Tracheostomized cats and piglets demonstrate respiratory stimulation d
uring experimental seizures, whereas airway intact piglets demonstrate
hypoventilation and increased subglottic resistances. The purpose of
this study was to characterize the role of the vocal folds in contribu
ting to these increased subglottic resistances during experimental sei
zures. A controlled animal study was performed in six anesthetized, sp
ontaneously breathing, hyperoxic piglets who had subglottic pressure a
nd airflow measured. A fiberoptic video scope directed into the cephal
ad trachea recorded subglottic images of the vocal folds. Glottal area
patency (GAP) was evaluated at inspiratory onset (I-o), peak inspirat
ory pressure (I-p), and expiratory onset (E(o)) for four to five conse
cutive breaths under baseline control, ictal, interictal, and anticonv
ulsant conditions. Seizures were induced with i.v. pentylenetetrazol o
r bicuculline. Normalized GAP was greatest at I-p under all conditions
, except anticonvulsant. During ictal periods, piglets demonstrated si
gnificant reductions in mean GAP throughout the respiratory cycle (I-o
, 98%; I-p, 78%; E(o), 98%), compared with baseline (p < 0.001, repeat
measures analysis of variance). During ictal discharges, hypoventilat
ion and glottal obstruction resulted in significant reductions in mean
arterial pH (-0.35) and PaO2 (-39 kPa) and elevations in PaCO2 (+8.1
kPa), compared with baseline conditions. During interictal conditions
mean GAP at I-p was increased, whereas at E(o) (-66%) GAP was reduced,
compared with control. These data demonstrate that the vocal folds ar
e tonically adducted throughout the respiratory cycle during ictal pha
ses and have increased expiratory adduction during interictal phases o
f seizures induced with standard i.v. convulsants in hyperoxic piglets
.