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Biomedical subjects

V Rehan

Publications and source records attributed to V Rehan.

9 recordsLinked to original sources

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

Specificity of a placental factor inhibiting breathing in fetal sheep.

We have found previously that the infusion of a placental extract inhibits breathing induced by 100% O2 plus umbilical cord occlusion in the fetal sheep, suggesting that a placental factor is responsible for the inhibition of fetal breathing. To test whether this factor is specific to the placenta and whether it also inhibits spontaneous fetal breathing (occurring in the absence of cord occlusion), we administered extracts from the placenta, muscle and liver of the pregnant ewe, extracts of fetal liver, and Krebs solution to 16 chronically instrumented fetal sheep at 135 +/- 5 days of gestation. Infusions were made during low-voltage electrocortical activity, 5 to 15 min after a switch from high voltage, when breathing was well established. Within 90 s of the infusion of the placental extract in the carotid artery of the fetus, breathing decreased in 79% (33/42) of the experiments and was completely abolished in 71% (30/42) of them (P < 0.0001 compared with the other infusates). No apnoeas were observed with the Krebs solution (0/19) and the maternal muscle (0/20). Extracts of maternal and fetal liver abolished breathing in only 17% (4/23) and 21% (6/29) of the experiments respectively (NS compared with Krebs solution). There were no significant changes in blood gas tensions, pH, blood pressure and heart rate associated with the infusion of the extracts. The electrocortical activity (ECoG) switched from low to high voltage in 50% of the experiments using placental extract compared with 0% with Krebs solution and maternal muscle, and with 9% and 17% with maternal and fetal liver respectively (P < 0.005). Breathing output (integral of EMGdi x f) during and after the infusions significantly decreased only with the placental extract. These findings indicate the presence of a factor produced by the placenta which inhibits fetal breathing and may be responsible for the normal inhibition of breathing observed in fetal life.

Animals

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

Effect of baseline oxygenation on the ventilatory response to inhaled 100% oxygen in preterm infants.

We tested the hypothesis that the immediate (< 1 min) ventilatory response to 100% O2 in preterm infants, a test of peripheral chemoreceptor activity characterized by a decrease in ventilation due to apnea, is more pronounced at lower baseline O2 concentrations. We studied 12 healthy preterm infants [birth weight 1,425 +/- 103 (SE) g; study weight 1,670 +/- 93 g; gestational age 30 +/- 1 wk; postnatal age 27 +/- 7 days] during quiet sleep. The infants inhaled 15, 21, 25, 30, 35, 40, and 45% O2 for 5 min in a randomized manner (control period), followed by 100% O2 for 2 min, and then the same initial O2 concentration again for 2 min (recovery period). A nose piece and a flow-through system were used to measure ventilation. The immediate decrease in ventilation with 100% O2 was 46% on 15% O2, 24% on 21% O2, 11% on 25% O2, 8% on 30% O2, 12% on 35% O2, and 8% on 40% O2; there was no decrease on 45% O2 (P < 0.01). The corresponding mean duration of apnea was 29 s during 15% O2, 18 s during 21% O2, 8 s during 25% O2, 9 s during 30 and 35% O2, and 3 s during 40% O2; only one infant developed a 5-s apnea during 45% O2 (P < 0.001). The findings suggest that 1) the ventilatory decrease in response to 100% O2 is dependent on the baseline oxygenation, being more pronounced the lower the baseline O2 concentration; and 2) this ventilatory decrease is entirely related to more prolonged apneas observed with lower baseline O2 concentrations. We speculate that the peripheral chemoreceptors, being so active in the small preterm infant with relatively low arterial PO2, are highly susceptible to changes in PO2, and this makes them prone to irregular or periodic breathing, especially during sleep.

Apnea

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

Spinal cord injury at birth: diagnostic and prognostic data in twenty-two patients.

OBJECTIVES: To establish criteria, evident soon after birth, that predict long-term outcome of neonates with spinal cord injury (SCI) at birth. DESIGN: Retrospective case-series. SETTING: Five Canadian regional neonatal tertiary care centers. PATIENTS: Consecutive samples of patients referred to five centers for a total of 22 subjects, in whom SCI was diagnosed during life. Sites of lesions were above the fourth cervical vertebrae (n = 14), at the fourth cervical to the fourth thoracic vertebrae (n = 6), and at the thoracolumbar region (n = 2). MEASUREMENTS AND MAIN RESULTS: All 14 patients with upper cervical SCI had cephalic presentations, whereas all 6 patients with cervicothoracic SCI had breech presentations (p < 0.0001). The site and extent of lesion were best diagnosed by clinico-imaging correlations. Ultrasonography appeared to be the most useful imaging study. In patients with upper cervical SCI who had no coexistent central nervous system abnormality associated with early death, long-term outcome in survivors (dependency on mechanical ventilation and on aids for upper limb activity and for ambulation) was best predicted by age when breathing was first observed and by rate of recovery of limb motor function in the first 3 months. The presence of breathing movements on day 1 (n = 2) was associated with mild disability. The absence of breathing movements on day 1 and little or no recovery of motor function in the first 3 months was associated with permanent total dependency on mechanical ventilation and severe quadriplegia (n = 5). Apnea on day 1 and intermediate recovery rates in the first 3 months was associated with variable long-term prognoses (n = 3).

Birth Injuries