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Of the two proteases produced by Pseudomonas aeruginosa, one whose optimal pH is neutral, exhibits elastolytic activity. This elastase is produced as a prepropeptide, subsequently modified by proteolysis, and finally secreted as an active enzyme. Both proteases act mainly on hydrophobic aminoacids. The most important site for the elastase seems to be the P'1 site where Phe, Tyr and Leu residues enhance hydrolysis. The alkaline protease is less specific of this site. At least four aminoacids are needed to obtain measurable rates of hydrolysis. A synthetic substrate, Ala-Ala-Phe-Ala, is proposed for conductimetric measurements of Pseudomonas aeruginosa elastase activities in the nanomolar range. A review of recent studies shows that a very wide range of proteins can be hydrolyzed by the two Pseudomonas aeruginosa proteases, a fact which may explain why these enzymes are major determinants of the bacteria's infectivity.

Kappa-elastin peptides, obtained from insoluble elastin by organo-alkaline hydrolysis, were fractioned by gel filtration on Biogel agarose. Rates of hydrolysis by pancreatic and leukocyte elastases of the fractions were measured using a conductometric method. Kinetics obey to Michaelis-Menten model for both substrates and enzymes. KM and Vmax values derived from Lineweaver-Burk plots indicate that, if KM remains quite constant, differences were observed in catalytic rates. The kcat values decreased with molecular-weight, the high-molecular-weight kappa-elastin peptides being hydrolyzed 3 to 5 times faster than the low-molecular-weight ones. Apparent differences between potentiometric (pH-Stat) and conductometric results were discussed, in relation with buffer capacity of soluble and insoluble elastins.

The conductimetric method was applied to the measurement of human leukocyte elastase activity, using insoluble elastin as a substrate. From conductance changes, initial rates of elastolysis were derived. A linear relationship of enzyme activity with enzyme concentration was demonstrated up to 400nM of enzyme, for three different substrates. In this concentration range, inhibition of elastolysis by eglin c was studied for different concentrations of eglin c. A 50% inhibitory concentrations of 0.13-0.15 microM of eglin c was derived from our results, corresponding to an inhibitor/enzyme ratio of about 0.5, indicating a strong inhibition, as previously demonstrated by authors using synthetic substrates.

A case of reentrant tachycardia with narrow and wide ventricular complexes without appearances of preexcitation is reported. Electrophysiological investigation showed complete retrograde atrioventricular block during tachycardia; left bundle branch block did not show the tachycardia rate. The reentry loop probably comprised: the His bundle, the right bundle branch, a right Mahaïm bundle and possibly a myocardial bridge. Possible intra-hisian reentry is discussed. The initiation of the tachycardia is analysed together with the possible consequences of permanent cardiac pacing.

The hemodynamic and electrophysiologic effects of rilmenidine were examined after single oral administration to hypertensive patients. In 8 untreated hypertensive patients, cardiac output, pulmonary pressure and blood pressure were measured before and for 10 hours after the administration of 25 micrograms/kg of rilmenidine (1.3 to 2.4 mg, mean 1.88). In addition, electrophysiologic investigations were performed before and 2 hours after administration. Hemodynamics were repeated in 8 other hypertensive patients receiving 50 micrograms/kg rilmenidine (3.0 to 4.8 mg, mean 3.85 mg). The electrophysiologic study was repeated in 8 other hypertensive patients receiving 50 micrograms/kg of rilmenidine (3.2 to 4.4 mg, mean 3.90). In contrast to the results obtained at the dose of 50 micrograms/kg, there was no significant variation in pulmonary arterial pressure, cardiac index or stroke index after administration of 25 micrograms/kg. No significant variation was observed in heart rate, sinus function, conduction parameters or atrial, nodal and ventricular refractory periods after administration of 25 and 50 micrograms/kg. Rilmenidine, after single oral administration at the 25 micrograms/kg dose, led to a significant reduction in blood pressure and peripheral resistance without any significant change in cardiac output; the 25- and 50-micrograms/kg doses led to no alteration in heart rate and cardiac electrophysiology.

Forty patients with normal resting ECGs and a history of paroxysmal junctional tachycardia underwent endocavitory electrocardiography. Accessory atrioventricular pathways were demonstrated in 34 patients (82.5%), 14 of whom (35%) had Kent bundles. The ventriculo-atrial conduction time during ventricular stimulation was constantin 85% of the 40 patients but increased after injection of striadyne (ATP). This may suggest a reentry circuit partially bypassing the atrioventricular node.

The authors have studied the haemodynamic role of atrial systole in patients in the acute stage of a myocardial infarction, usually with left ventricular failure. Their main comparison is between the results obtained with stimulation of the right ventricle at a fixed rate and those obtained with bifocal stimulation, thus restoring the atrio-ventricular sequence. The authors discuss their results, and especially their findings of improvement in cardiac output and systemic arterial blood pressure. They raise the question of synchronous stimulation in cases of infarction with heartblock complicated by left ventricular failure, and also of re-establishing sinus rhythm in cases of arrhythmia of supraventricular origin.

Bidirectional ventricular tachycardia, defined as the rapid alternation of the QRS complexes with successive opposing axial deviation, is a rare arrhythmia. In the rare cases which have undergone endocavitary investigations, an infrahisian origin has generally been proved. However, the mechanism of these tachycardias remains poorly understood and is discussed with respect to a new case. Bidirectional tachycardia occurred in a 79 year old woman with previous diaphragmatic and anterior wall infarction. It was a wide QRS tachycardia at 180/min with a succession of ventriculogrammes of opposing axis in the frontal plane and permanent right bundle branch block over the right precordium. The two types of tachycardia were observed, monomorphic type A or Type B or a combination of the two realising an A-B bidirectional tachycardia. The origin of these episodes, which occurred on a background of atrial tachycardia at about 100/min, was ventricular as shown by the absence of a His potential before the ventricular complexes in tachycardia. The presence of ventricular extrasystoles with relatively fixed coupling intervals, and the results of endocavitary investigation were suggestive of a reentry phenomenon ventricular extrastimuli were capable of transforming the bidirectional into monomorphic tachycardia and vice versa; this suggests that A was at times the origin of a reentry B, but protected by A, tachycardia B could be sustained. In the light of previously reported cases with documented endocavitary investigation and this new case, it seems possible to talk in terms of true "bidirectional ventricular tachycardia", a tachycardia whose mechanism is obscure but certainly not univocal.

Elastolysis of insoluble elastin by Pseudomonas aeruginosa elastase was found to be less specific (higher apparent Km value) but more active (higher activity) than with pancreatic elastase. Furthermore, pancreatic and P. aeruginosa elastases act synergistically during the initial stages of elastolysis. After extensive hydrolysis, the size distribution of digestion products was lower with P. aeruginosa than with pancreatic elastase. The higher extent of hydrolysis may be explained by the fact that, if pancreatic elastase needs at least six sub-sites for activity, P. aeruginosa elastase may hydrolyse tetrapeptides such as tetraalanine, or synthetic substrates such as furylacryloyltripeptides FA-X-Leu-Y, X and Y being Gly and/or Ala.