After the induction of an experimental algogenic focus in the left brachioradialis muscle of 15 healthy subjects, the algosensitive thresholds of the cutaneous, subcutaneous, and muscular tissues are studied in the painful region by means of electrical stimulation. Statistical analysis of the results shows (a) normal sensory thresholds in the three structures; (b) significantly lowered pain thresholds in a limited ellipsoid area in the skin and subcutaneous tissue and in the whole painful area in the muscle. These results clearly indicate a hyperalgesic condition in the parietal layers of the area examined.

Electrical stimulation pain thresholds and EMG activity were studied, using the vastus medialis muscle of healthy control subjects and of patients with osteoarthritis of the knee. Various categories of sensation elicited by progressive increases of the level of electrical stimulation (including one defined as pain threshold) were defined for control subjects. For patients, muscular pain thresholds differed significantly for the two sides of the body; they were usually lower in the more affected side. Involuntary activity of certain motor units and delayed relaxation following voluntary contraction were consistently observed in patients. The involuntary activity was affected by limb position and by mechanical stimulation of tender areas of the muscle or joint. Differences in pain threshold between the two sides were significantly reduced and the EMG pattern became normal following treatment with injections of local anaesthetic into tender periarticular areas and systemic administration of lysine acetylsalicylate. In standing patients, abnormal EMG activity (which was characteristically sensitive to body load and its variations) was found. Injection of a local anaesthetic into the joint cavity was able to induce a rapid subjective improvement and a consistent reduction of EMG activity.

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425trasylol and leupeptin on trypsin-like proteolytic enzymes such as kallikrein, CIr, tissue activator, pancreatin, plasmin and thrombin were studied. The derivatives of phenyl ester of these acids showed potent inhibitory effect on the trypsin-like enzymes. The effect of these esters on inflammation induced by croton oil and on experimental pancreatitis in animals will be reported. CI esterase activity and the conversion of CI to CI esterase were competitively inhibited by aromatic esters of guanidinocaproic acid. However, p-aminophenyl-phenylpropionate, chymotrypsin inhibitor, had no effect on CI esterase activity. Such synthetic inhibitors as described above reversibly inhibited trypsin, while derivatives of p-guanidinobenzoic acid inhibited trypsin irreversibly (E. Shaw; 1969).

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