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Biomedical subjects

J A Ferrero

Publications and source records attributed to J A Ferrero.

14 recordsLinked to original sources

Exhaustive physical exercise causes oxidation of glutathione status in blood: prevention by antioxidant administration.

We have studied the effect of exhaustive concentric physical exercise on glutathione redox status and the possible relationship between blood glutathione oxidation and blood lactate and pyruvate levels. Levels of oxidized glutathione (GSSG) in blood increase after exhaustive concentric physical exercise in trained humans. GSSG levels were 72% higher immediately after exercise than at rest. They returned to normal values 1 h after exercise. Blood reduced glutathione (GSH) levels did not change significantly after the exercise. We have found a linear relationship between GSSG-to-GSH and lactate-to-pyruvate ratios in human blood before, during, and after exhaustive exercise. In rats, physical exercise also caused an increase in blood GSSG levels that were 200% higher after physical exercise than at rest. GSH levels did not change significantly. Thus, both in rats and humans, exhaustive physical exercise causes a change in glutathione redox status in blood. We have also found that antioxidant administration, i.e., oral vitamin C, N-acetyl-L-cysteine, or glutathione, is effective in preventing oxidation of the blood glutathione pool after physical exercise in rats.

Animals

[Prediction of the tachycardia cycle based on auriculoventricular re-entry. Experimental study in dogs].

Seven anaesthesized mongrel dogs subject to thoracotomy were used in a electronic simile of A-V accessory pathway with retrograde conduction to generate reentrant tachycardias with different ventriculo-atrial delays. This was done both under control conditions and following amiodarone i.v. administration. The ability to predict tachycardia cycle length was studied, using a mathematical model of the circuit, in which the cycle length is obtained from the function of nodal conduction and the time of extranodal conduction of the circuit. An analysis was made of the repercussions in using four different mathematical functions describing nodal conduction: three were non-linear (exponential and hyperbolic A and B) and one linear. In the case of the first three, the consequences of using a direct non-linear data-fitting procedure or an indirect procedure by linear transformations of the functions were studied. The exponential and hyperbolic B functions provide a better prediction of tachycardia cycle length on being used in the model; in the case of these functions, a mean value of the squared differences between the real and estimated values of 19.1 +/- 31.0 ms2 and 19.1 +/- 26.7 ms2, respectively, was obtained.

Animals

[Quantification of concealed conduction in the atrioventricular node].

Twenty-eight anaesthetized open-chest mongrel dogs were used. Programmed atrial pacing was used and Hisian electrograms recorded through endocavitary electro-catheters to study and quantify the concealed conduction of non-transmitted atrial impulses in the A-V node. An exponential model was used in three situations to quantify the nodal conduction during incremental atrial pacing: a) during 1:1 conduction, b) during 2:1 nodal block, and c) during pacing, coupling an atrial impulse delivered at fixed intervals and blocked in the A-V node to each transmitted impulse. The relation between intranodal conduction times was analyzed both with and without the presence of blocked impulses, and the quotient between the obtained functions in situations b, c and situation a was determined. In a subgroup of 13 dogs the study was repeated following pharmacological block of the autonomic nervous system. In dogs with autonomic block, this relation always tended to decrease when the atrial pacing rate increased. The variations in the group of dogs with intact autonomic nervous systems were not homogeneous. During pacing with coupled block impulses, the progressive removal of conduction curves obtained for each coupling interval with respect to those obtained during 1:1 transmission, expresses the interval with respect ot those obtained during 1:1 transmission, expresses the lesser influence of the blocked impulses on decreasing their coupling interval.

Animals

Effects of propafenone on induction and maintenance of atrioventricular nodal reentrant tachycardia.

Electrophysiologic studies were performed in 10 patients with atrioventricular (A-V) nodal reentrant paroxysmal supraventricular tachycardias (PSVT), before and after intravenous administration of propafenone (1.5 mg/kg). All patients utilized an A-V nodal slow pathway for anterograde conduction and an A-V nodal fast pathway for retrograde conduction of the reentrant impulse. Propafenone depressed retrograde fast pathway conduction which was manifested by: 1) complete V-A block at all ventricular paced cycle lengths after propafenone in 3 cases; 2) increase in mean +/- SD of ventricular paced cycle length producing V-A block from less than 308 +/- 37 ms to 432 +/- 63 ms in the remaining 7 patients. Nine of the 10 patients had induction of sustained PSVT before propafenone. In 7 of the 9, PSVT could not be induced or sustained after propafenone, reflecting depression of the retrograde fast pathway conduction with either absence of atrial echoes (5 patients) or induction of nonsustained PSVT, with termination occurring after the QRS (2 patients). In 1 patient, single atrial echoes were induced before propafenone but none were noted after the drug. In only 2 patients was a sustained PSVT inducible after propafenone. In conclusion, propafenone inhibited induction of sustained A-V nodal reentrant PSVT in most patients, reflecting depression of retrograde A-V nodal fast pathway conduction.

Adult

Function of atrioventricular node conduction: hyperbolic model.

Twenty four patients were subjected to an electrophysiologic clinical procedure. The conventional extrastimulus test was applied to verify the relation between conduction time increase through the atrioventricular node of the extrastimulus beat (delta AH), and its preceding interval (A1A2). Following the least square root method the parameters of the hyperbolic model delta AH.A1A2 = m . delta AH + n were adjusted. The correlation coefficients obtained and tested in all cases were very high and significant. From this hyperbolic equation it was possible to determine the equations for the effective refractory period (ERPe = m) and functional refractory period (FRPe = ERPe + n). The theoretical values for refractoriness approached very closely those of the actually measured ERP and FRP, in all cases. This model proved to be, in respect to adjustments and especially in calculating refractory periods, at least as good as the exponential model proposed previously by other authors.

Adolescent