Intra-arterial injections of substance P in doses from 10 to 30 units potentiated the response of the nictitating membrane to submaximal stimulation of the preganglionic sympathetic nerve, while higher doses (30 to 100 units) usually depressed the response. The stimulating action of acetylcholine on the superior cervical ganglion (as judged by the response of the nictitating membrane) was also potentiated by substance P. The responses of the nictitating membrane to adrenaline, noradrenaline and tyramine were potentiated by substance P as well. It is concluded that the potentiating effect of substance P on the response of the nictitating membrane to submaximal stimulation of the preganglionic sympathetic nerve is probably due to sensitization of acetylcholine receptors in the postsynaptic neurone. The present experiments do not explain how substance P potentiated the response to sympathomimetic amines.It has been shown that substance P may restore peristalsis when injected into the lumen of the isolated guinea-pig ileum in which the peristaltic reflex has been abolished by fatigue, by external or internal application of 5-hydroxytryptamine, or by lowering the temperature of the bath (Beleslin and Varagic, 1958). Substance P. when acting on the outside of the isolated guinea-pig ileum, blocks the peristaltic reflex (Beleslin and Varagic, 1959). In previous work some evidence was obtained that this block of peristalsis might be at least partly produced by the action of substance P on the intestinal ganglia. On the other hand, Lechner and Lembeck (1958) writing point magnifying the movements of the membrane ten times. The cervical sympathetic chain was divided and, when stimulated electrically, its peripheral end was placed on shielded electrodes and covered with liquid paraffin. For stimulation an electronic stimulator delivering square wave pulses was used. The pulses had a duration of 0.8 msec. and a frequency between 4 and 15 per sec.In some experiments the intra-arterial injections were made without occluding the external carotid artery, thus allowing the injected substance to act directly on the nictitating membrane.Substance P was extracted and purified according to the method described by Zetler (1956).The following substances were used: substance P. acetylcholine hydrochloride, adrenaline hydrochloride, noradrenaline bitartrate and tyramine hydrochloride. With the exception of substance P all doses are expressed in terms of the salts. RESULTSSubstance P and Sympathetic Nervous Stimulation. -The intra-arterial injection of substance P in doses from 10 to 100 units changed the response of the nictitating membrane to submaximal stimulation of the preganglionic sympathetic nerve. With the stimulation in periods of 5 sec. every minute, a series of contractions of the nictitating membrane was recorded as shown in Fig. 1. At C the external carotid artery was occluded, and an intra-arterial injection of 18 units of substance P increased the response of the nictitating membrane to the preganglionic stimulation. The...

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Corneal graft survival in rabbits was significantly prolonged by topical treatment of the recipient eye with cyclophosphamide (0.1% in sterile isotonic NaCl) and methotrexate (0.1% in arachis oil) applied four times daily for 4 weeks. A control group of animals was treated with dexamethasone in the same way. The mean graft survival time was 52 +/- 18.5 days in the group treated with dexamethasone and 80 +/- 18.2 and 73 +/- 23.5, respectively, in the groups treated with cyclophosphamide and methotrexate. Cyclophosphamide and methotrexate applied topically produced no systemic side effects, and only one mild and transient local side effect in the form of hyperemia of the bulbar and palpebral conjunctiva. These two immunosuppressive drugs were more effective than the corticosteroid currently in clinical use, i.e., dexamethasone.

Summary1. The contractile response of the chronically denervated tongue of the cat to chorda stimulation, and to close arterial injections of bradykinin, acetylcholine (ACh) and other drugs was examined. 2. Bradykinin in doses of 50 ng-20 ,g injected close arterially always produced a contractile response of the denervated tongue. Sodium nitrite (1 mg i.a.) and isoprenaline (3-200 ng i.a.) also produced contracture; histamine (40-100 ng i.a.) evoked an increase in tension in only 2 out of 5 experiments. 3. Tubocurarine in doses of 0-25-1 mg injected intra-arterially, produced a large and long-lasting contracture of the denervated tongue. When the contracture was over, the effect of bradykinin was reduced to about half; the effects of ACh and chordo-lingual nerve stimulation were markedly reduced (over 80%), and those of sodium nitrite and isoprenaline were transiently abolished. Gallamine only slightly reduced the effect of bradykinin.4. Close intra-arterial injection of physostigmine (100 Itg) potentiated the effect of ACh and chordo-lingual nerve stimulation, but did not increase the response to bradykinin. 5. Cocaine (1 mg/kg i.v.) deeply depressed the response to bradykinin, and moderately reduced the responses to ACh (41%) and to chorda stimulation (66%). 6. In 2 out of 7 experiments, close arterial injections of bradykinin (100-500 ng) to the denervated tibialis anterior muscle of the cat, produced a contractile response. Bradykinin in small doses (200-250 ng) injected immediately before ACh potentiated its effect. On the other hand, the effect of ACh was depressed when given immediately after a big dose of bradykinin (10-15 ,tg). 7. The possible mechanism of action of bradykinin and other substances onl denervated muscle is discussed.

Prostaglandins E2 and F2 alpha at small concentrations inhibit the acetylcholinesterase activity in slices of caudate nucleus, thalamus and hypothalamus of the cat brain in vitro condition. Prostaglandin E2 (PGE2) at concentrations of 0.35 microM and 0.70 microM produces a dose-dependent inhibition of acetylcholinsteratse activity in slices of caudate nucleus, thalamus and hypothalamus. Higher concentration of PGE2 (2.1 microM) produces less inhibition of acetylcholinesterase activity than smaller concentration of PGE2. The highest concentration of PGE2 (6.3 microM) produces even less inhibition of the same enzyme, which is not significant to the control values of the enzyme activity. Prostaglandin F2 alpha (PGF2 alpha ) inhibits acetylcholinesterase activity in slices of thalamus and hypothalamus of the cat brain in a dose-dependent manner. In caudate nucleus the highest concentration of PGF2 alpha produces somewhat less inhibition than smaller concentration of that prostaglandin. These results are discussed in the context of established potentiating effect of small doses of prostaglandins of gross behavioural changes induced by cholinomimetic substances.