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PubMedDate not supplied

Inhibition and activation of acetaminophen reactive metabolite formation by caffeine. Roles of cytochromes P-450IA1 and IIIA2.

Caffeine has previously been shown to diminish or potentiate acetaminophen (APAP) hepatotoxicity in rats, depending on induction state. To elucidate the P-450 forms involved in these divergent effects, rat liver microsomes, prepared after pretreatment with various inducers, were used to examine the effect of caffeine on N-acetyl-p-benzoquinone imine (NAPQI) formation. The addition of caffeine to incubations with 3-methylcholanthrene (MC)-induced microsomes resulted in a biphasic effect on the formation of NAPQI. A 43% decrease in NAPQI formation was observed as caffeine concentration was increased from 0 to 0.5 mM; however, NAPQI formation was accelerated as caffeine concentration increased, exceeding the control (no caffeine) value, at caffeine concentrations greater than 2.5 mM. Incubations with purified P-450IA1 showed that as caffeine concentration increased from 0 to 5 mM, a 50% inhibition was observed with no evidence of acceleration. In contrast to MC microsomes, the addition of caffeine to incubations with uninduced and phenobarbital-induced adult rat microsomes resulted in a marked (3- to 4-fold) acceleration of NAPQI formation with no evidence of inhibition. Caffeine (5 mM) also accelerated NAPQI formation in microsomes isolated from diabetic rats, but to a substantially lesser extent (120%), suggesting a modest (if any) effect on P-450IIE1, a form previously shown to form NAPQI from APAP. Interestingly, caffeine caused a 3- to 4-fold increase in NAPQI formation by juvenile male and female rat microsomes, but no activation was observed with adult female rat microsomes. These results suggested that caffeine activated a member of the cytochrome P-450IIIA subfamily.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaminophen↗
PubMed1991

Role of adenosine receptors in caffeine tolerance.

Caffeine is a competitive antagonist at adenosine receptors. Receptor up-regulation during chronic drug treatment has been proposed to be the mechanism of tolerance to the behavioral stimulant effects of caffeine. This study reassessed the role of adenosine receptors in caffeine tolerance. Separate groups of rats were given scheduled access to drinking bottles containing plain tap water or a 0.1% solution of caffeine. Daily drug intake averaged 60-75 mg/kg and resulted in complete tolerance to caffeine-induced stimulation of locomotor activity, which could not be surmounted by increasing the dose of caffeine. 5'-N-ethylcarboxamidoadenosine (0.001-1.0 mg/kg) dose dependently decreased the locomotor activity of caffeine-tolerant rats and their water-treated controls but was 8-fold more potent in the latter group. Caffeine (1.0-10 mg/kg) injected concurrently with 5-N-ethylcarboxamidoadenosine antagonized the decreases in locomotor activity comparably in both groups. Apparent pA2 values for tolerant and control rats also were comparable: 5.05 and 5.11. Thus, the adenosine-antagonist activity of caffeine was undiminished in tolerant rats. The effects of chronic caffeine administration on parameters of adenosine receptor binding and function were measured in cerebral cortex. There were no differences between brain tissue from control and caffeine-treated rats in number and affinity of adenosine binding sites or in receptor-mediated increases (A2 adenosine receptor) and decreases (A1 adenosine receptor) in cAMP accumulation. These results are consistent with theoretical arguments that changes in receptor density should not affect the potency of a competitive antagonist. Experimental evidence and theoretical considerations indicate that up-regulation of adenosine receptors is not the mechanism of tolerance to caffeine-induced stimulation of locomotor activity.

Adenosine↗
PubMed1991

Caffeine potentiates vasodilator-induced renin release.

Previous studies strongly suggest that adenosine receptors on juxtaglomerular cells function to restrain the secretion of renin induced by a variety of stimuli. The clinical significance of this is that caffeine, a widely consumed adenosine receptor antagonist, could augment renin release responses to diseases such as renovascular hypertension, liver cirrhosis and heart failure and to therapeutic maneuvers such as salt restriction, diuretics and vasodilators. Caffeine may be particularly troublesome in this regard because this methylxanthine has central nervous system effects and intracellular actions that also might contribute to the overall ability of caffeine to potentiate renin secretion. The purpose of this study was to document the effects of caffeine on renin release responses to a vasodilator and to investigate what mechanisms were responsible for any augmentation of vasodilator-induced renin secretion. Accordingly, we compared the effects of caffeine vs. 1,3-dipropyl-8-p-sulfophenylxanthine (DPSPX; a xanthine that we documented in this study not to significantly enter the brain or penetrate cell membranes) on base-line and hydralazine-induced renin release in both normal and beta adrenoceptor-blocked (propranolol, 15 mg/kg) rats. Both xanthines (at a dose of 10 mg/kg plus 150 micrograms/min) attenuated adenosine-mediated hypotension and bradycardia, and DPSPX was at least as effective as caffeine in antagonizing peripheral adenosine receptors. Caffeine and DPSPX increased base-line plasma renin activity to a similar extent regardless of whether the animals were pretreated with propranolol. In rats with an intact beta adrenergic system, caffeine, but not DPSPX, increased the renin release response to low-dose hydralazine (1 mg/kg). Although both xanthines augmented the renin release response to high-dose hydralazine (10 mg/kg), caffeine was more efficacious in this regard. In beta adrenoceptor-blocked rats, neither caffeine nor DPSPX augmented the renin release response to low-dose hydralazine, whereas both xanthines equally potentiated the renin release response to high-dose hydralazine. These data demonstrate that caffeine increases base-line renin release primarily by blocking peripheral (most likely renal), cell-surface adenosine receptors; however, caffeine potentiates vasodilator-induced renin secretion in part by blocking peripheral (most likely renal), cell-surface adenosine receptors and in part by additional central nervous system and/or intracellular mechanism(s) that involve the beta adrenergic system.

Adenosine↗
PubMed1988

Caffeine: a new look at an age-old drug.

Caffeine is ubiquitous in our environment and is the most widely used psychoactive drug in the world. Caffeine works on every system in the body mediated by the central nervous system. Caffeine has the opposite effect of adenosine and is the antagonist at the inhibitory A1-receptor. Caffeine elevates the free fatty acid mobilization and could enhance weight loss through pre-exercise caffeine ingestion. However, this hypothesis remains to be proven until an increase in fat oxidation is found. Caffeine is metabolized to more than 25 metabolites in man. Less than 5% of the caffeine is found in the urine as unchanged drug. The half-life of caffeine ranges from 1.5 to 9.5 hours. Smoking decreases the half-life of caffeine. Caffeine is used for the treatment of apnea of prematurity and as an additive in several analgesics and migraine remedies, and as a panacea for hyperkinetic children. Although much work has been done to establish the relationship between caffeine and cancer and mutagenicity, none of these have established a cause-effect relationship. The consumption of caffeine products in moderation appears to be safe at this point.

Apnea↗
PubMed1988

Influence of caffeine consumption on 7,12-dimethylbenz(a)anthracene-induced mammary gland tumorigenesis in female rats fed a chemically defined diet containing standard and high levels of unsaturated fat.

The effect of caffeine (430-500 mg/liter of drinking water) on the initiation and promotion phases of 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary gland tumorigenesis in female Sprague-Dawley rats fed a chemically defined diet containing standard (5%) or high (20%) levels of fat (corn oil) was examined. In the initiation studies, caffeine and the standard or high fat diet treatments were provided for 34 days, from 24-29 days of age to 58-63 days of age. Three days prior to termination of caffeine-fat diet treatments, each rat received a single dose of DMBA. In the promotion studies, caffeine and the standard or high fat diets were provided commencing 3 days after a single dose of DMBA (at 56-61 days of age) and until termination of the study. Caffeine consumption, during the initiation phase significantly (P less than 0.05) reduced mammary carcinoma multiplicity (number of tumors/rat), in rats fed either a standard or high fat diet. In the promotion studies, prolonged consumption of caffeine in rats fed either a standard or high fat diet did not significantly effect mammary carcinoma multiplicity. In the early stages of promotion, an apparent increase in mammary carcinoma multiplicity was observed; this increase in mammary carcinoma multiplicity did not, however, reach the 5% level of statistical probability. When caffeine was administered during both the initiation and promotion phases, no significant effect on mammary carcinoma multiplicity was observed. Treatment of rats during the initiation or promotion phases with caffeinated coffee (via drinking water) mimicked the mammary tumor modulating activities of caffeine. Decaffeinated coffee consumption did not effect either the initiation or promotion phases of this tumorigenic process. In both the initiation and promotion studies, caffeine and/or coffee consumption did not significantly affect the incidence of mammary carcinomas (percentage of rats bearing mammary carcinomas) or the mean latency period of mammary tumor appearance. Thus, in female rats fed a chemically defined standard or high fat diet, caffeine consumption can significantly influence chemical carcinogenesis of the mammary gland; an effect that is dependent upon the duration and time-span of caffeine administration.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1988

Reinforcing effects of caffeine in humans.

The reinforcing and subjective effects of caffeine were studied under double-blind conditions in 12 normal humans. After 2 forced exposure days on which subjects received color-coded capsules containing either caffeine (100, 200, 400 or 600 mg) or placebo, subjects had a choice day on which they chose which one of the two types of color-coded capsules would be ingested. Subjects were exposed to 10 experimentally independent choices (i.e., involving exposure and choice between novel color-coded capsule conditions) at each of several dose levels. All forced exposure and choice opportunities occurred when subjects were overnight abstinent from their normal dietary caffeine intake (mean, 116 mg/day). Significant caffeine positive reinforcement was demonstrated in 5 of 12 subjects at one or more doses. Percentage of selection of caffeine was inversely related to dose, with four subjects showing significant caffeine avoidance at 400 and/or 600 mg. Choice behavior was correlated positively with feelings of contentedness and was correlated negatively with prestudy trait anxiety scores and with ratings of capsule disliking. Compared to placebo, caffeine produced increases in subjective ratings indicating arousal while producing decreases in headache and "craving" for caffeine-containing foods, even at the lowest dose of 100 mg. At higher doses caffeine produced dysphoric anxiety-like subjective effects. Overall, this study provides the first demonstration in humans of the positive reinforcing effects of caffeine alone (i.e., in capsules) and documents individual differences among normal subjects in both caffeine positive reinforcement and caffeine avoidance.

Adult↗
PubMed1987

Caffeine-induced contraction in vascular smooth muscle.

Characteristics of caffeine-induced contraction were compared with those of high K+- and norepinephrine-induced contractions in order to evaluate the participation of the Ca++-induced Ca++-release (CCR) from storage site in the vascular smooth muscle of rabbit aorta. Caffeine induced a transient contraction in a solution without MgCl2. One mM Mg++ selectively inhibited the caffeine-induced contraction. Two mM procaine inhibited the contractions induced by caffeine, high K+ and norepinephrine. One mM lidocaine and low temperature (23 degrees C) inhibited both high K+- and norepinephrine-induced contractions but rather potentiated the caffeine-induced contraction. Simultaneous addition of 10(-6) M verapamil and 10(-5) M sodium nitroprusside inhibited both high K+- and norepinephrine-induced contractions, but not the caffeine-induced contraction. In a Ca++-free solution, both caffeine and norepinephrine induced transient contractions. Norepinephrine-induced transient contraction was more strongly inhibited than caffeine-induced contraction by 2 mM procaine and 1 mM lidocaine, whereas 5 mM Mg++ inhibited only the caffeine-induced contraction. In sarcoplasmic reticulum of skeletal muscle, it has been shown that the CCR is activated by caffeine and inhibited by procaine, but not by lidocaine and low temperature. Although Mg++ is an inhibitor of CCR, changes in extracellular Mg++ concentrations do not seem to readily modify the intracellular Mg++ concentration in the intact smooth muscle, and the inhibitory effect of Mg++ on caffeine-induced contraction may not be attributable to the direct effect on sarcoplasmic reticulum. These results suggest that the CCR plays an important role in the contraction induced by caffeine but not in the contractions induced by high K+ and norepinephrine in the vascular smooth muscle of rabbit aorta.

Animals↗
PubMed1986

Tolerance to caffeine-induced stimulation of locomotor activity in rats.

The objective of this study was to quantify the rate and extent of tolerance development and loss of tolerance to caffeine-induced stimulation of locomotor activity in rats as a function of average daily caffeine dosage. Adult male rats were maintained chronically on 0.25, 0.5 or 1.0 mg/ml of caffeine in their drinking water by the method of scheduled access. These concentrations of caffeine yielded average daily doses of 19, 36 and 67 mg/kg, respectively. A control group received scheduled access to drug-free drinking water. A dose of 30 mg/kg of caffeine was administered by gavage periodically to all rats before, after the start of and following withdrawal from chronic caffeine treatment. Locomotor activity was measured either for 3 hr immediately after caffeine administration or for 30 min beginning 35 min after caffeine administration. In addition, dose-effect relationships for caffeine (5.6-175 mg/kg) were determined 3 to 5 weeks after the start of chronic drug treatment and were redetermined 2 to 4 weeks after withdrawal. Complete and reversible tolerance developed in the groups receiving the two higher daily doses of caffeine; nearly complete tolerance developed in the group receiving the lowest dose. Dose-effect curves were shifted downward and tolerance was not surmountable by increasing the dose of caffeine. Significant tolerance developed within 1 to 3 days of the start of chronic caffeine exposure and was lost within 3 to 4 days after the cessation of drug treatment. These results are reminiscent of a classical tachyphylaxis.

Animals↗
PubMed1985

Maturational changes of caffeine concentrations and disposition in infancy during maintenance therapy for apnea of prematurity: influence of gestational age, hepatic disease, and breast-feeding.

Twenty-three premature infants receiving caffeine maintenance therapy were followed prospectively for several months. Three to nine determinations of caffeine half-life (peak and trough caffeine levels) were made in each baby. This first longitudinal study confirmed that the half-life of caffeine is prolonged during the neonatal period (97.6 + 32 hours and for as many as 38 weeks' gestation in several very premature babies). Contrary to previous assumptions, gestational age and postconceptional age seem to be closely related to maturation of hepatic caffeine elimination after the neonatal period, although a high variability of caffeine half-life was observed between infants. Adult values (6 hours) were obtained about 60 weeks postconceptional. Caffeine half-life was greatly increased in two infants who had cholestatic hepatitis secondary to prolonged parenteral alimentation and one infant who was breast-fed exclusively. In this last case, the role of maternal hormones in repressing the normal enzymatic maturation process is strongly suspected. Adequate blood levels of caffeine were usually obtained with a caffeine half-life greater than 30 hours up to 46 weeks postconceptional with a dose of 5 mg/kg of caffeine citrate. Caffeine predose monitoring is adequate up to 46 weeks postconceptional, and caffeine half-life determination is mandatory whenever the trough level is too high or too low, icterus is present, and from 46 to 50 weeks postconception.

Aging↗
PubMed1982

Abolition by cycloheximide of caffeine-enhanced lethality of alkylating agents in hamster cells.

Greatly enhanced lethality for Syrian hamster cells (baby hamster kidney cells and polyomavirus-transformed derivative of baby hamster kidney cells) that had been treated with alkylating agents or ultraviolet light is produced by caffeine. Thus, nitrogen mustard [methylbis(beta-chloroethyl)amine] (HN2) at 0.5 microM decreased cell viability by only a few percent in the absence of caffeine. The addition of 2 mM caffeine during the first 24 hr after nitrogen mustard decreased viability more than 95%. Further kinetic studies of the caffeine effects using other alkylating agents indicate the existence of two modes which damaged cells become caffeine sensitive. Treatment with ultraviolet light or nitrogen mustard makes cells immediately sensitive to caffeine; cells treated with methyl methanesulfonate or N-methyl-N'-nitro-N-nitrosoguanidine, on the other hand, express their maximal caffeine sensitivity only about 15 to 20 hr later. A low concentration of cycloheximide completely abolished this caffeine effect. When 0.36 microM cycloheximide was present, loss of viability was negligible even in the presence of caffeine. Based on further experiments involving the timing of caffeine and cycloheximide additions, caffeine does not affect viability by itself but is involved with some substance such as a protein the rapid synthesis of which is prevented by cycloheximide. This substance does not appear to be needed for recovery from damage, but rather for the action of caffeine in fixing the damaging caused by alkylating agents.

Alkylating Agents↗
PubMed1995

Pharmacokinetics of caffeine in lactating dairy cows.

Because caffeine is metabolized by the hepatic P-450 cytochrome oxidase system, clearance of caffeine is an excellent quantitative test of hepatic function in human beings. It is currently used in much the same way that creatinine clearance is used to assess renal function. Caffeine clearance was measured in lactating dairy cows initially to determine the suitability of caffeine clearance as an indicator of hepatic function in cattle. Pharmacokinetic variables of caffeine were studied in 6 adult lactating dairy cows after i.v. administration of a single dose of caffeine sodium benzoate (2 mg of caffeine/kg of body weight). Caffeine concentration was analyzed by use of an automated enzyme immunoassay. The lower limit of detection of the assay for caffeine in serum was 0.079 micrograms/ml. Serum caffeine concentration-time curves best fit an open two-compartment pharmacokinetic model. Harmonic mean elimination half-life was 3.8 (range, 2.6 to 6.9) hours, and total clearance was 0.118 (range, 0.090 to 0.197) L/kg/h. Milk caffeine concentration was similar to serum concentration 1.5 to 24 hours after caffeine administration. Adverse effects were not observed in cows given caffeine.

Animals↗
PubMed1995

Effects of caffeine on ventilation during acute and chronic nicotine administration in rhesus monkeys.

This study characterized the effects of caffeine (1.0-30.0 mg/kg) and nicotine (0.1-3.0 mg/kg) administered alone and in combination on ventilation in unanesthetized rhesus monkeys. In seated monkeys prepared with a head plethysmograph, ventilation was measured during exposure to air (normocapnia), CO2 (3%, 4% and 5%) mixed in air (hypercapnia), 10% O2 mixed in N2 (hypoxia) and 100% O2 (hyperoxia). Caffeine produced marked, dose-dependent increases in ventilation during conditions of normocapnia and hypercapnia. In contrast, acute administration of nicotine had less pronounced respiratory-stimulant effects during all conditions. The joint effects of caffeine and nicotine on ventilation generally did not differ from those obtained with caffeine alone. Chronic administration of nicotine (1.0 mg/kg/day) for 4 consecutive wk via osmotic pumps significantly decreased the half-life of caffeine but had little effect on ventilation or on sensitivity to the respiratory-stimulant effects of caffeine. Two primary metabolites of caffeine, theophylline and paraxanthine, were active as respiratory stimulants and were equipotent to caffeine, and the joint effects of caffeine and its metabolites were additive. The results indicate that caffeine and nicotine stimulate respiration through different pharmacological mechanisms, in contrast to caffeine and its metabolites which exhibit a similar pharmacological profile. Moreover, significant pharmacokinetic interactions may be obtained when caffeine and nicotine are coadministered.

Animals↗
PubMed1993

Quantal Ca2+ release from caffeine-sensitive stores in adrenal chromaffin cells.

In populations of fura-2-loaded chromaffin cells, caffeine caused a concentration-dependent increase in the intracellular Ca2+ concentration ([Ca2+]i), in the presence or absence of external Ca2+ ([Ca2+]o), that was saturable, reversible, and inhibited in a use-dependent fashion by ryanodine. These data confirm that caffeine mobilizes Ca2+ from the ryanodine-sensitive intracellular stores in chromaffin cells. In nominally Ca(2+)-free medium, sustained stimulation of cell populations or single cells with low caffeine concentrations failed to completely empty the caffeine-sensitive stores. In each case, there was a transient [Ca2+]i elevation, but a subsequent challenge with a higher caffeine concentration evoked a further [Ca2+]i rise, indicating that Ca2+ stores within individual cells were heterogeneous in their sensitivities to caffeine and that caffeine-induced Ca2+ release was quantal. The heterogeneous sensitivity was also demonstrated using ryanodine; pretreatment of cell populations with increasing caffeine concentrations with a constant ryanodine concentration, caused a dose-dependent irreversible inhibition of the response to the subsequent addition of a maximal caffeine concentration. We conclude that, within single chromaffin cells, intracellular Ca2+ stores are heterogeneous in their sensitivity to caffeine and the fraction of Ca2+ stores mobilized by caffeine increases in direct proportion to the caffeine concentration.

Adrenal Medulla↗
PubMed1993

Blood pressure, plasma catecholamine and renin responses to caffeine in elderly hypertensives.

In young hypertensive patients, after a short period of abstention, caffeine ingestion has a significant pressor effect, although the acute cardiovascular responses have not been reported in elderly hypertensives. This study assessed the acute changes in BP, pulse rate, plasma renin activity (PRA) and arterialised plasma catecholamines after 250 mg of caffeine and matching placebo following 12 and 48 hours of caffeine abstention. After 48 hours caffeine abstention supine SBP was higher over the 120 minute study period following acute caffeine loading than following placebo (10 mmHg; 95% Cl 3-17 mmHg, P = 0.016) although the overall post-caffeine rise from baseline values was small (2 mmHg; -3 to 8 mmHg, P = 0.30). Similar differences were seen for supine DBP and standing SBP and DBP although pulse rate was unchanged throughout. After 12 hours abstention no acute pressor effect of caffeine was seen, in fact SBP fell over the study period (-5 mmHg; -10 to 0 mmHg, P = 0.05), and there was no difference between the caffeine and placebo phases. No change in plasma catecholamines or PRA values was found during any of the phases. These results suggest that in elderly hypertensives the pressor effect of caffeine (the equivalent of two to three cups of coffee) is small even after prolonged abstention. After the shorter abstention period, of the duration likely to be seen in clinical practice, no pressor response to caffeine was demonstrated. It is unlikely that acute caffeine ingestion has a significant effect on clinic BP measurements in elderly hypertensives who are regular caffeine consumers.

Aged↗
PubMed1994

Effects of caffeine deprivation on taste and mood.

Despite its ubiquitous consumption in the natural environment, caffeine has not been a reliable reinforcer in laboratory settings. The reinforcing effects of caffeine are greater in caffeine-dependent subjects relative to non-dependent subjects, but the mechanism underlying this difference remains unclear. We hypothesized that deprivation from caffeine would produce alterations in subjective ratings of stimuli commonly associated with caffeine consumption. Specifically, we hypothesized that hedonic ratings of the coffee taste would be selectively enhanced following caffeine deprivation. Twelve regular caffeine users received acute doses of caffeine (300mg) or placebo after 33h of caffeine deprivation or non-deprivation. They rated the taste of coffee and sucrose, saccharin, and quinine solutions on intensity, bitterness, sweetness, pleasantness, and unpleasantness. Contrary to our hypothesis, subjects' ratings of the pleasantness of the coffee taste were not significantly altered by caffeine deprivation. However, subjects' ratings of the bitterness and sweetness of the coffee taste and ratings of the sucrose solution were altered by caffeine. Implications of these data for caffeine self-administration are discussed.

Journal Article↗
PubMed1992

Factors influencing the subjective response to caffeine.

The subjective effects of caffeine, the most widely used psychoactive drug, vary widely from person to person. The factors responsible for these individual differences remain largely unknown. Data from 36 healthy adults who were light to moderate users of caffeine were examined with the goals of characterizing the subjective effects of caffeine and identifying factors which might correlate with or predict these effects. Subjective effects of 100 and 300mg caffeine were measured with standardized questionnaires. The low dose of caffeine was found to produce negligible subjective effects in the group as a whole, while the high dose produced mild stimulant and anxiogenic effects. As expected, there was considerable intersubject variability in the subjective effects of caffeine. There was no correlation between stimulant and anxiogenic effects after the high dose. Light caffeine users were more accurate than heavy caffeine users in identifying the high dose of caffeine as an active drug, but there was no evidence that light users were generally more sensitive to the subjective effects of caffeine. Current alcohol use, prior recreational use of stimulants, and baseline level of self-reported arousal appeared to influence subjective response to caffeine. Other variables (personality, gender, baseline anxiety, and prior use of other drugs) showed no relationship with mood response to caffeine.

Journal Article↗
PubMed2001

Regulation of in vitro penetration of frozen-thawed boar spermatozoa by caffeine and adenosine.

Effects of caffeine and adenosine on the function and in vitro penetration of frozen-thawed boar spermatozoa were examined. First, the effect on sperm function was determined by the chlortetracycline fluorescence assessment. Both caffeine and adenosine stimulated capacitation of spermatozoa. However, adenosine, but not caffeine, inhibited spontaneous acrosome loss. Second, sperm penetration into in vitro matured oocytes was compared among spermatozoa cultured in the absence or presence of caffeine or adenosine. Both caffeine and adenosine increased the penetration rate (99.1 +/- 0.9% in caffeine, 72.4 +/- 2.0% in adenosine vs. 54.8 +/- 5.1% in controls) but only caffeine decreased drastically the monospermic penetration rate (8.0 +/- 2.3% in caffeine vs. 75.4 +/- 4.8% in adenosine and 78.6 +/- 4.8% in controls). When oocytes were cocultured in various sperm concentrations, the proportion of monospermy changed in inverse proportion to sperm concentration in the presence of caffeine, but did not change in the presence of adenosine. A relatively high number of spermatozoa at the early stage of spontaneous acrosome reaction in the presence of caffeine may be one of the main causes of polyspermic penetration in porcine IVF system. These results indicate that replacement of caffeine with adenosine in fertilization medium improves monospermic penetration by frozen-thawed boar spermatozoa.

Acrosome Reaction↗
PubMed1989

Fasting plasma caffeine level in cirrhotic patients: relation to plasma levels of catecholamines and renin activity.

Fasting plasma caffeine concentrations, plasma levels of catecholamines and plasma renin activity were measured in patients with cirrhosis and control patients without hepatic dysfunction. A careful dietary history showed no significant difference in caffeine consumption (mean +/- S.E.) among 46 cirrhotics (86 +/- 7 mg per day) vs. 34 control patients (91 +/- 8 mg per day). Fasting plasma caffeine concentrations, however, were significantly higher (7.68 +/- 1.42 micrograms per ml) in cirrhotics than in controls (1.01 +/- 0.20 micrograms per ml) (p less than 0.01). Fasting plasma caffeine concentrations in cirrhotics varied significantly with Child's criteria, namely Child's A patients (2.06 +/- 0.38 micrograms per ml); Child's B patients (6.92 +/- 1.86 micrograms per ml), and Child's C patients (17.70 +/- 3.65 micrograms per ml) (p less than 0.001). In 44 cirrhotics, fasting plasma caffeine concentrations were compared with plasma levels of catecholamines and plasma renin activity. Plasma epinephrine concentrations were normal; however, plasma norepinephrine concentrations were increased in six cirrhotics, and plasma renin activities were increased in 28 cirrhotics. After a 3-day caffeine abstinence, plasma caffeine concentration and renin activity were significantly decreased (p less than 0.01), and high plasma norepinephrine levels were also decreased in 12 cirrhotics. Plasma caffeine concentration, renin activity and norepinephrine level did not change in a control group of cirrhotics who continued to receive caffeine for 3 days (n = 6). After abstinence from caffeine, the decrease of fasting plasma caffeine concentration correlated well with the decrease of plasma renin activity (r = +0.746, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗