. 34%) was significantly increased in Group 1 compared with Group 2 (p < 0.01). Fourteen (70%) patients in Group 1 and four (20%) in Group 2 reported an increase in mean IIEF EF domain score of > or = 4 (p < 0.01). Treatments were well tolerated and no patient discontinued study medication. Two patients in Group 1 reported mild gastric pain.CONCLUSIONS: Salvage therapy with PLC plus sildenafil was more effective than sildenafil in the treatment of ED in patients with diabetes refractory to sildenafil monotherapy.
 
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with Alpha-Burn anyone?

Coron Artery Dis. 2004 Feb;15(1):65-71.Click here to read Links
Improvement of cardiac function and beta-adrenergic signal transduction by propionyl L-carnitine in congestive heart failure due to myocardial infarction.
Sethi R, Wang X, Ferrari R, Dhalla NS.

Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre and Department of Physiology, University of Manitoba, Winnipeg, Canada.

OBJECTIVES: Earlier studies have revealed beneficial effects of metabolic therapy in animals with congestive heart failure (CHF) due to myocardial infarction. Because heart failure is also associated with attenuated response to catecholamines, we examined the effects of propionyl L-carnitine (PLC) (a carnitine derivative) therapy on the beta-adrenoceptor (beta-AR) signal transduction in the failing heart. METHODS: Heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated with or without 100 mg/kg (intraperitoneally, daily) PLC for 5 weeks. The animals were assessed for their left ventricular function and inotropic responses to isoproterenol. Crude membranes were isolated from the remote, nonischemic (viable) left ventricle and examined for changes in beta-AR and adenylyl cyclase (AC) activity. RESULTS: Animals with heart failure exhibited depressions in ventricular function, positive inotropic response to isoproterenol, beta-AR receptor density and basal AC activity; these changes were also attenuated by PLC treatment. The stimulation of AC activities with isoproterenol, 5'-guanyl imidodiphosphate, forskolin and sodium fluoride was decreased in the failing hearts and these changes were also prevented by PLC treatment. CONCLUSION: The results indicate that metabolic therapy with PLC not only attenuates the defects in heart function but also prevents changes in the beta-AR signal transduction in CHF due to myocardial infarction. Copyright 2004 Lippincott Williams & Wilkins
 
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1: Mol Genet Metab. 2000 Jan;69(1):69-75.Click here to read Links
Evidence for a short-chain carnitine-acylcarnitine translocase in mitochondria specifically related to the metabolism of branched-chain amino acids.
Roe DS, Roe CR, Brivet M, Sweetman L.

Kimberly H. Courtwright & Joseph W. Summers, Institute of Metabolic Disease, Dallas, Texas, 75226, USA.

Carnitine-acylcarnitine translocase (CATR) deficiency is a severe defect in fatty acid oxidation which presents early in life most frequently with hypoglycemia, hyperammonemia, and severe cardiac abnormalities. CATR exchanges acylcarnitines of various chain lengths for free carnitine across the mitochondrial membrane. In vitro studies in intact fibroblasts from patients with documented deficiency of CATR were probed with stable-isotope-labeled precursors and the resulting acylcarnitines were analyzed by tandem mass spectrometry. After a 72-h incubation with l-[(2)H(3)]carnitine the translocase-deficient cells produced acylcarnitines in which the deuterium was incorporated into short-chain acylcarnitines, C2-C5. Experiments with simultaneous incubation of l-[(2)H(3)]carnitine and l-[(13)C(6)]isoleucine produced [(13)C(5)]2-methylbutyryl-[(2)H(3)]carnitine and [(13)C(3)]propionyl-[(2)H(3)]carnitine indicating exchange of labeled acylcarnitine from inside the mitochondrial matrix with labeled free carnitine. These studies support the possible existence of a "branched-chain" carnitine-acylcarnitine translocator in mitochondria. Copyright 2000 Academic Press.
 
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Dsade, on it as usual
I found PLCAR in mid-2004, and had BIG plans for it at the time. It is such a badass compound that, unfortunately, most companies refuse to pay the premium for.

I applaud AX (and Matt Cahill) for having the guts to include it in 3-AD - and it is one of the hardcore keys to the effectiveness of DCP.
 
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The reason I chose this form of Carnitine for Eviscerate, and part of the key to the workout enhancement and localized growth seen thus far, as well as the excellent fatloss results:

1: J Vasc Surg. 1999 Jun;29(6):1097-103.Click here to read Links
Propionyl-L-carnitine dilates human subcutaneous arteries through an endothelium-dependent mechanism.
Cipolla MJ, Nicoloff A, Rebello T, Amato A, Porter JM.

Department of Surgery, Division of Vascular Surgery, Oregon Health Sciences University, Portland 97201, USA.

PURPOSE: The vasoactive effects of propionyl-L-carnitine (PLC) on human arteries, including endothelial and smooth muscle cell influences, were studied. METHODS: Small (less than 200 microm) subcutaneous fat arteries (n = 19), obtained from human patients undergoing vascular surgery, were dissected and mounted in an arteriograph system that allowed measurement of lumen diameter and control of transmural pressure. To investigate the role of the endothelium, arteries were compared intact, intact and in the presence of either 0.3 mmol/L nitro-L-arginine (an inhibitor of nitric oxide synthesis) or 10 micromol/L indomethacin (an inhibitor of prostaglandin synthesis), or denuded of endothelium. After a 1-hour equilibration at a pressure of 50 mm Hg, arteries were precontracted 50% with an intermediate concentration of norepinephrine, and clinically relevant concentrations of PLC (0.1 to 100 micromol/L) were cumulatively added to the bath while the lumen diameter was continually measured. RESULTS: Intact arteries dose-dependently dilated to PLC, with the half maximal dilation occurring at 2.9 +/- 1.2 micromol/L, increasing diameter 91% +/- 5% at 100 micromol/L. In contrast, PLC had significantly less effect on deendothelialized arteries, increasing diameter only 24% +/- 11% at 100 micromol/L (P <.01 vs. intact). This indicates the endothelial dependency of this compound. Blockade of nitric oxide did not inhibit this vasodilation, with the half-maximal response occurring at 8.6 +/- 7 micromol/L, increasing diameter 85% +/- 8% at 100 micromol/L ( P >.05 vs. intact). However, this vasodilation was significantly diminished in the presence of indomethacin, which dilated arteries only 53% +/- 18% at 100 micromol/L (P <.01 vs. intact; P >.05 vs. denuded). CONCLUSION: PLC is an endothelium-dependent vasodilator, the mechanism of which is partially mediated by prostaglandin synthesis, not nitric oxide. The beneficial effects of this compound may, in part, be related to vasodilation and enhanced blood flow.
 
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Anyone crying uncle yet?

1: Muscle Nerve. 1997 Sep;20(9):1115-20.Click here to read Links
Changes in skeletal muscle histology and metabolism in patients undergoing exercise deconditioning: effect of propionyl-L-carnitine.
Brevetti G, Fanin M, De Amicis V, Carrozzo R, Di Lello F, Martone VD, Angelini C.

Department of Medicine, University Federico II of Naples, Italy.

To define the skeletal muscle abnormalities in patients undergoing exercise deconditioning and evaluate the metabolic effect of propionyl-L-carnitine (PLC), muscle biopsies were obtained from 28 patients with effort angina and 31 control subjects. Coronary artery disease patients received either placebo (n = 12), PLC (1.5 g i.v. followed by infusion of 1 mg/kg/min for 30 min, n = 10), or L-carnitine (1 g i.v. followed by infusion of 0.65 mg/kg/min for 30 min, n = 6) for 2 days. Exercise deconditioned patients treated with placebo showed normal muscle content of total carnitine and glycogen, and decrease in percentage of type 1 fibers (P < 0.01) and in the activity of citrate synthase (P < 0.05), succinate dehydrogenase (P < 0.05), and cytochrome oxidase (P < 0.05), as compared to controls. Both PLC and L-carnitine did not modify muscle fiber composition or enzyme activities, but significantly increased muscle levels of total carnitine by 42% and 31%, respectively (P < 0.05). Moreover, PLC significantly increased glycogen muscle content (P < 0.01), while the equimolar dose of L-carnitine did not. This effect, probably due to the anaplerotic activity of the propionic group of PLC, suggests that this drug may be effective in improving energy metabolism of muscles with impaired oxidative capacity.
 
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How long can you go?

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Carnitines increase plasma levels of adenosine and ATP in humans.
Capecchi PL, Laghi Pasini F, Quartarolo E, Di Perri T.

Institute of Clinical Medicine, University of Siena, School of Medicine, Italy.

In order to help to clarify the mode of action of carnitine derivatives, plasma levels of adenosine, ATP and inosine were evaluated following the infusion of 0.75, 0.50 and 0.25 mg/kg/min propionyl-L-carnitine (PLC) for 30 min in patients affected with peripheral arterial disease. Moreover, the effects of 0.75 mg/kg/min acetyl-L-carnitine (ALC) and L-carnitine (LC) were studied in the same conditions. Finally, the activity of 7.5 mg/kg/min PLC administered for 3 min was also evaluated. PLC and ALC produced a significant increase in plasma levels of adenosine and ATP, whereas LC induced less relevant changes. The administration of the compounds did not affect the adenosine/inosine ratio. Peak plasma levels of adenosine preceded in any case those of ATP. The possibility can be suggested that the pharmacological activity of PLC, ALC, and LC may be mediated, at least in part, by an interference with the endogenous purine system. Since these effects may be related to physiological mechanisms of tissue protection, new pharmacological perspectives for the compounds may arise.
 
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Can you tell that I am a huge fan of this compound?

Can you tell WHY?
 
T-Bone

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I was studying it for about 6-7 hours online a few months, then I went to Nutraplanet to order and saw that it was out of stock. I emailed them and they said it had been discontinued!. So I just put it in the back of my mind for a while....Eveything I read online sounded so great about this stuff. Hopefully Nutraplanet will pick it up and keep carrying it forever and ever!!!.
 
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I was studying it for about 6-7 hours online a few months, then I went to Nutraplanet to order and saw that it was out of stock. I emailed them and they said it had been discontinued!. So I just put it in the back of my mind for a while....Eveything I read online sounded so great about this stuff. Hopefully Nutraplanet will pick it up and keep carrying it forever and ever!!!.
It'll be there tomorrow. :)
 

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about a month ago i got some bulk alcar and i want to get some of this too my q is
can i stack both together and how much would i use
 
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