Breathing of phrenicotomized rats.

Abstract

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)