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PubMed1992

Effects of caffeine, time of day and user history on study-related performance.

The individual and interactive effects of caffeine, time of day and history of caffeine consumption on several study-related tasks were investigated in 25 subjects (6 males, 19 females). Performance was measured on short term memory (STM), mental arithmetic (MA), reading comprehension, serial search (SS) and verbal reasoning (VR). Subjects attended eight experimental sessions, at four times of day (0100, 0700, 1300 and 1900 hours), after ingesting caffeine (4 mg/kg) or placebo. Subjects were assigned to a low, moderate or high user group on the basis of a caffeine consumption questionnaire. Reading comprehension was affected by time of day, while caffeine improved performance on all mental speed-related tasks. High caffeine users performed more poorly than other groups on the verbal reasoning task. Several interactions between the three independent variables were observed on a number of tasks, supporting the contention that different processes underlying various types of cognitive performance are differentially, and often jointly, affected by caffeine, time of day and user history. Implications of caffeine usage on academic performance were discussed.

Adult↗
PubMed1995

Pharmacokinetic and pharmacodynamic responses to caffeine in poor and normal sleepers.

Pharmacokinetic and pharmacodynamic responses to caffeine (2.5 mg/kg) were compared between ten healthy self-rated poor sleepers and ten normal sleepers. Sleep pattern assessed by the Pittsburgh Sleep Quality Index (PSQI). There was no significant difference in mean estimated daily caffeine consumption between the groups. The poor sleepers had significantly higher scores for neuroticism on the Eysenck Personality Questionnaire (EPQ) and anxiety on the Hospital Anxiety Depression (HAD) scale, compared with normal sleepers. Caffeine pharmacokinetics were assessed by measurement of saliva caffeine concentrations. Poor sleepers showed significantly greater variability in caffeine Cmax, clearance had half-life, compared to normal sleepers. Pharmacodynamic measures included heart rate, blood pressure, visual analogue scales for concentration, vigilance and relaxation, psychomotor performance [Digit Symbol Substitution Test (DSST) and tapping rate (TR)] and EEG activity [Contingent negative variation (CNV), auditory evoked potential and power spectral analysis]. Prior to caffeine administration, poor sleepers compared to normal sleepers had faster heart rates, lower ratings for concentration and relaxation, poorer performance on the DSST, greater CNV magnitude, faster peak alpha frequency and lower delta, theta and beta power. These differences persisted after caffeine ingestion and overall differences between the groups on these measures were significant (P < 0.01-.001). Post-dose, but not pre-dose, scores for vigilance and TR were significantly lower overall in poor compared with normal sleepers. Despite the baseline differences between poor and normal sleepers, the changes following caffeine administration were similar in direction and magnitude in both groups.

Adult↗
PubMed1994

Enhancing caffeine reinforcement by behavioral requirements following drug ingestion.

Each morning eight adults with caffeine versus placebo discrimination histories ingested letter-coded capsules containing 100 mg caffeine or placebo and then engaged in a relaxation or vigilance activity. Subjects were first exposed to caffeine and placebo once each with each activity. Then each day for 10 days subjects made two choices; they chose which compound they would prefer if vigilance were scheduled and which they would prefer if relaxation were scheduled, with the restriction that they could not choose the same compound with both activities; only one choice (randomly selected) was reinforced. Eight of eight subjects always chose caffeine with vigilance. The next choice condition was identical, except that subjects were free to take either compound with both activities. Six of six subjects reliably chose caffeine with vigilance. Four reliably chose placebo with relaxation. In the final condition, each day for 10 days subjects chose between each drug and each of 52 monetary values; those choices were made separately for vigilance and relaxation; only one choice (randomly selected) was reinforced. For six of seven subjects, the maximum dollar value at which subjects chose drug over money was higher for caffeine in vigilance than for placebo in either activity. For five subjects, the maximum value at which subjects chose caffeine over money was higher in vigilance than in relaxation. Overall, this study demonstrates enhanced caffeine reinforcement when a vigilance activity followed drug ingestion.

Adult↗
PubMed1985

Caffeine elimination: a test of liver function.

Fasting plasma caffeine concentration and various parameters of caffeine elimination from plasma obtained after a standardized oral dose of 140 mg caffeine have been compared in nine patients with liver cirrhosis, eight patients with non-cirrhotic liver disease and ten healthy volunteers with regard to their ability to discriminate between the different groups. Fasting plasma caffeine concentrations were significantly higher in cirrhotics (11.1 +/- 10.5 mumol/l) than in healthy volunteers (1.5 +/- 0.8 mumol/l). The respective values measured in patients with non-cirrhotic liver disease (3.1 +/- 3.1 mumol/l) did not differ significantly from the controls. Plasma disappearance rate and clearance of caffeine were significantly decreased in cirrhotics (0.11 +/- 0.02 h-1; 1.0 +/- 0.3 ml/min per kg) and in patients with non-cirrhotic liver disease (0.18 +/- 0.04 h-1; 2.2 +/- 0.7 ml/min per kg) as compared to healthy volunteers (0.23 +/- 0.04 h-1; 3.1 +/- 0.9 ml/min per kg). Plasma caffeine concentration determined 12 h after administration of the test dosage discriminated best between patients with cirrhosis (5.4 +/- 1.6 mumol/l), patients with non-cirrhotic liver disease (2.0 +/- 1.4 mumol/l) and healthy volunteers (0.8 +/- 0.2 mumol/l). These results, the safety of the test compound and the simplicity of a single caffeine determination in plasma 12 h after a standardized dose of caffeine make this test attractive for evaluation of liver function.

Adult↗
PubMed1995

Effect of dietary caffeine and zinc on the activity of antioxidant enzymes, zinc, and copper concentration of the heart and liver in fast-growing rats.

The purpose of this study was to determine the relationship between concentrations of Zn and Cu and the activities of superoxide dismutase and glutathione peroxidase in the heart and liver of young rat pups whose dams were fed a diet supplemented with caffeine and/or Zn. Four groups of dams with their newborn pups were fed one of the following diets for 22 d: 20% protein basal diet; the basal diet supplemented with caffeine (2 mg/100 body wt); the basal diet supplemented with Zn (300 mg/kg diet); or the basal diet supplemented with caffeine plus Zn. The Cu levels in the livers of the pups were decreased by maternal intake of the caffeine and Zn diet. The maternal intake of the caffeine diet increased Mn-superoxide dismutase (MnSOD) activity and Cu, Zn-superoxide dismutase (Cu,ZnSOD) in the heart of the pups. On the other hand, the activity of Cu,ZnSOD was significantly reduced in the liver of pups whose dams consumed a caffeine, Zn, or caffeine plus Zn diet. Cu,ZnSOD activity in the liver of the pups seems to be correlated with Cu levels in the tissue. Selenium-dependent glutathione peroxidase (GSH-Px) activities in the heart and liver showed no difference among the groups. The effect of dietary caffeine and/or Zn on the activity of antioxidant enzymes in the heart and liver were different in young rats. The activities of these enzymes in the heart were lower than in the liver of 22-d-old rats. Our experiments indicate that the heart has limited defenses against the toxic effects of peroxides when compared to the liver.

Animals↗
PubMedDate not supplied

Determination of N-acetylation phenotyping in a Greek population using caffeine as a metabolic probe.

Studies of isoniazid, the well known antituberculosis drug, have revealed that N-acetylation polymorphism, is of great clinical importance. In humans, N-acetylation is one of the most important pathways in the inactivation of isoniazid. Caffeine, which is also biotransformed by N-acetylation, has been widely used as an in vivo probe for the assessment of N-acetyltransferase polymorphism. The activity of N-acetyltransferase can be estimated from the urinary metabolic ratio of two caffeine metabolites, namely, 5-acetylamino-6-formylamino-3-methyluracil (AFMU), and 1-methylxanthine (1X) after the ingestion of caffeine. In the present study caffeine was used as a metabolic probe to determine N-acetyltransferase polymorphism in 83 healthy Greek volunteers by means of the molar ratio of AFMU and IX determined in urine following ingestion of 200 mg caffeine. Frequency distribution analysis of the metabolic ratios AFMU/1X revealed two distinct groups with 66.3% (n = 55) slow acetylators and 33.7 % (n = 28) rapid acetylators. No statistically significant difference was detected between slow and fast acetylators in terms of gender, smoking habits and caffeine-intake habits. These results are in agreement with previous studies on N-acetyltransferase activity in Caucasians using caffeine as a metabolic probe. They also agree with reports on N-acetyltransferase activity in Greek tuberculosis patients using isoniazid as a metabolic probe. Thus, the use of caffeine as a metabolic probe is a reliable method for the assessment of N-acetyltransferase activity in the Greek population.

Acetylation↗
PubMed2003

Caffeine raises the serum melatonin level in healthy subjects: an indication of melatonin metabolism by cytochrome P450(CYP)1A2.

Caffeine is metabolized in the liver by cytochrome P450(CYP)1A2. Recent findings imply that this enzyme may also be of importance for the metabolism of human melatonin (MT). If caffeine and MT are metabolized by the same enzyme, one may expect to find different serum MT levels after ingestion of coffee compared with placebo. Although coffee is consumed by people all over the world, few studies have focused on whether caffeine actually affects serum MT levels in normal subjects. We decided to study that particular topic. For that purpose 12 healthy individuals were tested on two occasions, one week apart. On one of these occasions they were given a capsule containing 200 mg caffeine in the evening. On the other, they received placebo. The experimental order was randomized. Serum MT levels were determined every second hour between 22:00 h and 08:00 h, and the melatonin areas under the curve (MT-AUCs) were calculated. After caffeine the serum MT level rose from 0.09 +/- 0.03 nmol/l at 22:00 h to 0.48 +/- 0.07 nmol/l at 04:00 h. The corresponding rise after placebo was less prominent (from 0.06 +/- 0.01 to 0.35 +/- 0.06 nmol/l). This was reflected by the MT-AUC which was 32% larger after ingestion of caffeine compared with placebo (MT-AUC(caffeine) 3.16 +/- 0.44 nmol/l x h vs MT-AUC(placebo) 2.39 +/- 0.40 nmol/l x h; p < 0.02). These findings imply that caffeine, ingested in the evening at a dose corresponding to two ordinary cups of coffee, augments the nocturnal serum MT level, which in turn supports the notion that cytochrome P450(CYP)1A2 is involved in the hepatic metabolism of human MT.

Caffeine↗
PubMed2002

Tetrandrine potentiates caffeine-induced contraction but inhibits phenylephrine-induced contraction in perfused rat mesenteric artery.

Effects of tetrandrine (TET), a bisbenzylisoquinoline alkaloid, on the contractile responses of perfused rat mesenteric arteries to phenylephrine (PE) and caffeine were investigated. TET concentration-dependently (1-30 micro M) attenuated phenylephrine-induced responses but potentiated the contractile responses to caffeine (5-40 mM) in the presence and absence of Ca(2+). Berbamine (BER), a structural analogue of TET, elicited a relatively smaller inhibitory effect on the responses to PE due to Ca(2+) release or Ca(2+) influx. However, both TET and BER elicited a comparable potentiating effect on caffeine-induced contraction. Cyclopiazonic acid (CPA; 10 micro M), a selective sarcoplasmic reticulum Ca(2+)-ATPase pump inhibitor, mimicked the potentiating effect of TET when added 5 min prior to caffeine in Ca(2+)-free medium. However, CPA did not augment and might even inhibit the caffeine-induced response when it was preincubated with the tissue for 25 min prior to the addition of caffeine. We propose that TET elicits differential effects on PE- and caffeine-induced responses in perfused rat mesenteric arterial bed. The inhibitory effect of TET on PE-induced responses is probably due to its direct interactions with alpha-adrenoceptors and PE-sensitive Ca(2+)-channels. The augmentation of caffeine-induced responses by TET, particularly in Ca(2+)-free medium, is likely to be due to its partial inhibition of the sarcoplasmic reticulum Ca(2+)-ATPase pump.

Alkaloids↗
PubMed2002

The moderating effect of anxiety sensitivity on caffeine-induced hypoalgesia in healthy women.

RATIONALE: Caffeine is an analgesic adjuvant, but also has panicogenic properties. Anxiety sensitivity is a trait vulnerability factor related to negative responses to pain, and is known to moderate negative psychological responses to caffeine. OBJECTIVES: The current study sought to investigate whether anxiety sensitivity moderates the effect caffeine has on the pain responses of healthy women. METHODS: Caffeine (250 mg) was administered to women pre-selected as high, medium or low in anxiety sensitivity. Measures of arousal and mood were taken before and after drug administration. The cold pressor pain task was used to induce pain. Pain threshold, tolerance, sensory and affective pain responses were also recorded. RESULTS: Caffeine increased systolic blood pressure and mood. Additionally, those low in anxiety sensitivity exhibited caffeine-induced improvement in negative mood (less depressed) and caffeine-related hypoalgesia. CONCLUSIONS: These results suggest that the analgesic effects of caffeine may depend on anxiety sensitivity status, and that the fear of bodily sensations should be considered in pain management programmes.

Adolescent↗
PubMed2005

Nicotine antagonizes caffeine- but not pentylenetetrazole-induced anxiogenic effect in mice.

RATIONALE: Nicotine and caffeine are widely consumed licit psychoactive drugs worldwide. Epidemiological studies showed that they were generally used concurrently. Although some studies in experimental animals indicate clear pharmacological interactions between them, no studies have shown a specific interaction on anxiety responses. OBJECTIVES: The present study investigates the effects of nicotine on anxiety induced by caffeine and another anxiogenic drug, pentylenetetrazole, in mice. The elevated plus-maze (EPM) test was used to evaluate the effects of drugs on anxiety. METHODS: Adult male Swiss Webster mice (25-32 g) were given nicotine (0.05-0.25 mg/kg s.c.) or saline 10 min before caffeine (70 mg/kg i.p.) or pentylenetetrazole (15 and 30 mg/kg i.p.) injections. After 15 min, mice were evaluated for their open- and closed-arm time and entries on the EPM for a 10-min session. Locomotor activity was recorded for individual groups by using the same treatment protocol with the EPM test. RESULTS: Nicotine (0.05-0.25 mg/kg) itself did not produce any significant effect in the EPM test, whereas caffeine (70 mg/kg) and pentylenetetrazole (30 mg/kg) produced an anxiogenic effect, apparent with decreases in open-arm time and entry. Nicotine (0.25 mg/kg) pretreatment blocked the caffeine- but not pentylenetetrazole-induced anxiety. Administration of each drug and their combinations did not produce any effect on locomotor activity. CONCLUSIONS: Our results suggest that the antagonistic effect of nicotine on caffeine-induced anxiety is specific to caffeine, instead of a non-specific anxiolytic effect. Thus, it may extend the current findings on the interaction between nicotine and caffeine.

Animals↗
PubMed2005

Effects of caffeine on performance and mood: withdrawal reversal is the most plausible explanation.

RATIONALE: Although it is widely believed that caffeine can enhance human performance and mood, the validity of this belief has been questioned, giving rise to debate. The central question is whether superior performance and mood after caffeine represent net benefits, or whether differences between caffeine and control conditions are due to reversal of adverse withdrawal effects. OBJECTIVES: To provide a focussed review of relevant experimental studies with the aim of clarifying current understanding regarding the effects of caffeine on human performance and mood. METHODS: To avoid the shortcomings of standard placebo-controlled studies, which are ambiguous due to failure to control for the confounding influence of withdrawal reversal, three main experimental approaches have been employed: studies that compare consumers and low/non-consumers, pre-treatment and ad lib consumption studies, and long-term withdrawal studies. RESULTS: Of the three approaches, only long-term withdrawal studies are capable of unambiguously revealing the net effects of caffeine. Overall, there is little evidence of caffeine having beneficial effects on performance or mood under conditions of long-term caffeine use vs abstinence. Although modest acute effects may occur following initial use, tolerance to these effects appears to develop in the context of habitual use of the drug. CONCLUSIONS: Appropriately controlled studies show that the effects of caffeine on performance and mood, widely perceived to be net beneficial psychostimulant effects, are almost wholly attributable to reversal of adverse withdrawal effects associated with short periods of abstinence from the drug.

Affect↗
PubMed2005

The effect of caffeine on cognitive task performance and motor fatigue.

RATIONALE: In everyday life, people are usually capable of performing two tasks simultaneously. However, in a previous study we showed that during a fatiguing motor task, cognitive performance declined progressively. There is extensive literature on the (positive) effects of caffeine on cognitive and motor performance. These effects are most pronounced under suboptimal conditions, for example during fatigue. However, little is known about the effects of caffeine on cognitive performance during a fatiguing motor task. OBJECTIVE: This study was aimed to investigate whether a moderate dose of caffeine could attenuate the decline in cognitive performance during a fatiguing motor task. METHODS: The study consisted of a placebo and a caffeine (3 mg/kg) session. A total of 23 subjects completed these sessions in a semi-randomized and double-blind order. In each session, subjects performed maximal voluntary contractions of the index finger, a choice reaction time (CRT) task and a dual task consisting of a fatiguing motor task concomitantly with the same CRT task. After the fatiguing dual task, the CRT task was repeated. RESULTS: Caffeine improved cognitive task performance, in both the single and dual task, as shown by decreased reaction times together with unchanged accuracy. Cognitive performance in the dual task deteriorated with increasing fatigue. However, the decrease in cognitive performance in the beginning of the dual task, as observed in the placebo condition, was partly prevented by caffeine administration (i.e., no increase in reaction times). We found no effects of caffeine on motor parameters (absolute force, endurance time or electromyographic amplitude). CONCLUSIONS: Caffeine improved cognitive performance. This effect also extends under demanding situations, as was shown by the performance during the dual task, even during progressive motor fatigue.

Adolescent↗
PubMed2000

The anxiogenic-like effect of caffeine in two experimental procedures measuring anxiety in the mouse is not shared by selective A(2A) adenosine receptor antagonists.

RATIONALE: The elevated plus-maze and the light/dark box are two established anxiety tests in rodents, which are useful to screen putative anxiogenic effects of drugs. OBJECTIVE: Caffeine is well known to promote anxious behaviour in humans and animal models, but the precise site of action of the drug is still a matter of debate. The present study investigated whether the anxiogenic effects of caffeine observed in mice depend on the blockade of A(2A) receptor. First, the effects induced by the non-selective drug caffeine were compared with those elicited by two selective A(2A) receptor antagonists over a wide range of doses in the same experimental conditions. The effects of A(2A) or A(1 )adenosine receptor agonists and of a selective A(1) adenosine receptor antagonist were also investigated. Second, wild-type and A(2A) receptor knockout mice offered another approach to delineate the role played by A(2A) receptor in caffeine's anxiogenic effects. METHODS: Mice were exposed to the elevated plus-maze or to the light/dark box for 5 min after acute or chronic administration of tested drugs. RESULTS: Caffeine acutely administered (50 or 100 mg/kg IP) induced anxiety-like effects in both procedures. Its chronic administration (50 mg/kg IP twice daily) for 1 week or consumption in the drinking water (0.3 g/l) for 8 days or 2 months were also anxiogenic in the plus-maze test. The A(2A) receptor antagonists ZM241385 (up to 60 mg/kg IP) and SCH58261 (up to 10 mg/kg IP) were devoid of acute effects in both tests. One week administration of ZM241385 (30 mg/kg IP) or SCH58261 (3 mg/kg IP) had no effects in the plus-maze test. An antagonist (DPCPX) and an agonist (CPA) at A(1) receptors had no acute effects on anxiety-related indices, whereas an A(2A) receptor agonist (CGS 21680) displayed non-specific motor effects in the plus-maze test. Acute administration of caffeine (50 mg/kg IP) induced no clear-cut anxiety-like effects in the plus-maze test in A(2A) receptor knockout mice that exhibited higher basal anxiety levels than wild-type mice. Chronic administration (50 mg/kg IP twice daily) for 1 week elicited less anxiety-like behaviour in A(2A) receptor knockout than in wild-type mice. CONCLUSIONS: Adaptative mechanisms following mutation in A(2A) receptors or their long-term blockade after chronic ingestion of caffeine may be responsible for increase proneness to anxiety. However, the short-term anxiety-like effect of caffeine in mice might not be related solely to the blockade of adenosine A(2A) receptors, since it is not shared by A(2A) selective antagonists.

Adenosine↗
PubMed1998

Physical dependence increases the relative reinforcing effects of caffeine versus placebo.

Using a within-subject cross-over design, this study examined the role of physical dependence in caffeine reinforcement by experimentally manipulating physical dependence. Each subject was exposed to two chronic drug phases (300 mg/70 kg/day caffeine and placebo) for 9-12 days, with order of phases counterbalanced across subjects. On 2 separate days immediately following each of the chronic drug exposures, subjects received acute doses of either caffeine (300 mg/70 kg) or placebo in counterbalanced order. The reinforcing effects of these drugs were then determined by using a multiple-choice procedure in which subjects made a series of discrete choices between receiving varying amounts of money or receiving the drug again, and a choice between the two drugs. To ensure that subjects completed the form carefully, following exposure to both of the acute drug administrations, one of the subject's previous choices from the multiple-choice form was randomly selected and the consequence of that choice was implemented. When subjects were maintained on chronic caffeine, they were willing to forfeit significantly more money and showed significant increases in typical withdrawal symptoms (e.g. fatigue, mood disturbance) after receiving placebo as compared to the other three conditions. When subjects were maintained on chronic caffeine, they also chose to receive caffeine over placebo twice as often than when they were maintained on chronic placebo. These findings provide the strongest evidence to date indicating that caffeine physical dependence increases the relative reinforcing effects of caffeine versus placebo.

Adult↗
PubMed2001

Caffeine, nicotine and mecamylamine share stimulus properties in the preexposure conditioned taste aversion procedure.

RATIONALE: The present study examined whether nicotine and caffeine, two of the most widely used psychoactive drugs, share stimulus properties in the preexposure conditioned taste aversion (CTA) procedure. OBJECTIVES: To determine whether nicotine would attenuate the formation of a caffeine-induced CTA and further assess whether pretreatment with mecamylamine, a nicotinic receptor antagonist, would reverse nicotine's attenuating effect of a caffeine-induced CTA. METHODS: Male Wistar rats were preexposed with one of three doses of nicotine (0.6, 1.2 and 2.0 mg/kg, s.c.) for three consecutive days, then 24 h following the final preexposure injection were conditioned with caffeine (20 mg/kg and 30 mg/kg, i.p.) in a standard two-bottle test. There were four conditioning trials and four drug-free test days. In a follow-up study, rats were pretreated with mecamylamine (2 mg/kg, i.p.) prior to preexposure injections with nicotine (0.6 mg/kg, i.p.), then subsequently conditioned with caffeine (20 mg/kg, i.p.) as described above. RESULTS: The lowest nicotine dose (0.6 mg/kg) attenuated the caffeine induced CTAs (20 mg/kg and 30 mg/kg) but the higher nicotine doses showed no such attenuating effect. In addition, mecamylamine reversed the nicotine-induced attenuation of the caffeine-induced CTA and also directly attenuated it. CONCLUSIONS: These results suggested that caffeine, nicotine and mecamylamine share overlapping stimulus properties and that the nature of this relationship may involve action at the nicotinic-cholinergic receptor.

Animals↗
PubMed2003

Effects of caffeine on potassium currents in isolated rat ventricular myocytes.

Rapid exposure of cardiac muscle to high concentrations of caffeine releases Ca(2+) from the sarcoplasmic reticulum (SR). This Ca(2+) is then extruded from the cell by the Na(+)/Ca(2+) exchanger. Measurement of the current carried by the exchanger (I(Na/Ca)) can therefore be used to estimate of the Ca(2+) content of the SR. Previous studies have shown that caffeine, however, can also inhibit K(+) currents. We therefore investigated whether the inhibitory effects of caffeine on these currents could contaminate measurements of I(Na/Ca). Caffeine caused partial inhibition of the inward rectifier K(+) current (I(K1)): the outward current at -40 mV was 1.15+/-0.24 pA/pF in control and decreased to 0.34+/-0.15 pA/pF in the presence of 10 mmol/l caffeine (P<0.05, n=15). This was similar to the effect of caffeine on the holding current observed at -40 mV in the absence of K(+) channel block and could therefore account for the contaminating effects of caffeine observed during measurements of I(Na/Ca). Moreover, caffeine also partially inhibited the transient outward ( I(to)) and the delayed rectifier (I(K)) K(+) currents.

Animals↗
PubMed1998

Comparison of the effects of theophylline and caffeine on serum erythropoietin concentration in premature infants.

UNLABELLED: Theophylline administration has been shown to attenuate erythropoietin (EP) production in adults; the effect of caffeine is not known. Our aim was to determine whether caffeine and theophylline had similar effects on EP production in the premature newborn. If caffeine was found to have a greater effect, this would influence prescribing habits. Fifty preterm infants (mean gestational age 28 weeks) who had clinically significant apnoea were randomized to receive theophylline (4 mg/kg then 2 mg/kg twice daily) or caffeine (10 mg/kg then 2.5 mg/kg once daily). The methylxanthines were continued at least until discharge from the NICU and the dosage altered to keep the levels within the therapeutic range. As an assessment of EP production, serum EP concentrations were measured. Blood for EP, haemoglobin, reticulocyte count, theophylline and caffeine levels was obtained prior to treatment and at least during weeks 3 and 7. There was no significant difference in the mean EP level in the two groups taken prior to treatment at a median age of 2 days of life. There were similar falls in haematocrit and haemoglobin in the two groups during the study period compared to pre-treatment values. At that time, however, the median reticulocyte count was higher in the caffeine compared to the theophylline treated infants (P < 0.05). This was associated with a rise compared to baseline (median 10.0-0.2 mU/ml) in the mean EP levels in the caffeine group and a decrease from a median of 10.1 to 8.3 mU/ml in the theophylline group, but the EP levels in the two groups at week 7 did not differ significantly. CONCLUSION: These results suggest that caffeine does not have a greater impact than theophylline on EP production.

Anemia↗
PubMed2006

Simultaneous determination of acetylsalicylic acid and caffeine in pharmaceutical formulation by first derivative synchronous fluorimetric method.

A sensitive, rapid, and specific assay has been developed for the simultaneous determination of acetylsalicylic acid and caffeine in commercial tablets based on their natural fluorescence. The mixture of these drugs was resolved by first derivative synchronous fluorimetric technique using two scans. At Deltalambda=106 nm, using first derivative synchronous scanning, only acetylsalicylic acid yields a detectable signal at 316 nm (peak to zero method) which is unaffected by caffeine. At Deltalambda=30 nm, the signal of caffeine at 288 nm (peak to zero method) is not affected by acetylsalicylic acid. The range of application is between 0.021 and 41.62 microg ml(-1) (correlation coefficient, R=0.9995) for acetylsalicylic acid and between 0.4486 and 44.86 microg ml(-1) (correlation coefficient, R=0.99786) for caffeine. The recovery range of 98.40-102% for acetylsalicylic acid and 90-100.5% for caffeine from their synthetic mixture was reported. Overall recovery of both compounds about 97-99% for acetylsalicylic acid and 97-98% for caffeine was obtained from real sample analysis. The detection limits are 0.0013 microg ml(-1) and 0.0306 microg ml(-1) for acetylsalicylic acid and caffeine, respectively. The relative standard deviation (n=10) for 20 microg ml(-1) of acetylsalicylic acid is 2.75% and for 2.2 microg ml(-1)of caffeine is 1.7%.

Aspirin↗