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The effects of L ‐lysine and diethanolamine‐rutin on blood ethanol levels and withdrawal convulsions following a 4‐day exposure to ethanol vapors were evaluated in 30–40‐g male Swiss‐Webster mice. The animals were exposed in groups, along with simultaneous controls, in a 34‐liter dynamic Plexiglas exposure chamber. Blood was collected by retro‐orbital puncture and analyzed enzymatically for ethanol. At the end of the inhalation period, convulsions on handling were scored over 24 hr. In addition, the effects of L‐lysine and diethanolamine—rutin on blood ethanol levels and on acute ethanol toxicity following oral and intraperitoneal administration were evaluated. L ‐Lysine lowered blood ethanol levels following inhalation or oral administration of ethanol. Diethanolamine-rutin had no effect on blood ethanol levels. Both L ‐lysine and diethanolamine-rutin decreased the withdrawal reaction in dependent mice. L ‐Lysine increased the oral LD 50 of ethanol, while diethanolamine-rutin decreased the intraperitoneal LD 50 of ethanol.

In this study, an operant conditioning and extinction technique is used to compare the effects of various so-called tranquilizing agents. In addition, a method is presented for the preparation of 2-ethyl-2-(3-methyl)-butylmalondiamide. The statistical analysis of the data obtained is supported by observations which indicate that some of the effects of these drugs can be ascribed to secondary or side-effects.

The effect of mescaline on respiratory dynamics, right ventricular pressure, and the ECG in the guinea pig is presented. A procedure for the acquisition of normal right ventricular pressure is described. The mean value for the latter was 13.4 ± 4.6 mm. Hg. Mescaline in low dosages (1 to 20 mg./Kg.) produced a slight increase in heart rate; higher dosages (50 to 240 mg./Kg.) induced bradycardia and conduction disturbances. Respiratory rate, resistance of the airways, and minute volume increased significantly, while tidal volume and compliance decreased. The decrease in compliance was near maximum (−70 and − 77 per cent) with high dosages (50 and 100 mg./Kg.). Right ventricular pressure increased, average 45 per cent, following moderate dosages of mescaline (25 mg./Kg.). Diphenhydramine and chlorpheniramine (range 0.4 to 0.7 mg./Kg.) in sufficient concentration to block the effect of histamine (4 mg./Kg.) were utilized to observe possible mescaline antagonistic activity. However, the antihistamines were ineffective against mescaline. It appears probable that mescaline does not owe its activity on these parameters to histaminic receptor stimulation.

Mescaline (TMPEA) elicited a motor response (dependent upon segment and concentration) from isolated guinea pig, rat, and cat ileum. It did not alter inotropic or chronotropic activity of isolated mammalian atria. Estrogen dominated uteri responded similarly. TMPEA antagonized serotonin-induced motor responses of rat and guinea pig uteri. High concentrations of ganglionic blocking agents potentiated TMPEA motor effects. Evidence suggests that TMPEA does not act via a cholinergic mechanism, but rather through catecholamine mechanisms. The end result varies in definite situations. The primary site of action of TMPEA appears to be at the α-adrenergic receptor site.

Myocardial infarctions were produced in rats by electro-cauterization of the left anterior descending artery, and the extent of myocardial damage was measured by serial serum levels of creatine phosphokinase activity utilizing spectrophotometric analysis. All animals were also evaluated for myocardial damage by electrocardiographic wave alterations. A correlation between myocardial infarct size and serum creatine phosphokinase was demonstrated. Significant arrhythmias and death occurred only in experimental groups where myocardial infarction had been produced. This small animal model offers a quick, inexpensive, and simple method for screening therapeutic agents that alter infarct size.

A survey of the prevalence of boric acid toxicity indicates the difficulty encountered in detecting cases of poisoning by this commonly used substance. Because of this situation, an investigation was carried out utilizing a previously reported method for the detection of borates by the polyvinyl alcohol-borate-iodine reaction. The test was extended in this study to permit the detection of boric acid in the urine of poisoned animals. Rabbits were fed varying quantities of boric acid, and urine samples were collected. After concentration of the urine sample, the polyvinyl alcohol-iodine reagent was applied to the residue. Results of both in vitro and in vivo studies indicate that this method is capable of detecting as little as 0.3 mg. of boric acid (0.05 mg. B).

Several therapeutic agents that alter infarct size were administered to rats with myocardial infarcts induced by electrocauterization. The myocardial tissue damage and infarct size correlated well with the creatine phosphokinase myocardial band activity, and these markers were utilized to assess the action of the therapeutic agents on myocardial tissue damage. Hyaluronidase, insulin, potassium chloride, and isoproterenol increased myocardial tissue damage whereas heparin and prednisolone administration resulted in decreased myocardial tissue damage after induced myocardial infarction in rats.

While the PVA-borate-iodine complex is shown to be suitable for the qualitative determination of boric acid, attempts to adapt this to a colorimetric procedure were of no avail. A possible explanation is suggested as a dilution phenomenon.