| 1. |
|
|
| 2. |
- Hafström, Ola, 1960, et al.
(författare)
-
Cardiorespiratory effects of nicotine exposure during development
- 2005
-
Ingår i: Respir Physiol Neurobiol. - 1569-9048. ; 149:1-3, s. 325-41
-
Tidskriftsartikel (refereegranskat)abstract
- Exposure to tobacco smoke is a major risk factor for the sudden infant death syndrome. Nicotine is thought to be the ingredient in tobacco smoke that is responsible for a multitude of cardiorespiratory effects during development, and pre- rather than postnatal exposure is considered to be most detrimental. Nicotine interacts with endogenous acetylcholine receptors in the brain and lung, and developmental exposure produces structural changes as well as alterations in neuroregulation. Abnormalities have been described in sympathicovagal balance, arousal threshold and latency, breathing pattern at rest and apnea frequency, ventilatory response to hyperoxia or hypoxia, heart rate regulation and ability to autoresuscitate during severe hypoxia. This review discusses studies performed on infants of smoking mothers and nicotine-exposed animals yielding varying and sometimes inconsistent results that may be due to differences in experimental design, species and the dose of exposure. Taken together however, developmental nicotine exposure appears to induce vulnerability during hypoxia and a potential inability to survive severe asphyxia.
|
|
| 3. |
- Hafström, Ola, 1960
(författare)
-
Perinatal nicotine exposure. Effects on the defense against hypoxia in lambs
- 2002
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- The aim of the present study was to evaluate whether perinatal nicotine exposure could impair cardiorespiratory defense mechanisms to hypoxia. The rationale for this approach is that exposure to tobacco smoke, particularly before birth, is a risk factor for the sudden infant death syndrome as well as for obstructive airway disease in childhood. Chronically instrumented lambs were studied unanesthetized after birth. Ventilatory and cardiovascular variables were recorded in normoxia, acute hypoxia (0.1 FiO2) and brief hyperoxia (1.0 FiO2) in wakefulness (W) and quiet sleep (QS). Time from start of hypoxia to arousal from QS and hemoglobin oxygen saturation (SaO2) at arousal was measured.Arousal from QS was delayed during a low dose postnatal nicotine infusion (N) compared with control (C) and occurred at lower SaO2. The ventilatory response to hypoxia was similar during N and C in W, but was attenuated during N in QS. The blood pressure (BP) and heart rate (HR) responses to hypoxia were similar during N and C.Effects of prenatal nicotine (pN) exposure were studied in lambs exposed to a low dose of nicotine during the last trimester of pregnancy and compared with C. The ventilatory response to hypoxia was similar in the two groups during W, but was attenuated in pN lambs during QS. Arousal occurred later in pN lambs than C. The HR response to hypoxia was attenuated in pN lambs during both W and QS. The ventilatory response to hyperoxia was attenuated in pN lambs during both activity states. C lambs had lower resting minute ventilation ( ) during QS compared with W, whereas N lambs had similar resting during W and QS.Prenatally nicotine-exposed lambs (pN) had similar resting as C but a markedly different breathing pattern. At both 5 and 21 d of age, pN lambs had lower resting tidal volumes (VT) and higher respiratory rates than C. Inspiratory drive (P0.1) and effective impedance were higher in pN lambs compared with C only at 5 d of age. Combined pre- and postnatal nicotine exposure (ppN) had no significant effect compared with prenatal (pN) exposure alone on resting , resting P0.1 or resting effective impedance during both W and QS. Resting VT was significantly higher in ppN lambs than pN lambs during both W and QS. The ventilatory response to hypoxia and hyperoxia was similar in the two groups during both activity states. Time to arousal from QS was similar in the two groups. Resting HR and BP as well as HR and BP responses to hypoxia were similar in both groups during both activity states. Conclusions. Perinatal nicotine exposure blunts cardiorespiratory and arousal responses to acute hypoxia. These effects may be due to attenuation of carotid body oxygen chemoreceptors or the central respiratory integration of their input. Prenatal nicotine exposure affects postnatal breathing pattern indicating altered lung mechanics. Continued postnatal nicotine exposure after prenatal exposure does not further compromise defense mechanisms against hypoxia or the altered breathing pattern after birth. Nicotine substitution may not be safe during pregnancy.
|
|
| 4. |
|
|
| 5. |
- Silberberg, Ants, 1955, et al.
(författare)
-
Resuscitation in Preterm Infants; Extended Documentation of Procedures
- 2013
-
Ingår i: Pediatric Academic Societies Annual Meeting, May 4-7, 2013, Washington DC USA.
-
Konferensbidrag (refereegranskat)abstract
- Background: A lung protective strategy of ventilation is recommended during resuscitation in newborn infants limiting tidal volume to less than 8 ml/kg to reduce the risk of lung overdistention, volutrauma. As the mechanical properties of the respiratory system change rapidly after birth monitoring of respiratory function is recommended also during the first minutes of life to avoid lung injury (J Pediatr 2008;153:741)Objective: To follow respiratory function parameters, such as tidal volume (Vt), respiratory system compliance (Crs) and resistance (Rrs) during resuscitation in preterm infants. Derived data together with the clinical signs are used to describe and document the course of the resuscitation .Design/Methods: A pneumotachometer with a pressure port was attached to the face mask (Neopuff® or Laerdal®) or to the ET-tube (for intubated patients). Flow and pressure were measured and used to derive respiratory system mechanics (Crs and Rrs) together with corresponding positive inspiratory pressure (PIP) and Vt. Ten infants [median (range) birth weight 0.84 (0.47-1.3) kg; GA 25.5 (25-29) weeks] with apnoea and bradycardia (heart rate (HR)
|
|
| 6. |
- Stichel, H, et al.
(författare)
-
Inflammatory cytokines in gastric fluid at birth and the development of bronchopulmonary dysplasia
- 2011
-
Ingår i: Acta paediatrica (Oslo, Norway : 1992). - : Wiley. - 1651-2227 .- 0803-5253. ; 100:9, s. 1206-1212
-
Tidskriftsartikel (refereegranskat)abstract
- Aim: To assess whether the levels of inflammatory and anti-inflammatory proteins in gastric fluid of premature infants shortly after birth are associated with the development of bronchopulmonary dysplasia (BPD). Methods: Gastric fluid retrieved within 1h of birth of premature infants (gestational age <29weeks) was analysed for interleukin (IL)-8, growth-related oncogene (Gro)-α, epithelial cell-derived neutrophil-activating peptide (ENA)-78, IL-1β and Clara cell secretory protein with ELISA. Results: Of 51 enrolled infants, 86% had BPD. Of these, 54% had mild BPD, 30% had moderate BPD and 16% had severe BPD. Clinical chorioamnionitis was associated with high levels of IL-8, Gro-α, Epithelial cell-derived neutrophil-activating peptide-78 (ENA-78) and IL-1β in gastric fluid. Gastric fluid levels of IL-8, Gro-α, ENA-78 and IL-1β were higher in infants with moderate or severe BPD than in those with no or mild BPD. Ligation of the patent ductus arteriosus was associated with the development of moderate or severe BPD. These associations were no longer significant after adjustment for gestational age. Conclusion: The levels of inflammatory mediators in gastric fluid samples retrieved soon after birth from intubated or nonintubated infants can be used to assess the infants' perinatal exposure to inflammatory mediators and its association with neonatal outcome.
|
|
