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Biomedical subjects

L Alcidi

Publications and source records attributed to L Alcidi.

6 recordsLinked to original sources

Implantable pharmacological defibrillator (AIPhD): preliminary investigations in animals.

The treatment of ventricular fibrillation (VF) by means of automatic implantable cardioverter defibrillators (AICD) poses many severe problems and limitations at the present time. In order to overcome these problems, we propose a totally new way to terminate VF or ventricular sustained tachycardia (VST). Our proposal consists of replacing the electric shock, which is dangerous, delayed, and sometimes ineffective, with a "chemical" shock: i.e., a chemical bolus retroperfused in the coronary sinus (CS) immediately after VF arises. The possible device is hypothesized and preliminary investigations in animals, performed to verify the theoretical assumption, are presented. In rabbits, and in larger animals (sheep and swine). Drugs were perfused in the coronary bed: lidocaine was used in 86% and bretylium tosylate in 14% of the animals. The results were: lidocaine immediately terminated VF in 100% and sinus rhythm was restored in rabbits; lidocaine terminated VF in VST in sheep; and in swine, bretylium immediately produced sinus rhythm in one case; in another one, only delayed sinus rhythm was achieved but lasted a short time; in the last case ventricular tachycardia at 128 beats/min appeared. Because new drugs, which are really "defibrillating" drugs, are available (bretylium tosylate, bethanidine, clofilium, tricyclic antidepressants, phenotiazine derivatives), we plan to investigate these defibrillating drugs in isolated hearts, found in suitable animals like dogs (sheep and swine are difficult to defibrillate) and in humans during routine electropharmacological studies.

Animals

[Electrocardiogram simulation. A theoretical model of ischemia].

Using an electric circuit model, made of two segments formed of sections that behave electrically as subendocardial and subepicardial cells, we simulated myocardial ischemia in one of the two segments. The changes in the ST segment and in the T wave were obtained respectively by diminishing the intercellular potential from -90 mV to -60 mV and by shortening or prolonging the duration of action potentials. In order to simulate acute subendocardial, subepicardial and transmural ischemia, the potentials of the internal section, the outer section, and of both sections were diminished respectively. The ST segment appeared depressed both in the segment involved and in the undamaged one in subendocardial ischemia. In subepicardial ischemia it appeared elevated in the segment involved and was normal in the undamaged one. In transmural ischemia it was elevated in the segment with reduced potential and it was depressed in the undamaged segment. The depression of the ST segment in the undamaged part, both in subendocardial ischemia and in transmural ischemia, depends on the imbalance of the central point and therefore the whole subendocardial layer behaves electrically as if it really were ischemic. The T-wave changes in acute ischemia are in keeping with those of the ST segment.

Action Potentials

Preliminary experience with the pH-triggered pacemaker.

A cardiac pacemaker capable of responding to blood acidosis by change in its stimulation rate allows adjustment to a patient's metabolic needs. The blood pH is sensed by an iridium oxide electrode in the right atrium. During exercise, the venous pH decreases and the paced ventricular rate increases. If acidosis persists, the paced rate gradually returns to baseline and reaches it after about 70 minutes. A pH-triggered pacemaker has been implanted in a 72-year-old male. The pacemaker remained responsive one year after implant, increasing rate during exercise, cold pressor stress, ischemia of the arms and emotional stress.

Aged

[Clinical and biological aspects in patient with pH-triggered implanted pacemaker (author's transl)].

The Authors have selected the variations of blood pH to drive the pacing rate according to the new biological balance created by exercise. The clinical tests performed on the patients who have had a pH-triggered pacemaker implanted one year previously demonstrated that: a) during physical exercise there is an increase of cardiac rate triggered by the pacemaker, comparable with that noted when sinus rhythm is present; b) situations causing an increased production of cathecolamines and thus a pH variation--Cold Pressor Test, Ischaemic Test, as well as emotional stress--cause an increase of the stimulation rate of pH triggered pacemaker.

Blood