48 research outputs found
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Effects of Epinephrine on the Cardiorespiratory Response to Hypoxia in Sedated Newborn Piglets with Intact and Denervated Carotid Bodies
In order to evaluate the effects of epinephrine on the cardiorespiratory response to hypoxia in the neonate, 35 sedated, spontaneously breathing newborn piglets (X ± SD, age 5 ± 0.8 days; weight 1.6 ± 0.3 kg) with intact (ICB) or denervated (DCB) carotid bodies were studied before and during an infusion of saline or epinephrine (2.2 ± 1.0 μg/kg/min, i.v.). Cardiorespiratory measurements were performed while the animals breathed room air and after 10 min of hypoxia (FiO2 0.10) during saline or epinephrine infusion. During epinephrine infusion, the ICB animals had a sustained increase in minute ventilation during hypoxia while the control group showed a biphasic ventilatory response with depression during sustained hypoxia. After the chemodenervation, the ventilatory response to hypoxia was completely blunted in saline and epinephrine animals. In the ICB and DCB animals, the arterial blood pressure decreased significantly with hypoxia during epinephrine infusion, while cardiac output increased significantly in all ICB and DCB saline animals. The oxygen consumption (VO2) decreased significantly after 10 min of hypoxia in all groups except in the ICB epinephrine animals, in whom the VO2 did not change with hypoxia. In conclusion, the administration of epinephrine to newborn piglets reverses the depressed ventilatory response to hypoxia and this effect requires the activity of the peripheral chemoreceptors
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A Simple Method for Measuring Functional Residual Capacity by N2 Washout in Small Animals and Newborn Infants
Serial determination of pulmonary function in infants with chronic lung disease
Pulmonary function was measured in 39 infants with chronic lung disease who had required mechanical ventilation starting during the first week of life for a median of 9 days (range 1 to 46 days) and supplemental oxygen for a median of 48 days (range 28–162 days). Their mean birth weight was 1140 g (range 550 to 2325 g), and mean gestational age 29.8 weeks (range 26 to 37 weeks). Ventilation was measured by pneumotachography, esophageal pressure through a water-filled feeding tube, and functional residual capacity (FRC) by a modified nitrogen washout technique. Lung compilance, pulmonary conductance, and FRC were determined at 1, 3, 6, 12, 18, 24, and 36 months after birth. Pulmonary function was also determined in 40 normal children, ranging in age from neonates to 5 years, who served as controls. In infants with chronic lung disease, growth in weight and length followed the 10th to 25th percentiles of the normal curve. Minute ventilation and respiratory effort remained elevated throughout the follow-up. FRC per kilogram of body weight was decreased at 1, 3, and 6 months after birth, but thereafter was in the normal range. FRC increased in proportion to weight at the same rate as in the controls. Lung compliance was only half of normal at 1 month, increased with growth in close correlation with weight, and was approximately 80% of normal at the end of follow-up. Pulmonary conductance was 50% of normal at 1 month, increased little during the first 6 months, but reached 85% of normal at 3 years of age. There was no evidence of gas trapping. These results indicate that in infants with chronic lung disease after mechanical ventilation, lung volume increases normally, probably by formation of new alveoll, which also leads to improvement in lung compliance. Airway growth is slow during the first 6 months after birth, but the subsequent faster growth leads to conductance values close to normal at 3 years of age
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Decreased ventilatory response to hypoxia in sedated newborn piglets prenatally exposed to cocaine
OBJECTIVE: Infants exposed to cocaine in utero have been reported to have a higher incidence of apnea and altered ventilatory response to carbon dioxide and hypoxia. We investigated whether in utero cocaine exposure results in greater ventilatory depression during hypoxia in piglets.
METHODS: Cocaine hydrochloride, 1.0 or 2.0 mg/kg given intramuscularly, or saline solution was administered daily to pair-fed pregnant sows during the last month of gestation. Thirteen cocaine-exposed piglets (mean ± SD: age, 4.4 ± 1.3 days; weight, 2.10 ± 0.10 kg) and 15 saline solution-exposed piglets (age, 4.6 ± 1.1 days; weight, 2.32 ± 0.42 kg) were studied under chloral hydrate sedation. Minute ventilation (v̇
E), arterial blood pressure (BP), heart rate (HR), oxygen consumption (v̇
O
2), and arterial blood gases were measured in room air. During hypoxia (fraction of inspired oxygen = 0.10), the values for v̇
E, BP, and HR were obtained at 1, 5, and 10 minutes, v̇
O
2 was calculated during the last 5 minutes, and arterial blood gas samples taken after 10 minutes.
RESULTS: Basal v̇
E did not differ between saline solution- and cocaine-exposed animals. The increase in v̇
E at 1 minute of hypoxia was also similar. However, at 5 and 10 minutes of hypoxia, v̇
E was significantly lower in the cocaine group than in the saline group (6% ± 9% and 4% ± 10% vs 15% ± 13% and 21% ± 14%;
p <0.02). Mean baseline BP and the initial increase in BP during hypoxia were not different between groups. However, BP remained increased throughout hypoxia only in the saline solution-exposed animals (
p
<0.05). Changes in HR, v̇
O
2, arterial oxygen tension, and base excess during hypoxia were similar between groups.
CONCLUSIONS: These results show a decrease in the ventilatory response to hypoxia in newborn piglets prenatally exposed to cocaine. This change is most likely to be centrally mediated because the initial hypoxic hyperventilation was not modified by the intrauterine cocaine exposure. This decrease in ventilation cannot be explained by changes in metabolic rate or in cardiovascular or acid-base status. (J P
EDIATR 1996;128:389-95
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Brainstem Amino Acid Neurotransmitters and Ventilatory Response to Hypoxia in Piglets
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Effects of Intermittent Nebulization of NONOate, DPTA/NO, on Group B Streptococcus-Induced Pulmonary Hypertension in Newborn Piglets
Background: A single dose of NONOate attenuates pulmonary hypertension (PH) induced by group B Streptococcus (GBS) infusion and this is accompanied by a decrease in systemic vascular resistance (SVR). Objective: The objective of the study was to determine whether two doses of the NONOate sustain the attenuation in GBS-induced PH without further systemic compromise. Methods: 15 anesthetized newborn piglets were randomized to receive placebo (n = 8) or two doses of nebulized DPTA/NO (n = 7) at 15 and 75 min after GBS-induced PH. Pulmonary artery (Ppa) and systemic (Psa) pressures, cardiac output (CO) and arterial blood gases were obtained at baseline and every 15 min until 180 min during GBS infusion. Results: Ppa and pulmonary vascular resistance (PVR) decreased significantly after the first dose of nebulized DPTA/NO and this effect was maintained after the second dose. Psa and SVR decreased after the first dose of DPTA/NO to values close to baseline and no further changes in systemic circulation were observed with repeated treatment. PVR/SVR increased with GBS infusion, but decreased after the first dose of DPTA/NO and remained significantly lower for 180 min. CO was significantly higher in the DPTA/NO group. Changes in Ppa, PVR, Psa, SVR, and CO with GBS infusion were not modified by placebo infusion. PaCO2, base deficit, and pH did not differ between groups. PaO2 was significantly lower in the DPTA/NO group after the second dose. Conclusion: These data demonstrated that GBS-induced PH is attenuated with two doses of DPTA/NO without significant systemic effect. The vasodilatory effect is more pronounced in the pulmonary than in the systemic vasculature, as suggested by lower PVR/SVR in the DPTA/NO group. We speculate that NONOates may have a clinical application in the management of PH in neonates