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PubMed2002

Evidence for a relationship between daily caffeine consumption and accuracy of time estimation.

The present study examined the relationship between regular caffeine consumption and time estimation. Sixty participants (aged 18-57 years, mean 24 years) completed a 47 s time estimation exercise and questionnaires related to daily caffeine consumption and perceptions of time. We hypothesized that the effects of caffeine on time estimation would follow a U-shaped pattern such that individuals who reported moderate amounts of daily caffeine would be more accurate in their perceptions of time than would those who reported high amounts of caffeine intake or no daily caffeine consumption. Timing accuracy was computed by dividing participant-reported time by actual time (47 s). Timing accuracy followed a U-shaped curve such that those respondents who reported 'low' daily caffeine consumption (< or = 135 mg/day, n = 24) were the most accurate in their time estimates (mean= 44.2 s). Individuals who reported no caffeine (mean= 69.3 s; n= 7) or 'high' daily caffeine consumption (mean=56.2 s; >135 mg/day, n = 28) were less accurate in their time estimates [F(2, 56)= 3.34, p< 0.05]. Findings suggest that 'low' daily caffeine consumption may enhance time estimation accuracy above that of 'high' or no daily caffeine consumption.

Adolescent↗
PubMed1991

Validity of self-reports of caffeine use.

The relationship between self-reports of caffeine ingestion on two occasions and measured plasma concentrations of caffeine and its major metabolites was examined. A subject population [25 men and 25 women, age 20-45 years (mean: 28.7 yr)] that was enrolled in a benzodiazepine pharmacokinetic study underwent general medical screening on two occasions, each including detailed caffeine histories. Before beginning their scheduled study, plasma samples were obtained and evaluated by HPLC for caffeine, paraxanthine, theophylline, and theobromine. These values were compared with estimates of caffeine consumption in mg/day generated from both histories. There was no significant difference between plasma levels of caffeine, metabolites, or caffeine plus metabolites for categories corresponding to reports of low, intermediate or high caffeine use. A self-reported caffeine consumption of greater than 300 mg/day (high) did correlate, however, with a significant smoking history. The authors conclude that self-reports of caffeine ingestion do not accurately reflect acute exposure, and that if caffeine use is of importance in a given setting, reports should be confirmed by biochemical means.

Adult↗
PubMed1998

Response to nimodipine in caffeine-induced neurotoxicity in cerebellar granular cell culture of rat pups.

Methylxanthines (theophylline, theobromine and caffeine) are widely used as central nervous system stimulants and caffeine is used in the treatment of apnea in newborns. Plasma therapeutic concentration of caffeine is around 110 microM. Caffeine diffuses the blood brain barrier easily, increasing oxygen consumption in neurones and leading to cell death. In the present study, 4-7-day-old rats were used to obtain cerebellar granular cell cultures. Caffeine was used 50, 150, 250 and 350 microM concentrations and the most toxic dose for it was found to be 350 microM. Death cell scores were 0.9+/-0.63 for control, 1.1+/-0.63 for 50 microM, 0.89+/-0.47 for 150 microM (P>0.05 for both), 3.84+/-0.8 for 250 microM (P=0.024) and 6.2+/-0. 86 for 350 microM (P=0.001) caffeine concentrations. The role of voltage-dependent calcium channels in caffeine-induced neurotoxicity was tested with the doses of 100 and 200 microM nimodipine 45 min before or after the 350 microM caffeine. Both doses of nimodipine after caffeine administration were found to be ineffective in blocking neurotoxicity. Doses administered 45 min prior to caffeine, reduced death cell score to 0.89+/-0.23 (P=0.000) for 100 microM nimodipine and 2.35+/-0.96 (P=0.000) for 200 microM nimodipine administration into the cultures. A dose-dependent manner of nimodipine in ischemic states is well-known. In the light of these results, nimodipine may be used in the treatment of newborn apneas together with caffeine to prevent neurotoxic side effects of high or repeated doses of it.

Animals↗
PubMed2000

Is caffeine associated with bone mineral density in young adult women?

BACKGROUND: By increasing the urinary excretion of calcium, caffeine consumption may reduce bone mineral density (BMD) and subsequently increase the risk for osteoporotic fracture. Although negative associations between caffeine consumption and BMD have been reported for postmenopausal women, in particular for those who consume low amounts of dietary calcium, the relation between caffeine and BMD in younger women is unclear. Therefore, we evaluated the association between caffeine consumption and BMD in a cross-sectional study of 177 healthy white women, age 19-26 years, who attended a Midwestern university. METHODS: Average caffeine intake (milligrams per day) was calculated from self-reports of the consumption of coffee, decaffeinated coffee, tea, colas, chocolate products, and select medications during the previous 12 months (mean caffeine intake = 99. 9 mg/day). BMD (grams per square centimeter) at the femoral neck and the lumbar spine was measured by dual-energy X-ray absorptiometry. RESULTS: After adjusting in linear regression models for potential confounders, including height, body mass index, age at menarche, calcium intake, protein consumption, alcohol consumption, and tobacco use, caffeine consumption was not a significant predictor of BMD. For every 100 mg of caffeine consumed, femoral neck BMD decreased 0.0069 g/cm(2) (95% confidence in terval [CI] = -0.0215, 0. 0076) and lumbar spine BMD decreased 0.0119 g/cm(2) (95% CI = -0. 0271, 0.0033). No single source of caffeine was significantly associated with a decrease in BMD. Furthermore, the association between caffeine consumption and BMD at either site did not differ significantly between those who consumed low levels of calcium (< or =836 mg/day) and those who consumed high levels of calcium (>836 mg/day). CONCLUSIONS: Caffeine intake in the range consumed by young adult women is not an important risk factor for low BMD.

Absorptiometry, Photon↗
PubMed1987

Pharmacologic specificity of tolerance to caffeine-induced stimulation of locomotor activity.

The pharmacologic specificity of tolerance to caffeine-induced stimulation of locomotor activity was studied in adult male rats that were given access to either caffeine solution (0.5 or 1.0 mg/ml) or plain water for 10 min every 6 h on a chronic daily basis; daily caffeine intake averaged 41 and 62 mg/kg, respectively. Dose-effect curves were determined for behavioral stimulant and depressant drugs in control and caffeine-treated groups. Drugs were injected IP and locomotor activity was measured for 30 min beginning 35 min later. Rats tolerant to stimulation of locomotor activity by caffeine were also tolerant to theophylline and 7-(2-chloroethyl)theophylline, but not to any of six nonxanthine stimulants, including cocaine, methylphenidate, and d-amphetamine. The adenosine analogs, R(-)-N6-2-(phenylisopropyl)adenosine(R(-)-PIA) and 5'-(N-ethyl)carboxamidoadenosine (NECA), decreased locomotor activity of control and caffeine-treated (0.5 mg/ml) rats; dose-effect curves in rats consuming caffeine chronically were displaced to the right of the control curves by 10-fold for R(-)-PIA and 100-fold for NECA. Dose-effect curves for the nonadenosine behavioral depressants chlorpromazine and diazepam were unchanged by chronic treatment with caffeine, but the curve for pentobarbital, which is thought to inhibit adenosine receptor binding, was shifted to the right by a factor of 3. Rats withdrawn from chronic caffeine for 24 h were still completely tolerant to caffeine-induced stimulation of locomotor activity. Dose-effect curves for R(-)-PIA and d-amphetamine in rats withdrawn from chronic caffeine for 24 h were not different from curves in control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Caffeine- and histamine-induced oscillations of K(Ca) current in single smooth muscle cells of rabbit cerebral artery.

In the present experiment, we characterized the intracellular Ca2+ oscillations induced by caffeine (1mM) or histamine (1-3microM) in voltage-clamped single smooth muscle cells of rabbit cerebral (basilar) artery. Superfusion of caffeine or histamine induced periodic oscillations of large whole-cell K+ current with fairly uniform amplitudes and intervals. The oscillatory K+ current was abolished by inclusion of ethylenebis(oxonitrilo)tetraacetate (EGTA, 5mM) in the pipette solution. Caffeine- and histamine-induced periodic activation of the large-conductance Ca2+-activated K+ [K(Ca)] channel was recorded in the cell-attached patch mode. These results suggest that the oscillations of K+ current are carried by the K(Ca) channel and reflect the oscillations of intracellular Ca2+ concentration ([Ca2+]i). Ryanodine (1-10microM) abolished both caffeine- and histamine-induced oscillations. Caffeine-induced oscillations were abolished by the sarcoplasmic reticulum Ca2+-adenosine 5'-triphosphatase (Ca2+-ATPase) inhibitor, cyclopiazonic acid (10microM), and a high concentration of caffeine (10mM). Inclusion of heparin (3mg/ml) in the pipette solution blocked histamine-induced oscillations, but did not block caffeine-induced oscillations. By the removal of extracellular Ca2+, but not by the addition of verapamil and Cd2+, the caffeine-induced oscillations were abolished. Increasing Ca2+ influx rate increased the frequencies of caffeine-induced oscillations. Spontaneous oscillations were also observed in cells that were not superfused with agonists, and had similar characteristics to the caffeine-induced oscillations. From the above results, it is concluded, that in smooth muscle cells of the rabbit cerebral (basilar) artery, ryanodine-sensitive Ca2+-induced Ca2+ release pools play key roles in the generation of caffeine- and histamine-induced intracellular Ca2+ oscillations.

Animals↗
PubMed1985

Behavioral effects of caffeine, (-)N-((R)-1-methyl-2-phenylethyl)-adenosine (PIA), and their combination in the mouse.

The effects of caffeine (1-100 mg/kg, IP), (-)N-((R)-1-methyl-2-phenylethyl)-adenosine (PIA) (0.01-1 mg/kg, IP), and of the two drugs in combination were studied in mice responding under a mult FR30 FI600 s schedule of food presentation. The lowest dose of caffeine, 1 mg/kg, had no effect on responding under either component of the mult schedule. Intermediate doses of caffeine (3 and 10 mg/kg) slightly increased responding under the FI component, while higher doses decreased responding. Caffeine only decreased responding, at doses above 30 mg/kg, under the FR component. PIA decreased responding under both components of the mult schedule in a dose-dependent, and similar, manner. In most cases, the rate-increasing effect of caffeine on FI responding was diminished when combined with a rate-decreasing dose of PIA. However, when 0.01 mg/kg PIA, a dose that had no effect alone, was combined with 3 mg/kg caffeine, the increase in rate exceeded that of caffeine alone. Rate-decreasing effects of PIA were antagonized by caffeine; with larger doses of PIA, larger doses of caffeine were required for antagonism. Thus, while the rate-increasing effects of caffeine can be either enhanced or diminished, when combined with different doses of PIA, the rate-decreasing effects of PIA are clearly antagonized by caffeine in a dose-dependent manner.

Adenosine↗
PubMed1989

Reinforcing and subjective effects of caffeine in normal human volunteers.

The reinforcing and subjective effects of caffeine (100 and 300 mg, PO) were determined in a group of 18 normal, healthy adults. Subjects (eight females, ten males) were light to moderate users of caffeine, and had no history of drug abuse. A discrete-trial choice procedure was used in which subjects were allowed to choose between the self-administration of color-coded capsules containing either placebo or caffeine. The number of times caffeine was chosen over placebo was used as the primary index of reinforcing efficacy. Subjective effects were measured before and several times after capsule ingestion. The low dose of caffeine was chosen on 42.6% of occasions, not significantly different from chance (50%). The high dose of caffeine was chosen on 38.9% of occasions, significantly less than expected by chance, indicating that this dose served as a punisher. Both doses of caffeine produced stimulant-like subjective effects, with aversive effects such as increased anxiety predominating after the high dose. When subjects were divided into groups of caffeine-sensitive choosers and nonchoosers, a consistent relationship emerged between caffeine choice and subjective effects; nonchoosers reported primarily aversive effects after caffeine (increased anxiety and dysphoria), whereas choosers reported stimulant and "positive" mood effects. When compared with previous findings, these results demonstrate that caffeine is less reinforcing than amphetamine and related psychomotor stimulants.

Adult↗
PubMed1984

Caffeine contractures in denervated frog muscle.

Caffeine contracture tension, effect of caffeine on the resting membrane potential, and caffeine influx in normal and denervated frog sartorius muscle have been investigated. Peak caffeine contracture tension is increased after denervation at all caffeine concentrations. The percentage increases in tension are highest for lower caffeine concentrations. The caffeine concentration required for half maximum tension is decreased from about 3.6 mM in control muscles to 2.6 mM in denervated muscles. Caffeine at 3.5 mM produces a depolarization of about 6 mV in control muscles and 16mV in denervated muscles. The large contracture tensions observed in denervated muscles are not due to the greater depolarization produced by the drug in denervated muscles since innervated muscles depolarized to the same level by external K+ do not enhance caffeine contracture tension. Both control and denervated muscles are highly permeable to caffeine. The increases in sarcoplasmic reticulum development ( Moscatello et al. 1965) and calcium content ( Picken and Kirby 1976) promoted by denervation may explain the larger tension elicited by caffeine in denervated muscles.

Animals↗
PubMed1989

The effects of maternal caffeine intake during pregnancy on mineral contents of fetal rat bone.

Various levels of maternal caffeine ingestion during pregnancy were investigated to determine whether caffeine will affect the mineral contents of the growing bones of fetal rats. On day 8 of gestation, rat dams were fed with a 20% protein diet supplemented with 0.5 mg, 1 mg, or 2 mg caffeine/100 g of dams body weight as an experimental group and the same without caffeine as a control until day 22 of gestation. Fetuses were removed by cesarean section on day 22 and mandibular bones were removed to study the mineral contents of calcium, phosphorus, magnesium, and zinc. Although the mandible weighed more in the 0.5-mg caffeine group as compared to the controls, an additional increase of caffeine resulted in a decrease in weight. All calcium, magnesium, and zinc contents per bone decreased in the 1- and 2-mg caffeine groups as compared to either controls or 0.5-mg caffeine group, whereas phosphorus stayed relatively constant regardless of the different levels of caffeine intake. When data are expressed as per gram of bone tissue, most of the mineral contents among the groups disappeared suggesting that normal growth and development of the fetal bone are impaired as a results of maternal caffeine intake. Caffeine intake during gestation in the present study indicates that different levels of caffeine intake may exert not only different effects on mineral contents in bone development, but also affect the growth of the fetal bone.

Animals↗
PubMed1980

[Pharmacokinetics of caffeine in mice and its modification by ethanol].

In experiments on mice the pharmacokinetics (absorption, distribution, metabolism) of orally administered caffeine (18 mg/kg) using 14C caffeine as marker and the influence of simultaneously applied ethanol (1,8 g/kg) was tested. The following results were obtained: 1. Caffeine was very quickly absorbed from the gastro-intestinal tract of mice. Addition of ethanol had no noticeable influence on the absorption of caffeine. 2. The elimination of caffeine from the serum and tissues examined (liver, kidney, brain, muscle) showed an exponential course with a half life of 40-60 minutes and was completed after 4 to 5 hours. 3. By giving ethanol the elimination of caffeine was significantly decreased and its half life increased to 160-240 minutes. 4. The caffeine metabolites reached their maximal concentration in serum and tissues examined within two hours. In the liver and kidney the concentration of caffeine metabolites was greater than in the serum, whereas they were lower in the brain and muscle. At the end of the experimental the concentration of caffeine metabolites reached only very low values. 5. After administration of ethanol the caffeine metabolites were significantly decreased from the 30th to 180th minute in the liver and kidney; they were only slightly lowered in the serum and almost unchanged in the muscle and brain. The results of these experiments suggest that ethanol inhibits the metabolism of caffeine in the liver, especially by influencing its demethylation to other dimethyl- and monomethylxanthines and probably also its oxidation ot methyluric acids.

Absorption↗
PubMed1984

[Effect of caffeine on various metabolic parameters in vivo].

The metabolic actions of caffeine were investigated in the rat (90 mg/kg bw caffeine intravenously during 3 hours) and in human volunteers (35 mg/kg bw caffeine orally) in the fasting state. Additionally, the effects of caffeine were measured during simultaneous intravenous glucose infusion (0.25 mg/kg bw/h during 6 hours in humans and 1.8 mg/kg bw/h during 3 hours in the rat). In the fasting rat, intravenous caffeine caused an increase in the serum concentrations of glucose, urea, insulin, and free fatty acids, whereas a decrease in glucoplastic amino acids was found. As the liver glycogen concentration was not altered, the increase in blood glucose should be due to an increase in glyconeogenesis. During simultaneous application of carbohydrates and caffeine, the increases in the concentration of blood glucose and serum insulin were intensified, whereas the serum concentrations of lactate and urea as well as hepatic glycogen were not altered. In fasting male volunteers caffeine caused an increase in the concentrations of blood glucose, cortisol, insulin, free fatty acids, free glycerol and ketone bodies. During intravenous glucose infusion, caffeine intensified the decrease in serum phosphate induced by carbohydrates. Neither in volunteers nor in the experimental animal, an alteration in the concentrations of cholesterol or serum triglycerides or serum uric acid was effected by caffeine. It is concluded that high dosed caffeine causes peripheral insulin resistance in the human being as well as in the experimental animal. This peripheral insulin resistance is shown by the simultaneous large increases in concentrations of serum insulin, blood glucose and concentration of free fatty acids. In this situation insulin obviously is not able to inhibit lipolysis or gluconeogenesis nor to increase peripheral glucose utilisation. These metabolic effects of caffeine show some similarities to the metabolic situation in diabetes mellitus type 2 (Non Insulin Dependent Diabetes mellitus).

3-Hydroxybutyric Acid↗
PubMed1994

Influence of caffeine on information processing stages in well rested and fatigued subjects.

The effects of caffeine on different information processing stages were examined by using choice reaction time tasks. Independent variables were stimulus degradation, stimulus-response compatibility, time-uncertainty, state of the subject, and caffeine treatment. The task variables were assumed to affect the following processing stages; encoding, response selection and motor preparation, respectively. A 200 mg dose at the beginning of the experiment and a maintenance dose of 50 mg caffeine or lactose half-way through the session were administered to well rested and fatigued subjects, double-blind and deceptively. Behavioural measurements, event-related potentials (ERPs) and mood questionnaires were used to assess caffeine effects. The data showed that caffeine shortened reaction time. This effect showed an interaction with stimulus degradation and time uncertainty. In addition, ERP results supported the view that caffeine increases cortical arousal and perceptual sensitivity. Stimulating effects of caffeine were mainly located at input and output stages of the information processing system. Central processes were unaffected by caffeine. Fatigued subjects showed larger improvements in performance after caffeine than well-rested subjects. The results also indicated that caffeine effects were not stimulating in all subjects: 6 out of 30 subjects did not show arousing effects of caffeine.

Adolescent↗
PubMed1992

Drug discrimination studies in rats with caffeine and phenylpropanolamine administered separately and as mixtures.

The discriminative stimulus effects of mixtures of caffeine and phenylpropanolamine (PPA) have been investigated because these drugs have been abused together. Rats were trained to discriminate caffeine (20 mg/kg), PPA (20 mg/kg), or a mixture of both drugs, from saline in a two-bar operant conditioning procedure with food reinforcers presented on a tandem VI-FR schedule. Discriminations of mixture, caffeine alone and PPA alone were 90% accurate after 40 sessions. Generalisation to both PPA and caffeine was weak (25-47%) at the doses used in the training mixture, although there was almost complete generalisation to larger doses of PPA. Under these conditions, there was a possible synergistic interaction between caffeine and PPA because the discriminative effect of the mixture could not be fully explained by the combined effects of its component drugs. However, in rats trained on caffeine, PPA had no effect on the dose-response relationship for caffeine; similarly, in rats trained on PPA, caffeine had no effect on the dose-response relationship for PPA (no synergism or antagonism). Generalisation to (+)-amphetamine and cocaine was weakest in rats trained on caffeine, was partial in rats trained on the mixture, and was complete in rats trained on PPA; thus, the mixture of caffeine and PPA was not more like cocaine or amphetamine than PPA alone. The results are in agreement with reports that caffeine and PPA may interact in a complex manner, but do not support the view that the interaction enhances their resemblance to highly abused stimulants such as amphetamine and cocaine.

Animals↗
PubMed2002

Caffeine potentiates the discriminative-stimulus effects of nicotine in rats.

RATIONALE: Caffeine and nicotine are the main psychoactive ingredients of coffee and tobacco, respectively, with a high frequency of concurrent use in humans. OBJECTIVES: The aim of the present study was to examine the interaction of caffeine and nicotine in rats trained to discriminate nicotine from saline. METHODS: Two groups of male Sprague-Dawley rats ( n=8 per group) were trained to discriminate 0.4 mg/kg nicotine, SC, from saline under a fixed ratio schedule of food presentation. One group of rats was chronically exposed to caffeine (1.0 mg/ml) dissolved in their drinking water whereas the other group was exposed to tap water. Effects of IP injections of caffeine on nicotine-lever selection were subsequently examined. In separate groups of rats exposed to the same caffeine-drinking or water-drinking regimen, effects of caffeine pretreatment on nicotine plasma levels were evaluated. RESULTS: Although caffeine (1.0-30.0 mg/kg) did not generalize to nicotine when administered alone, it markedly potentiated discriminative-stimulus effects of the threshold dose of nicotine (0.05 mg/kg) in both water- and caffeine-drinking rats. Nicotine plasma levels were, however, not affected by acute or chronic caffeine exposure. CONCLUSIONS: Caffeine appears to enhance the discriminative-stimulus effects of the threshold dose of nicotine by a pharmacodynamic rather than a pharmacokinetic interaction. This suggests that caffeine consumption may be a contributing factor in the onset, maintenance of and relapse to tobacco dependence.

Animals↗
PubMed1997

Caffeine reinforcement: the role of withdrawal.

This study examined caffeine's acute and withdrawal effects in moderate caffeine consumers (mean = 379 mg/day caffeine) to compare the relative contributions each might have to caffeine reinforcement. Subjects were caffeine restricted on the night before each of three sessions, which generally occurred at weekly intervals; these restrictions lasted until the session was completed approximately 19 h later. During the first two sessions, subjects received either placebo or caffeine (each subject's average daily intake). These two conditions occurred using a double-blind, quasi-random, crossover design. At the end of each session subjects completed the POMS, a caffeine withdrawal questionnaire, and a Multiple-Choice Form on which subjects made a series of discrete choices between receiving the drug again or receiving varying amounts of money. This form also included negative money amounts to assess how much subjects would forfeit to avoid placebo (e.g., withdrawal symptoms after placebo). During the third session, one of the previous choices was randomly selected and the consequence of that choice was implemented. Placebo increased self-reported feelings of "worn out," "headache," and "flu-like feelings," and decreased "alert," "upset stomach," "helpful," and "well-being" relative to caffeine. On the Multiple-Choice Forms, subjects chose to receive caffeine rather than an average of $0.38 and to forfeit $2.51 to avoid receiving placebo again. "Headache" was significantly correlated with amount of money forfeited to avoid placebo. These results suggest that, under these conditions, choice of caffeine is more potently controlled by avoiding withdrawal than it is by the positive effects of caffeine.

Adult↗
PubMed2000

The effects of acute falciparum malaria on the disposition of caffeine and the comparison of saliva and plasma-derived pharmacokinetic parameters in adult Nigerians.

OBJECTIVES: The pharmacokinetics of caffeine and its dimethylxanthine metabolites were evaluated in Nigerians, for whom it is normal to consume caffeine-containing beverages during ill health and recuperation in the belief that caffeine aids early recovery from illness; however, there are no data defining the kinetics of caffeine in healthy and ill Nigerians. MATERIALS AND METHODS: A single oral dose of 300 mg caffeine was given to ten healthy adult Nigerians and ten adults suffering from acute uncomplicated Plasmodium falciparum malaria infection. Caffeine and its dimethylxanthine metabolites were measured in plasma and saliva of healthy subjects and in plasma of patients suffering from malaria using high-performance liquid chromatography. RESULTS: The plasma pharmacokinetics of caffeine per se in both groups was similar (P > 0.05). The maximum plasma concentration (Cmax) of paraxanthine was significantly lower (P < 0.05) in malaria (0.9 +/- 0.4 microg/ ml) than in healthy controls (1.4 +/- 0.5 microg/ml), and the paraxanthine:caffeine area under the plasma concentration time curve ratio, an index of cytochrome P450 (CYP)IA2 activity was significantly lower (P < 0.05) in malaria patients (0.5 +/- 0.1) than in healthy controls (0.3 +/- 0.2). The elimination half-life of theophylline was longer in malaria, while the area under the plasma concentration time curve of theobromine was significantly higher (P < 0.05) in malaria (7.1 +/- 3.4 microg ml(-1) h) than in healthy adults (4.1 +/- 2.2 microg ml(-1) h). Excellent correlations were found between saliva and plasma concentrations of caffeine (r2 = 0.98) with a mean saliva:plasma concentrations ratio of 0.7 +/- 0.1. The plasma concentrations (Cmax and AUC) were therefore higher than the corresponding salivary levels, so that the apparent oral clearance calculated for saliva exceeded the true oral clearance based on plasma data. CONCLUSIONS: Acute Plasmodium falciparum malaria produced significant changes in the disposition of caffeine metabolites. Analysis of concentrations in saliva is a useful non-invasive method for monitoring the kinetics of caffeine and paraxanthine in Nigerians.

Acute Disease↗
PubMed1985

Effects of caffeine on vascular resistance, cardiac output and myocardial contractility in young men.

The mechanisms by which caffeine typically elevates blood pressure (BP) in humans have not been previously examined using a placebo-controlled design. Accordingly, oral caffeine (3.3 mg/kg body weight, equivalent to 2 to 3 cups of coffee) was given on 2 days and a placebo was given on 1 day to 15 healthy young men using a double-blind, crossover procedure. All 3 test sessions were held during a week of caffeine abstinence. Multiple measurements were made on subjects at rest (baseline values) and over a 45-minute interval after ingestion of caffeine for BP, heart rate, systolic time intervals and thoracic impedance measures of ventricular function. Baseline measurements were highly reliable for each subject across all sessions and yielded means for placebo vs caffeine days that were not different. Caffeine increased systolic and diastolic BP (p less than 0.01) and decreased heart rate (p less than 0.05). The pressor effect was due to progressively increased systemic vascular resistance and resulted in greater stroke work (p less than 0.01). There was no indication that caffeine increased cardiac output or contractility. These actions of caffeine were replicable when each caffeine day was tested separately against the placebo day. These results suggest that caffeine use by persons with cardiovascular diseases should be examined to determine whether caffeine's enhancement of vascular resistance may contribute to systematic hypertension and/or create excessive demands for cardiac work.

Adult↗