Biomedical subjects

B Nowaczyk

Publications and source records attributed to B Nowaczyk.

9 recordsLinked to original sources

PubMed1998

Effect of norepinephrine on fetal breathing in sheep.

We tested the hypothesis that the surge of norepinephrine at birth is associated with the establishment of continuous breathing. Therefore, we studied whether the administration of norepinephrine could enhance fetal breathing during administration of oxygen, or 100% O2 plus cord occlusion, and if phenoxybenzamine would reverse these changes. Fetal sheep were instrumented in late gestation to measure electrocortical activity and diaphragmatic electromyography. These parameters and blood gases were measured before and during in utero administration of nitrogen, 100% O2, 100% O2 plus umbilical cord occlusion, and subsequently during umbilical reperfusion and recovery. Nine fetuses (14 experiments) received continuous norepinephrine (0.13 microgram/kg/min) throughout the experiment while 9 other fetuses (18 experiments) underwent the same treatment without the hormonal infusion. We found that norepinephrine inhibited the breathing induced by 100% O2 plus cord occlusion, despite a significant increase in the duration of low-voltage electrocortical activity; phenoxybenzamine reverted these changes. The findings suggest that the surge of norepinephrine at birth is probably not the primary mechanism for establishment of continuous breathing.

Adrenergic alpha-Agonists↗

PubMed1996

The biphasic ventilatory response to hypoxia in preterm infants is not due to a decrease in metabolism.

The mechanism underlying the biphasic ventilatory response to hypoxia in neonates is poorly understood. Because alveolar PCO2 (PaCO2) decreases and remains low during hypoxia, it has been argued that a decrease in metabolism may occur. We hypothesized that if the late decrease in ventilation during hypoxia is due to a decrease in CO2 production, an increase in PACO2 should abolish it. We studied 27 preterm infants [birth weight, 1,700 +/- 41 g (mean +/- SEM); study weight, 1,760 +/- 36 g; gestational age 32 +/- 0.2 weeks; postnatal age, 17 +/- 1 days]. A flow-through system and Beckman analyzers were used to measure ventilation and alveolar gases. Metabolism was expressed as changes in oxygen consumption. Infants were studied randomly during hypoxia alone (15% O2 + N2, n = 55) and during hypoxia plus CO2 (0.5% CO2, n = 30; 2% CO2, n = 10). Each experiment consisted of 2 minutes of control measurements (21% O2), 5 minutes of measurements during hypoxia alone or hypoxia plus CO2, followed by 2 minutes of recovery (21% O2). We found a biphasic response to hypoxia with or without CO2 supplementation, the percent change in ventilation from initial peak hyperventilation to late hypoventilation at 5 minutes being -16 +/- 2 on 15% O2; -9 +/- 3 on 15% O2 + 0.5% CO2; and -15 +/- 9 on 15% O2 + 2% CO2 (P < 0.05). The decrease in ventilation was primarily due to a significant decrease in frequency; tidal volume increased. Oxygen consumption decreased similarly with the various inspired gas mixtures during hypoxia. These findings indicate that the decrease in ventilation during hypoxia is unlikely to be solely due to a decrease in metabolism since the late decrease in ventilation following initial hyperventilation still occurred despite the elimination of a fall in PACO2. We speculate that the mechanism underlying the late decrease in ventilation is likely of central origin, probably mediated through the release of inhibitory neurotransmitters.

Carbon Dioxide↗

PubMed1996

Influence of sleep state and respiratory pattern on cyclical fluctuations of cerebral blood flow velocity in healthy preterm infants.

To examine the influence of sleep state, respiratory pattern, and ventilation on cyclical fluctuations (CF) in cerebral blood flow (CBF) velocity (CBFV), we studied 21 'healthy' preterm infants: birth weight 1,790 +/- 162 g (SEM), study weight 1,960 +/- 165 g, gestational age 32 +/- 1 weeks, postnatal age 20 +/- 4 (range 8-57) days. The CBFV was measured using on-line pulsed Doppler ultrasound by insonating the middle cerebral artery. Breathing was measured using a flow through system. The sleep state was monitored according to conventional criteria. Three hundred and seventy-five epochs of 1 min each were analyzed; 207 during quiet sleep (QS) and 168 during rapid eye movement (REM) sleep. CFs in CBFV were detected in all babies. The frequency of CF ranged from 0.5 to 6 cycles/min. The proportion of epochs showing CF was similar during both sleep states (56% QS vs. 59% REM; p = NS). Although the mean CBFV (cm/s) was similar in these two sleep states, the mean coefficient of variation, a measure of CF amplitude, was significantly higher during REM as compared with QS (6 +/- 0.5 vs. 4.3 +/- 0.2%; p < 0.05). Similarly, the mean CBFVs were similar with various respiratory patterns, but the coefficient of variation was significantly higher in periodic and apneic patterns as compared with regular and irregular respiratory patterns (5.6 +/- 0.6% periodic, 5.6 +/- 0.3% apneic, 3.6 +/- 0.3% regular, and 4.1 +/- 0.5% irregular, p < 0.05). The amplitude of CF was associated with the variability of the heart rate (p < 0.05), but not with the variability of the respiratory measurements. These findings suggest: (1) REM sleep is associated with a greater CBF variability than QS, and (2) periodic and apneic breathing are associated with a greater CBF variability than regular or irregular breathing. We speculate that sleep state and respiratory pattern do not determine but modulate the CBF. Our data suggest that in studies involving interpretation of CBFV data using the Doppler technique, breathing patterns should be taken into account in addition to sleep state.

Apnea↗

PubMed1995

Prevalence and characterization of spontaneous oral breathing in preterm infants.

Oral breathing is an important defense mechanism, yet its prevalence and relationship to behavioral activities have not been studied in preterm infants. We tested the hypothesis that oral breathing is rare in these infants and likely to be restricted to periods of body movements. Ten healthy preterm infants (birthweight 1300 +/- 100 g [SE]; gestational age 29 +/- 1 weeks; postnatal age 36 +/- 7 days) were studied. Ventilation was measured with a nose piece and screen flowmeter. Oral breathing was detected with a carbon dioxide sampler at the mouth. Movements were classified according to intensity into type I (localized, minor signal distortion) and type II (generalized, moderate signal distortion). Oral breathing was present 10% of the time, with a mean duration of 27 +/- 3 seconds. Of 104 episodes of oral breathing, 13 (13%) occurred during type I movement, 89 (86%; p < 0.01) during type II, and 2 (2%) in the absence of movement. The delay from beginning of movements to the beginning of oral breathing was 20 +/- 3 seconds. Nasal minute ventilation decreased from 0.203 +/- 0.013 L.min-1.kg-1 during movements in the absence of oral breathing to 0.167 +/- 0.013 L.min-1.kg-1 during movements plus oral breathing (p = 0.017). In 496 type I and II movements, the prevalence of oral breathing was 21 of 165 (13%) in quiet sleep, 37 of 194 (19%) in rapid eye movement sleep, 6 of 12 (50%) in transitional sleep, and 44 of 125 (35%) in indeterminate sleep (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗

PubMed1994

The effect of nasal occlusion on the initiation of oral breathing in preterm infants.

The ability to switch from nasal to oral breathing in response to nasal obstruction is crucial for survival, and has been suggested to be an important mechanism in preventing sudden infant death syndrome (SIDS). To know whether the ability to switch from nasal to oral breathing is uniformly present during the early neonatal period, we examined the effects of slow and fast nasal occlusions on the establishment of oral breathing in preterm infants. Slow occlusions were used to mimic more closely occlusions occurring spontaneously. We studied 17 healthy preterm infants [birth weight, 1830 +/- 27 g (mean +/- SE); study weight, 1800 +/- 109 g; gestational age, 32 +/- 1 weeks; postnatal age, 12 +/- 2 days]. We used a nosepiece with a nasal occluder and a flow-through system to measure ventilation. A CO2 sampling catheter at the mouth was used to detect oral breathing. Of 58 occlusions, 29 were slow [resistance increasing slowly from 0 to infinite (occlusion)], and 29 were fast (infinite elastance applied in < 1 sec). Oral breathing was always established following slow and fast occlusions. In 44% of the slow occlusions, oral breathing started before complete occlusion. Arousal was observed in 12/58 (17%) of all occlusions, occurring primarily after initiation of oral breathing. Oxygen saturation and respiratory rate decreased significantly following occlusions, from 96 +/- 0.6 to 87 +/- 1.2% and 49 +/- 2.8 to 38 +/- 2 breaths/min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Obstruction↗

PubMed1993

A placental extract inhibits breathing induced by umbilical cord occlusion in fetal sheep.

Umbilical cord occlusion in the presence of adequate oxygenation induces continuous breathing and arousal in the chronic unanesthetized fetal sheep preparation. The mechanism responsible for this is unknown. We hypothesized that if a placental factor is responsible for the inhibition of breathing in the fetus, the administration of a placental extract while the fetus is breathing continuously after cord occlusion should reverse these changes. Thus, at about 10 min after the induction of continuous breathing by cord occlusion, we administered a placental extract and three subfractions separated by ultrafiltration to 14 chronically instrumented fetal sheep at 133 +/- 1 day gestation. The Krebs solution in which the placental extract was prepared was used as control. Within two minutes of the infusion of the whole placental extract in the carotid artery of the fetus, breathing output (integral of EMGdi x f) diminished in all experiments and was completely abolished in 15/17 (88%). Krebs solution had no effect on breathing. The infusion of subfractions of different molecular weight showed that the inhibition was primarily related to the subfraction between 3.5 and 10 kD. There were no significant changes in blood gas tensions, pH, blood pressure, and heart rate associated with the infusions of the extracts. The ECoG switched from low to high voltage in the majority of the experiments using whole extract and the subfraction 3.5 to 10 kD. These findings suggest that a placental factor, probably a peptide with a molecular weight between 3.5 and 10 kD, inhibits breathing in fetal life.

Animals↗

PubMed1992

The effects of gestational age and labour on the breathing and behaviour response to oxygen and umbilical cord occlusion in the fetal sheep.

We tested the hypothesis that the continuous breathing response to oxygen or oxygen plus umbilical cord occlusion, in the fetal sheep, could be modified by gestational age or labour. We studied 35 chronically instrumented fetal sheep on 84 occasions during late gestation (124 to 141 days), using our window model (Rigatto, 1984). After a resting cycle (1 low-voltage followed by 1 high-voltage electrocortical activity epoch), the fetal lung was distended via an endotracheal tube using mean airway pressure of about 30 cm H2O. Inspired nitrogen, and 100% O2 were given to the fetus during one cycle each. While on 100% O2 the umbilical cord was occluded using a balloon cuff. We found that: (1) the continuous breathing response to 100% O2 occurring in 8% of the experiments at a gestational age less than 130 days, in 25% from 130 to 134 days and in 45% at gestational ages greater than 134 days (P < 0.01); (2) at similar gestational age intervals the breathing responses to umbilical cord occlusion were 67%, 84%, and 100% (P < 0.01); and (3) in the presence of labour, 45% of the experiments responded to O2 with continuous breathing as compared to 23% in the absence of labour (P < 0.01). Cord occlusion did not affect these values. Because the highest PaO2 achieved increased significantly to 128 days but not thereafter it is unlikely that these results can be explained on the basis of an increase in PaO2 alone. We speculate that there is an age related maturation of the inhibition of breathing normally present in the fetus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

The effects of 21 or 30% O2 plus umbilical cord occlusion on fetal breathing and behavior.

We have shown previously that continuous fetal breathing can be induced by 100% O2 alone or combined with umbilical cord occlusion (Baier, Hasan, Cates, Hooper, Nowaczyk & Rigatto, 1990). To know whether it could also be induced by lower O2 concentrations plus cord occlusion, we studied 9 chronically instrumented fetal sheep (16 experiments) using our window model. After a baseline cycle [1 low voltage + 1 high voltage electrocortical activity (ECoG) epoch] the fetal lung was distended via an endotracheal tube to about 30 cm H2O. Inspired N2 (control) and 21 or 30% O2 were given for one cycle each. While on 21% or 30% O2 the umbilical cord was occluded (balloon cuff). In 10 out of 16 experiments breathing output (% maximum of integral of EMGdi x f) increased after cord occlusion from 80 +/- 48 (N2) to 2871 +/- 641 (SEM; P < 0.01); in 7 of them breathing became continuous. Arterial PO2 increased from 14 +/- 1 (N2) to 33.5 +/- 5 Torr (occlusion; P < 0.01). In the other 6 experiments breathing output decreased from 319 +/- 116 (N2) to 86 +/- 38 (occlusion; P < 0.01) and arterial PO2 changed from 18 +/- 1 (N2) to 22 +/- 5 Torr (occlusion; P = 0.4). Arterial PCO2 increased similarly after occlusion in both groups, those which did respond with increased breathing (to 46 +/- 2 Torr) and those which did not respond (to 48 +/- 3 Torr; P = 0.6). The percent low voltage ECoG and the behavioral score increased after occlusion in the responder group only.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Effects of various concentrations of O2 and umbilical cord occlusion on fetal breathing and behavior.

To test the hypothesis that continuous fetal breathing could be induced by hyperoxemia alone or by hyperoxemia and umbilical cord occlusion, even in the absence of a rise in arterial PCO2 (PaCO2), we studied 18 chronically instrumented fetal sheep on 34 occasions using our window model (18). After a resting cycle (1 low-voltage followed by 1 high-voltage electrocortical activity epoch), the fetal lung was distended via an endotracheal tube using mean airway pressure of approximately cmH2O. Inspired N2, 17% O2, and 100% O2 were given to the fetus during one cycle each. While 100% O2 was given, the umbilical cord was occluded (balloon cuff).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗