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1. The effect of sodium acetylo-salicylate (2 g per os) on the thermoregulatory responses of 10 male subjects was studied by direct and indirect calorimetry during two tests : heat exposure at 37 degrees C and exercise (50 W) at 25 degrees C. Both test were performed twice : with salicylate treatment and with a placebo. 2. During heat exposure at 37 degrees C for 75 min, the rise in tympanic temperature (Tty) and in mean skin temperature Ts, the time course of heat losses by radiation (R), convection (C) and evaporation (E), and the metabolic rate (M), measured by oxygen consumption, were not altered by salicylate treatment. 3. During exercise, salicylate treatment did not affect the time course of Tty and Ts, (R + C) and M. However, salicylate treatment decreased the delay for triggering the evaporative response (E) to the thermal load; similarly, the increase in cutaneous blood flow was triggered sooner in subjected receiving salicylate than in controls. 4. In conclusion, these results suggest that, during exercise, the thermal controller triggers thermoregulatory responses during passive hyperthermia by heat exposure.

The in vitro effect of oxidative agents, b-naphthol, p-aminophenol, phenylhydrazine, hydroxylamine, methylene blue, hydroquinone and 1,4-naphthoquinone and of analgesics, acetylsalicylic acid, sodium salicylate and dipyrone, on the electrophoretic pattern of the red cell membrane proteins, is described. The electrophoresis was effected in acid urea-starch gel vertical system. All the agents studied altered the red cell membrane protein electrophoretic pattern, causing a total loss of certain protein bands or a loss of some bands and the diminution of others simultaneously.

The effects of peritubular salicylate for chloride substitution were studied in the isolated perfused Necturus kidney. This substitution resulted in changes of cell membrane p.d., varying from tubule to tubule; the withdrawal of the test-anion invariably produced a steep and prolonged depolarization. Exposure of the tissue to salicylate brought about, in addition, electrical uncoupling of junctional membranes, which was not related to concomitant changes of membrane p.d.

The study of the effects of varying pH and ionic composition of external solution on the uric acid ratio (see article) for human erythrocytes at equilibrium and on its permeability constant shows that the distribution of uric acid agrees with the laws of the Gibbs-Donnan equilibrium and its passage across the human erythrocyte membrane with the law of ionic diffusion.

Sodium salicylate 10(-3) M is able to limit the number of plaques induced by RNA viruses on monkey kidney cell cultures (Cercopithecus aethiops and Macaccus rhesus). However, the inhibition rate changes with the virus type or even the strain used. Poliovirus 2, Coxsackie B3, echovirus and reovirus 1 were the most susceptible to the inhibitory effect of the drug. Latent infection caused by SV5 decreases the antiviral activity of salicylate. The stages of the poliovirus type 2 growth affected by sodium salicylate, were studied. The drug has no direct activity on the infectivity of the virus. It decreases adsorption and penetration. In spite of heavy virus concentration (10(-5,5) to 10(-7)) ID/ml) the eclipse phase is delayed about 3 hours. After 6 hours, viral maturation proceeds and reaches the same level as the controls, and virus quantities recovered are equivalent after 12 hours. Viral infectious RNA fails to induce plaques on salicylate treated cultures. The drug seems to act during the eclipse phase.

In order to assess the role of inflammation and its components in spontaneous cure of Strongyloides ratti infestation, rats were treated with non-steroid anti-inflammatory agents (indometacin; sodium salicylate) or with antagonists of certain mediators (dexchlorpheniramin; cyproheptadin, promethazin). Results were compared with those obtained in similar treatments of rats infested by other Nematoda which also give rise to spontaneous cure: especially Trichinella spiralis, and Nippostrongylus brasiliensis. Coordinating the various findings made it possible to devise a pattern accounting for the chain of reactions that lead to rejection of the parasite.

Aspirin-sensitive asthma is a common and severe disorder characterized by asthmatic attacks after oral ingestion of cyclooxygenase inhibiting drugs. Yet its pathophysiology remains unknown, and no specific in vitro abnormality, neither humoral nor cellular, has been detected in these patients. We have recently described a new model of platelet activation--IgE-dependent platelet activation--expressed by the release of cytocidal mediators and oxygen metabolites. We have now investigated whether cyclooxygenase inhibitors induce a similar response in platelets from aspirin-sensitive asthmatics in vitro. Aspirin or indomethacin strikingly activated platelets from 12 aspirin-sensitive asthmatics to the same extent as IgE-dependent stimuli, but had no effect on platelets from 18 controls (p less than 0.0001). Sodium salicylate, which does not inhibit cyclooxygenase, did not trigger platelets from aspirin-sensitive asthmatics. Preincubation with sodium salicylate or prostaglandin endoperoxides (PGH2), selectively prevented further platelet activation by aspirin or indomethacin (90% inhibition), suggesting that this abnormal platelet activation is the consequence of cyclooxygenase inhibition. This represents the first identification of a specific abnormal cellular response in aspirin-sensitive asthma, provides the basis for an in vitro diagnostic test of the disease, and for new insights on its pathogenesis and its prevention.