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Biomedical subjects

M Manoach

Publications and source records attributed to M Manoach.

At least 55 records · Page 3Linked to original sources
PubMed1980

Ventricular self-defibrillation in mammals: age and drug dependence.

Ventricular fibrillation (VF) was electrically induced in cats, rabbits, guinea pigs and rats. In young animals of all species and also in old rats short transient VF (TVF) was followed by spontaneous reversion to normal sinus rhythm. Old cats, rabbits and guinea pigs had episodes of sustained VF (SVF) which did not terminate spontaneously; artificial electro-defibrillation was required. Dibenzepin converted the sustained response of old animals to a transient one. Verapamil antagonized the effect of dibenzepin in old animals and also changed the TVF in young animals to SVF. The effect of calcie age of the animal is an important factor in determining whether the fibrillatory red to an alteration in the properties of the cell membrane.

Aging↗
PubMed1979

Dibenzepin as an antifibrillatory agent for spontaneously terminating electrically induced ventricular fibrillation.

The effect of dibenzepin, a tricyclic antidepressant drug, on electrically induced ventricular fibrillation was studied in 20 cats and nine dogs. The ventricular fibrillation threshold and the ability of the ventricle to defibrillate spontaneously were determined before and after the administration of dibenzepin, with each animal serving as its own control. The drug raised the ventricular fibrillation threshold in all the animals tested. Before treatment, spontaneous ventricular defibrillation occurred in only 8 of the 20 cats and in none of the dogs. After treatment, all of the cats and eight of the dogs exhibited spontaneous ventricular defibrillation. The study of drugs that have a self-defibrillatory effect may serve to further understanding of the mechanism of ventricular fibrillation and its spontaneous termination.

Animals↗
PubMed1977

Mammalian embryo: a model for congenital prolonged QT syndrome.

The QT interval has been studied in ECG in mouse and rat embryos during two stages of development. The QT interval during the early stage of development is prolonged and an ST segment clearly exists. Both disappear during fetal development and do not exist in adult animals in which the T wave immediately follows the QRS. Mammalian embryos have therefore been proposed as a model for the study of QT prolongation. It is suggested that the origin of the QT prolongation in the young embryos is caused by the prolonged duration of the action potentials of the primordial cardiac tissue. During embryonic development this tissue becomes organized as a conductive system surrounded by "neomyocardial" tissue with a shorter duration of action potential, which causes the shorter QT interval at this stage. Our working hypothesis is that the pathogenesis of the prolonged QT syndrome in children could be interpreted as an incomplete or delayed differentiation between the primordial or primordial-like myocardium retaining prolonged action potential duration, and "neomyocardium" with short duration.

Animals↗