Cardio-respiratory response to moderate chloral hydrate sedation in young lambs.

Aim: Chloral hydrate (CH) is the most commonly used sedative for medical procedures and lung function tests in infancy. The aim was to determine whether moderate CH sedation affects airway function, lung volume and ventilation.

Methods: Thirteen chronically instrumented 7- to 8-week-old lambs were studied both before and after CH sedation (50 mg/kg as intravenous bolus followed by 25 mg/kg/hour as continuous infusion).

Fetal nicotine exposure increases airway responsiveness and alters airway wall composition in young lambs.

To test the hypotheses that fetal nicotine exposure alters airway wall composition and enhances the airway response to inhaled methacholine (MCh), lambs were exposed during the last fetal trimester to (1) a low dose (LN) (n=13, 0.5mg/kg/d (maternal weight) of free base nicotine, (2) a moderate dose (MN) (n=10, 1.5mg/kg/d) or (3) saline (n=14).

Prenatal nicotine exposure transiently alters the lung mechanical response to hypoxia in young lambs.

To test the hypothesis that fetal nicotine exposure alters the lung mechanical response to hypoxia (10% O(2)) 10 lambs were exposed during the last fetal trimester to a low dose nicotine (LN) and 10 to a moderate dose (MN) (maternal dose 0.5 and 1.5mg/(kgday) free base, respectively).

Inhaled nitric oxide attenuates hyperoxic lung injury in lambs.

Cytochrome P450 (CYP) inhibition with cimetidine reduces hyperoxic lung injury in young lambs. Nitric oxide (NO), also a CYP inhibitor, has been shown to either aggravate or protect against oxidant stress depending on experimental context. The objective of this study was to determine whether NO, like cimetidine, would protect young lambs against hyperoxic lung injury, and whether its effect was associated with CYP inhibition.

Cardiorespiratory effects of nicotine exposure during development.

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.

Altered lung development after prenatal nicotine exposure in young lambs.

There is compelling evidence that prenatal nicotine exposure permanently alters lung development and airway function. The aim of this study was to determine how prenatal nicotine exposure alters proximal and distal airway function. Thirteen lambs were continuously exposed during the last fetal trimester to low-dose nicotine (LN) and 12 to a moderate dose (MN) (maternal s.

Impaired cardiorespiratory recovery after laryngeal stimulation in nicotine-exposed young lambs.

The hypothesis that postnatal nicotine exposure weakens cardiorespiratory recovery from reflex apnea and bradycardia was tested in eight lambs continuously infused with nicotine from the day of birth at a dose of 1 to 2 mg.kg(-1).d(-1).

Prenatal nicotine exposure blunts the cardiorespiratory response to hypoxia in lambs.

Because smoking during pregnancy is a major risk factor for late fetal death and the sudden infant death syndrome, we investigated cardiorespiratory defense mechanisms to hypoxia in 7 prenatally nicotine-exposed (N) lambs (approximate maternal dose: 0.5 mg/kg/day) and 11 control (C) lambs all at an average age of 5 days. The ventilatory response to 10% oxygen (hyperpnea) was significantly attenuated during quiet sleep in N lambs compared with C lambs and in N lambs aroused from sleep later compared with C lambs (161 +/- 90 versus 75 +/- 66 seconds, p < 0.

Altered breathing pattern after prenatal nicotine exposure in the young lamb.

Maternal smoking during pregnancy is a risk factor for sudden fetal and infant death as well as obstructive airway disease in childhood. Fetal nicotine exposure affects organ development. The aim of the present study was to investigate effects of fetal nicotine exposure on lung function in young lambs.

Robot-assisted endoscopic intrauterine myelomeningocele repair: a feasibility study.

Background: Animal experiments have suggested that the intrauterine environment causes secondary injury to the congenitally dysplastic spinal cord. This in turn suggests that early closure of the myelomeningocele sac might prevent secondary injury and therefore improve neurologic outcome. This study was designed to examine the technical feasibility of performing intrauterine myelomeningocele repair using a robot-assisted endoscopic system in an animal model.