Evaluation of cognitive brain functions in caffeine users: a P3 evoked potential study.

Caffeine is one of the most widely consumed stimulant drugs of the modern world. It brings about a feeling of well-being, relaxation, increased alertness and concentration. Its effects have been studied on brain function and behavior using mood questionnaires, reaction time tests, memory tests, EEG and of late Event Related Potentials (ERPs). This study evaluates the response of caffeine on ERPs and Reaction Time (RT) using auditory "oddball" paradigm. Forty undergraduate medical students volunteered for the study and their ERPs and RT were recorded before and after 40 minutes of ingestion of caffeine. There was a non-significant decrease in latency of N1, P2, N2 and P3 and a significant decrease in Reaction Time after caffeine consumption. The amplitude of P3 showed a significant increase after intake of caffeine. The results of this study indicate that caffeine leads to facilitation of information processing and motor output response of the brain.

Adenosine-induced chest pain: is it due to myocardial ischaemia? Clinical, electrocardiographic, haemodynamic and metabolic study.

Adenosine has recently been demonstrated to be a mediator of angina in human beings. The present study was undertaken to document the presence or absence of myocardial ischaemia on clinical, haemodynamic, electrocardiographic and metabolic evidences after intracoronary administration of adenosine. Fifteen patients with chronic stable angina (12 males and 3 females), positive exercise stress test and documented significant stenosis of the left anterior descending coronary artery (LAD) were included in the study. The surface and intracoronary electrocardiograms (ECGs), pulmonary artery diastolic pressure and coronary sinus lactate levels were monitored at baseline and after intracoronary administration of adenosine in all patients. Adenosine was administered intracoronary in doses of 1000-8000 microgram depending on the provocation of chest pain. Typical angina was observed in all patients. There were no signs of ischaemia on surface or intracoronary ECG. There was no statistically significant difference between the pulmonary artery diastolic pressure and coronary sins lactate levels at baseline and post-adenosine administration (p > 0.05). It is concluded that intracoronary administration of adenosine produces chest pain in patients with chronic stable angina by mechanism other than myocardial ischaemia.

Antinociceptive effect of purine nucleotides

The antinociceptive effect of purine nucleotides administered systemically (sc) was determined using the formalin and writhing tests in adult male albino mice. The mechanisms underlying nucleotide-induced antinociception were investigated by preinjecting the animals (sc) with specific antagonists for opioid (naloxone, 1 mg/kg), purinergic P1 (caffeine, 5, 10 or 30 mg/kg); theophylline, 10 mg/kg) or purinergic P2 receptors (suramin, 100 mg/kg; Coomassie blue, 30-300 mg/kg; quinidine, 10 mg/kg). Adenosine, adenosine monophosphate (AMP), diphosphate (ADP) and triphosphate (ATP) caused a reduction in the number of writhes and in the time of licking the formalin-injected paw. Naloxone had no effect on adenosine- or adenine nucleotide-induced antinociception. Caffeine (30 mg/kg) and theophylline (10 mg/kg) reversed the antinociceptive action of adenosine and adenine nucleotide derivatives in both tests. P2 antagonists did not reverse adenine nucleotide-induced antinociception. These results suggest that the antinociceptive effect of adenine nucleotides is mediated by adenosine.