Forty-nine inpatients with abnormal EEG patterns were administered nialamide at dose levels of 75 - 150 mg per day for one week. During that period EEG recordings were performed two or three times successively on the 1st - 2nd day, 3rd - 4th day, and 5th - 7th day. There were four cases of epilepsy, two cases of narcolepsy and one case of anorexia nervosa among the 49 patients. The remaining 42 cases were brainstem dysfunction syndrome (diencephalosis and diencephalic seizures). Out of 49 patients, 35 cases (7 1.4%) showed increased centrencephalic discharges.

Coronary arteries were isolated from mongrel dogs and placed in a tension measuring apparatus inside a tissue bath. The nutrient solution of the bath contained NaC1, 119.7 mM; KC1, 5.4 mM; NaHCO3, 20.0 mM; CaC12, 2.2 mM; MgCl2, 1.0 mM; and dextrose, 5.6 mM. The temperature was maintained at 37 deg-C with a pH of 7.4 - 7.4 in a 5% CO2 atmosphere. Preparations were allowed to equilibrate for 90 - 120 minutes with solution replacement every 10 - 15 minutes. Nialamide was added to the bath 60 minutes prior to experiments. Platinum electrodes were used to conduct transmural electrical stimulation, and coronary arteries were contracted spontaneously or with prostaglandin F2a in low concentrations before electrical stimulation. The preparations were transmurally stimulated by a train of square pulses of 6.0V intensity at frequencies of 5 and 20 Hz for a period of 10 sec, with 0.2 msec (coronary arteries) or 0.3 msec (mesenteric arteries) duration. Pretreatment of mesenteric arteries with nialamide in a concentration of 10^5 M markedly shifted the dose-contraction curve to the left (nialamide-induced potentiation). The nialamide induced potentiation appears to be specific for tyramine since nialamide (10^5 M) did not affect dose-concentration curves of prostaglandin F2a; the ED50 values in the absence and presence of nialamide were (5.5_+ 1.5) x 10^5 M and (4.5+ 1.3) x 10^5 M (N = 5), respectively.