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Experiments with rabbits (30) and albino rats (110) demonstrated that morphine (1 mg/kg), promedol (trimeperidine) (2 mg/kg) and phentanyl (0.02 mg/kg), while raising by 21-24 per cent of the algesia threshold, produced an analgesic effect differeing in its duration (morphine-130 min, trimeperidine-70 min, phentanyl-17 min). This is attended by changes in respiration (greater on introduction of phentanyl, and lesser, following administration of morphine) and by shifts in the functional state of the tissues (greater on introduction of trimeperidine and lesser after aministration of morphine).

Experiments were conducted on chloralose-anesthetized cats. The action of morphine and promedol upon the potentials of the cortical and subcortical structures occurring after the visceral nerve stimulation was studied. Morphine proved to depress the potentials evoked by stimulation of the inferior cardiac and vagus nerves, in the specific, associative and nonspecific structures of the brain; promedol produced an analogous effect. Morphine also inhibited the potentials occurring after the stimulation of the splanchnic nerve in the associative and nonspecific structures; depression of the responses in the specific pathways was less pronounced.

A study was made of the effect of morphine and promedol on the content, uptake, and release of norepinephrine (NE) on rat myocardium. Promedol proved to decrease the NE level in the myocardium. Morphine failed to influence the release of the NE-14C from the isolated perfused heart, whereas promedol increased it significantly, altering both the "slow" and the "rapid" release of the mediator. Promedol failed to influence the uptake of NE-14C by the perfused heart, whereas morphine decreased it significantly. The competition between morphine and NE was characterized by the effect of incomplete inhibition: morphine and NE produced reciprocal effects on the affinity of one another to the receptor, and their interaction depended on the ratio of the concentrations of these drugs.

The effect produced by narcotic analgetics with their intravenous administration on the process of cortical control over the transmission of impulses along specific routes of the sciatic nerve was studied. The conditioning stimulation of the cortex was effected by using a monopolar electrode through single electric impulses. The interval between conditioning and test (on sciatic nerve) impulses was of 80-120 ms. Morphine (1-2 mg/kg), promedol (trimeperidin) (1-2 mg/kg) and phentanyl (100 gamma/kg) potentiated the inhibition of evoked potentials in the nucleus gracilis and in VPL, observed upon stimulation of the cortex of optic lobuses. The intensification of inhibitory corticifugal mechanisms occurring under the effect of narcotic analgetics takes place both on the level of the medulla oblongata and of the thalamic one.

With a single parenteral introduction of thyrocalcitonin (TCT) the algesthesia of soft tissues (tall skin, paw) is moderately increasing, while the algesic action of morphine and promedol against the background of TCT-gets weaker. And contrarywise algesthesia of hard tissues of the tooth becomes significantly lower under the effect of TCT and this continues for a long time.

In tests with determination of pain reaction in rats registered by their squeak and arising in reponse to a single electric irritation of the tail evidence was obtained to the effect that substances both lowering the serotonin content in the brain (p-chlorphenylalanine, reserpine) and raising it (5-oxytryptophan, pargilin) cause a fall of the threshold, viz. 5-oxytryptophan and pargilin display antagonism to the analgetic effect of trimeperidine hydrochloride, whereas p-chlorphenylalanine, and inhibitor of trypophan-hydroxylase and tipindol, an antagonist of serotonin, do not exert any noticeable influence on the extent of the analgesic effect of trimeperidine hydrochloride.