Two patients who ingested therapeutic doses of acetaminophen and who developed a severe hepatotoxicity are reported. Both patients had a rather high alcohol consumption, which probably made them susceptible to the toxic effects of acetaminophen.

Duct pressure and salivary flow were recorded in submaxillary glands of anaesthetized dogs, to study whether parasympathetic stimulation caused effects referable to activity in myoepithelial cells. At fairly low frequency of stimulation, e.g. 3 Hz, the pressure curve had two distinct components, with an initial steep and a secondary gradual rise. It resembled that obtained on sympathetic stimulation, where the first phase is ascribed to myoepithelial contraction, the second phase to secretion. When parasympathetic stimulation ceased, there was first a steep fall, then a more gradual decline of the pressure. The steep fall was of the same magnitude as the steep rise; both increased with the frequency of stimulation. The size of the initial fall was fairly independent of the pressure level from which it started. Such a steep fall did not occur subsequent to parasympathetic stimulation if the myoepithelial cells were already in a state of strong contraction caused by sympathetic impulses or bradykinin. The phase of steep fall was inferred to be due mainly to relaxation of contracted myoepithelial cells, the following decline to back-flow of fluid into the gland.The salivary flow rate was highest at the beginning of a period of parasympathetic stimulation, particularly if the duct system was well filled and the saliva thin. It was concluded that myoepithelial contraction had initially expelled saliva. A brief period of parasympathetic stimulation while a slow basal secretion at constant rate was going on was found to accelerate this flow, and afterwards there was a transient deceleration of the flow. Acceleration was attributed partly to myoepithelial contraction, mainly to superimposed secretion; retardation to myoepithelial relaxation. The effect appeared independently of the way in which the basal flow was evoked, and the retardation resembled that seen after sympathetic stimulation or bradykinin.Morphological investigations suggest that cholinergic nerves innervate myoepithelial cells in salivary glands [Garrett, 1966]. Motor effects of electrical stimulation of parasympathetic salivary nerves have been

In the parotid gland of the rat intracellular recordings were made 13–30 hours after section of the auriculo‐temporal nerve or excision of the superior cervical ganglion. Shortlasting membrane potential changes (hyperpolarisation or depolarisation) and resistance decreases, much larger and more frequent than in the control gland, were observed. The degeneration activity after parasympathectomy was blocked by atropine, whereas the sympathetic degeneration activity was blocked by the α‐blocker dihydroergotamine. The electrical activity is thus believed to be due to release of neurotransmitter from degenerating nerve fibres; β‐blockers and tetrodotoxin did not significantly affect the activity.

The effects of SP and VIP were studied in vitro in normal and denervated parotid glands of the rat using electrophysiological techniques. After sympathetic, and especially after parasympathetic, denervation the number of cells responding to peptides increased significantly. Furthermore, sub-threshold doses for control glands induced membrane potential changes after denervation. It seems reasonable to correlate these findings to the development of supersensitivity. The underlying mechanisms, however, require further investigation.

SUMMARY1. In cats under chloralose anaesthesia micro-electrodes were inserted into parotid gland cells.2. The average resting potential was found to be -356 + 4.7 (S.D.) mV. 3. Stimulation of the auriculo-temporal nerve caused hyperpolarizing, or occasionally depolarizing, secretary potentials of 5-10 mV, which were abolishable with atropine.4. Stimulation of the cervical sympathetic trunk regularly caused, after long latency (several seconds), slow depolarizations of 15-20 mV, accompanied by a decrease in input resistance. They were antagonized by practolol and therefore assumed to be mediated bv fl1-adrenoceptors. Occasionally hyperpolarization, ascribed to an effect on x-adrenoceptors, was observed.5. In many units the slow depolarization on sympathetic stimulation was preceded by short-lasting hyperpolarizing (sometimes depolarizing) transients. They resembled the evoked cholinergic responses but could be abolished not only by atropine but also by guanethidine.