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Biomedical subjects

J Nacházel

Publications and source records attributed to J Nacházel.

7 recordsLinked to original sources
PubMed1993

Respiration after phrenicotomy and hydrocortisone treatment in anaesthetized rats.

The study was designed to determine the extent to which respiratory muscle wasting, resulting from corticosteroid-induced atrophy, may affect respiration in normal rats and in rats with denervated diaphragm. Twenty four male Wistar rats were divided into four groups: 1) controls with sham operation (SX) and vehicle injections: 2) SX with eight hydrocortisone (HC) injections (60 mg.kg-1.day-1 i.m.); 3) phrenicotomized (PX), injected with vehicle; 4) PX and HC-treated. HC treatment was started on the thirteenth day after surgery. Under urethane anaesthesia, tidal volume, respiratory rate, arterial carbon dioxide tension (PaCO2) and occlusion pressure were measured at rest and after 5 min of stimulated-breathing induced by added dead space 22nd day after surgery. All HC-treated animals decreased body weight by 32% compared to untreated rats. The diaphragm weight was reduced in PX rats by 29%, and after HC by 44%, while in PX rats with HC treatment diaphragm weight decreased by only 21%. PX rats (HC-untreated) had the lowest minute ventilation and occlusion pressure. There was no difference in ventilation between control and both HC-treated groups at rest. However, ventilation in PX and HC-treated rats did not increase upon stimulation, and the occlusion pressure increased significantly only in the HC-untreated animals. We conclude that in the rat, HC treatment did not affect resting ventilation, but it impaired ventilation performance, during increased demand, in animals handicapped by diaphragm denervation.

Anesthesia, General↗
PubMed1992

Hypoventilation after acute phrenicotomy of the urethane anaesthetized rats.

The aim of this study was to explore the mechanism resulting in hypoventilation in rats with denervated diaphragm. Bilateral cervical phrenicotomy (PX) was performed in 15 male rats anaesthetized with urethane (1.3 g/kg i.p.); other 8 rats were sham operated (SX). Ventilation, PaCO2 and the integrated EMG of the external intercostal muscles (iEMG) were measured before and after the surgery, at regular intervals, up to 4 hours postoperatively. During the 4 hours after PX there was a progressive decrease in minute ventilation and an increase in PaCO2 compared with the control values and with that in the SX rats. The increase in PaCO2 was accompanied by an increase in the peak amplitude of the iEMG to 155 +/- 18% of control values after PX and to 228 +/- 33% 4 hours later. Despite the augmented EMG activity tidal volume gradually decreased. The iEMG of the intercostal muscles, however, did not reach a maximum because the shortlasting stimulation of breathing by acute hypercapnia and hypoxia as the result of added dead space (0.5 ml) increased the iEMG still further. These results indicate that both the central and peripheral mechanisms contribute to hypoventilation in anaesthetized rats with denervated diaphragm.

Anesthesia↗
PubMed1990

Breathing of phrenicotomized rats.

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)

Animals↗
PubMed1990

Aminophylline enhances ventilation in phrenicotomized rats.

The aim was to test the effects of aminophylline (AP) on breathing of phrenicotomized rats. Fifty seven male rats of the Wistar strain were anaesthetized with 1.3 g.kg-1 urethane i.p. They were phrenicotomized, divided into 6 groups and given 5, 10, 20, 40 and 80 mg.kg-1 AP i.v. or a corresponding volume of saline. Ventilation, tracheal occlusion pressure and arterial blood gases were measured. In all animals phrenicotomy resulted in hypoventilation with corresponding hypoxaemia (from control 11.9 +/- 1.0 to 10.4 +/- 0.8 kPa) and hypercapnia (from control 4.6 +/- 0.5 to 5.5 +/- 0.6 kPa). In the control group (with saline) 4 h later the PaO2 was 8.6 +/- 1.1 kPa and PaCO2 7.2 +/- 0.6 kPa. After AP 1 h after phrenicotomy the minute ventilation increased in a dose-dependent manner by 1-66%. 4 h after phrenicotomy the minute ventilation of rats with 20 and 40 mg.kg-1 of AP was significantly higher than that of the control group. AP prevented hypoventilation when injected into phrenicotomized rats. The results give no unequivocal basis from which to decide the proportion of central and peripheral effects of AP.

Aminophylline↗
PubMed1986

Hyperthermic effect of neurotensin in the rabbit.

Neurotensin injected into the anterior hypothalamus of the rabbit induces a consistent upward shift of the threshold core temperatures for inducing cold thermogenesis, peripheral vasomotor tone and respiratory evaporative heat loss, while leaving the efficiency and the intensity of these thermoregulatory outputs unchanged. Neurotensin injections into the PH are without effect on body temperature control. The effect of neurotensin is interpreted as a selective inhibition of activity of warm sensors in the anterior hypothalamus. The possible mediating role of dopaminergic pathways in the neurotensin action is discussed.

Animals↗