P724
Physiol Bohemoslov 1990;39(5):435-42
Breathing of phrenicotomized rats.
Nacházel J, Paleček F.
Institute of Pathological Physiology, Faculty of Paediatrics, Charles
University, Prague.
Bilateral paralysis of the diaphragm can result in normo or
hypoventilation, according to the species studied. Our aim was to
ascertain the results of bilateral phrenicotomy in the rat and, if
hypoventilation should be present, to try to identify its
pathophysiology. We used 33 male rats under urethane anaesthesia (1.3
g/kg i.p.). They were divided into three groups: control animals, rats
with bilateral phrenicotomy and a group with two doses of pentobarbital
(25 mg/kg i.p. each) on top of the urethane anaesthesia. We observed
pronounced hypoventilation both in the rats after phrenicotomy and those
with pentobarbital. At comparable levels of hypoventilation (PaCO2 =
5.61 0.28 kPa immediately after phrenicotomy and 5.91 0.25 kPa
after the first dose of pentobarbital; and 7.21 0.47 kPa 4 hours
after phrenicotomy and 7.38 0.39 kPa after the second dose of
pentobarbital) the only difference was a longer relative duration of
inspiration in phrenicotomized rats; (0.39 0.04 and 0.34 0.04
after phrenicotomy; 0.32 0.04 and 0.24 0.05 in rats after
pentobarbital). Immediately after phrenicotomy and 2 and 4 hours later,
and also after both doses of pentobarbital breathing was stimulated by
hypoxia and hypercapnia due to the additional external dead space (0.5
ml) for 5 min. There was no pronounced differences in the ventilatory
response to the dead space between the two groups; the response changed
from an isocapnic (in control rats and before phrenicotomy or
pentobarbital) to an isoventilatory one (four hours after phrenicotomy
and after the second dose of pentobarbital). The rats after the second
dose of pentobarbital did not, however, survive the added dead
space.(ABSTRACT TRUNCATED AT 250 WORDS)