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(Circulation. 2002;106:2301.)
© 2002 American Heart Association, Inc.
Brief Rapid Communications |
From the Laboratoire de Neurobiologie et Pharmacologie Cardiovasculaire (A.L., J.F., P.B.), Faculté de Médecine, Université Louis Pasteur, Strasbourg; Unité de Recherches dEpidémiologie Génétique (J.F.), INSERM-155, Faculté des Sciences de Jussieu, Paris; and Fédération de Pédiatrie (A.L., L.W., Y.A., I.M.S.-A., M.F., J.M.), Hôpital de Hautepierre, Strasbourg, France.
Correspondence to Angelo Livolsi, Laboratoire de Neurobiologie et Pharmacologie Cardiovasculaire, Faculté de Médecine, 11 rue Humann, 67000 Strasbourg, France. E-mail Angelo.Livolsi{at}chru-strasbourg.fr
Background The main purpose of our study was to define an animal model of vagal hyperreactivity and its genetic transmission.
Methods and Results We first investigated the vagal reactivity with phenylephrine in conscious rabbits. Barosensitivity and the maximal bradycardic response were measured at the upper mean blood pressure plateau. Hyperreactive (H) animals were selected and crossbred with normal (N) ones. Results showed no significant difference between calculated barosensitivity values after the different doses of phenylephrine. In contrast, an increase of the values and a great dispersion appeared 1 to 5 beats after the end of the ramp. Marked pauses (6000 to 20 000 ms) were obtained with some rabbits, which were blocked by atropine. A significant excess of hyperreactive offspring was observed in HxH crossings compared with NxN ones (39.4% male and 42.3% female offspring versus 14.4% and 4.4%, respectively). Few female offspring were hyperreactive compared with males in NxH and NxN crossings (4.1% versus 23.4% and 4.4% versus 14.4%, respectively).
Conclusions This study describes the first model of spontaneous vagal pauses. The inheritance could be polygenic with a partial sex-limited character.
Key Words: syncope arrhythmia genetics
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