Midazolex® binds to benxodiazepine receptors in various regions of the brain such as the spinal cord, brain stem, cerebellum, limbic system, and the cercbral cortex. Benzodiazepines like Midazolex® block EEG arousal from stimulation of the brain stemcticular formation. Midazolex® acts as CNS depressant on CNS reflexes via the brain stem reticular form tion. Midazolex® is an anxiolytic in animal test systems such as the fear of electroshock in rats or monkey. It is sedative as judged by reduction of fighting in n ice of monkeys. The hypnotic effects of Midazolex® hat are demonstrable in humans are difficult to show in animals even in very high doses. Midazolex® produces anterograde amnesia similar to that produced by diazepam but neither benzodiazepine produces retrograde amnesia. Midazolex® has a more rapid one et of action and shorter duration of effect than diazepam in most animal test systems. The antinociceptive effect of intrathecal Midazolex® inay involve interaction with a delta opiate receptor. Midazolex® has a marked anticonvulsant effect with a nonlinear relationship between concentration and effect without an apparent ceiling at higher concentrations. The EC350 was 0.067 ??? 0.01 mg l-1 for Midazolex®. Antagonism of the anticonvulsant effect of Midazolex® by flumazenil suggested that there might be two separate sites of action, of which only one is antagonized by flumazenil. This study concluded that the effect of benzodiazepines on seizures induced by cortical stimulation in vivo cannot be fully accounted for by an interaction at the GABA A receptor. At high concentrations, Midazolex® can inhibit calcium entry into cells by a non- GABA dependent mechanism and thereby relaxes bronchial and vascular smooth muscle, but the relevance of this finding to the concentrations achieved in humans is doubtful. 

Chlorpheniramine antagonizes competitively the effects of histamine on H1 receptors, and the constrictor responses to histamine of intestinal and bronchial smooth muscle are readily blocked by chlorpheniramine. Phenyleprine is considered a relatively selective ?1-adrenoceptor agonist. Most of the ?1-stimulant activity is the result of a direct action on the receptors. Phenylpropanolamine is often regarded as an ?1-adrenoceptor agonist, but its main pharmacological action appears to be as an indirectly acting sympathomimetic which causes release of norepinephrine from adrenergic nerve endings. 

Acetaminophen has antipyretic and mild analgesic actions together with some anti-inflammatory activity. These effects are thought to be related to inhibition of prostaglandin synthesis. Chlorpheniramine antagonizes competitively the effects of histamine on H1 receptors, and the constrictor responses to histamine of intestinal and bronchial smooth muscle are readily blocked by chlorpheniramine. Phenyleprine is considered a relatively selective ?1-adrenoceptor agonist. Most of the ?1-stimulant activity is the result of a direct action on the receptors. 

Both dextromethorphan and its major metabolite dextrorphan have non-opiate-mediated cough suppressant actions. Animal studies suggest that the main site of action of dextromethorphan is on the centrally induced cough response. Pseudoephedrine is a sympathomimetic agent with direct and indirect effects on adrenergic receptors. It has direct agonist activity, particularly on cardiac ?-adrenoceptors and peripheral ?adrenoceptors, and indirect sympathomimetic activity because it displaces norepinephrine from the cytoplasmic pool.