| Ημερομηνία | barcode | code | περιεχομενο | τιμή παραγωγός | χονδρική | λιανική |
|---|---|---|---|---|---|---|
| 05/2018 | 2801854117016 | 185411701 | APOTEL SOL.IV.INF 1G/6,7ΜL AMP BT x 3 AMPS x 6,7 ML | 3.89 | 04.08 | 5.61 |
| 05/2018 | 2801854118020 | 185411802 | APOTEL MAX SOL.INF 1G/100 ML BTx12 VIALSx100 ML | 13.20 | 13.85 | 19.09 |
| 05/2018 | 2801854118044 | 185411804 | APOTEL MAX SOL.INF 1G/100 ML BTx12 BAGS x100 ML | 13.20 | 13.85 | 19.09 |
| 05/2018 | 2802459301015 | 245930101 | APOTEL PLUS INJ.SOL (600+20)MG/4ML AMP BTx3(AMPx4ML) | 2.66 | 2.79 | 3.85 |
For temporary relief of fever and minor aches and pains.
Acetaminophen is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis. Unlike NSAIDs, acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, thus, has no peripheral anti-inflammatory affects. While aspirin acts as an irreversible inhibitor of COX and directly blocks the enzyme's active site, studies have found that acetaminophen indirectly blocks COX, and that this blockade is ineffective in the presence of peroxides. This might explain why acetaminophen is effective in the central nervous system and in endothelial cells but not in platelets and immune cells which have high levels of peroxides. Studies also report data suggesting that acetaminophen selectively blocks a variant of the COX enzyme that is different from the known variants COX-1 and COX-2. This enzyme is now referred to as COX-3. Its exact mechanism of action is still poorly understood, but future research may provide further insight into how it works. The antipyretic properties of acetaminophen are likely due to direct effects on the heat-regulating centres of the hypothalamus resulting in peripheral vasodilation, sweating and hence heat dissipation.
Oral, mouse: LD50 = 338 mg/kg; Oral, rat: LD50 = 1944 mg/kg. Acetaminophen is metabolized primarily in the liver, where most of it is converted to inactive compounds by conjugation with glucuronic acid and, to a lesser extent, sulfuric acid. Conjugates are then excreted by the kidneys. Only a small portion is excreted in unchanged in urine or oxidized via the hepatic cytochrome P450 enzyme system (CYP2E1). Metabolism via CYP2E1 produces a toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI). The toxic effects of acetaminophen are due to NAPQI, not acetaminophen itself nor any of the major metabolites. At therapeutic doses, NAPQI reacts with the sulfhydryl group of glutathione to produce a non-toxic conjugate that is excreted by the kidneys. High doses of acetaminophen may cause glutathione depletion, accumulation of NAPQI and hepatic necrosis. The maximum daily dose of acetaminophen is 4 g. Liver failure has been observed at doses as low as 6 g per day. As such, the maximum daily and single dose of acetaminophen is currently being reviewed in some countries. N-acetyl-cysteine, a precursor of glutathione, may be administered in the event of acetaminophen toxicity.
Rapid and almost complete
1 to 4 hours
Approximately 80% of acetaminophen is excreted in the urine after conjugation and about 3% is excreted unchanged.
For management of fatigue, orthostatic hypotension, and for the short term treatment of apnea of prematurity in infants.
Caffeine stimulates medullary, vagal, vasomotor, and respiratory centers, promoting bradycardia, vasoconstriction, and increased respiratory rate. This action was previously believed to be due primarily to increased intracellular cyclic 3′,5′-adenosine monophosphate (cyclic AMP) following inhibition of phosphodiesterase, the enzyme that degrades cyclic AMP. It is now thought that xanthines such as caffeine act as agonists at adenosine-receptors within the plasma membrane of virtually every cell. As adenosine acts as an autocoid, inhibiting the release of neurotransmitters from presynaptic sites but augmenting the actions of norepinephrine or angiotensin, antagonism of adenosine receptors promotes neurotransmitter release. This explains the stimulatory effects of caffeine. Blockade of the adenosine A1 receptor in the heart leads to the accelerated, pronounced "pounding" of the heart upon caffeine intake.
LD<sub>50</sub>=127 mg/kg (orally in mice)
Readily absorbed after oral or parenteral administration. The peak plasma level for caffeine range from 6-10mg/L and the mean time to reach peak concentration ranged from 30 minutes to 2 hours.
3 to 7 hours in adults, 65 to 130 hours in neonates
In young infants, the elimination of caffeine is much slower than that in adults due to immature hepatic and/or renal function.
* 0.8 to 0.9 L/kg [infants] * 0.6 L/kg [adults]