Pre-hospital discharge car safety seat testing in infants following congenital heart surgery.

The purpose of this study was to expand the American Academy of Pediatrics' (AAP) car safety seat testing recommendation to include high-risk infants following cardiac surgery. Car safety seat testing (< or =4 days prior to discharge) was retrospectively reviewed for 66 postoperative infants. Car safety seat testing was performed according to AAP guidelines. Failure of the test was defined as the occurrence of apnea, bradycardia, or oxygen desaturation. Average birth weight was 3.1 +/- 0.5 kg. Two patients were born <37 weeks of gestation. Surgical procedures included modified Blalock-Taussig shunt (15), arterial switch operation (12), Norwood-Sano modification (11), coarctation repair (8), repair of tetralogy of Fallot (6), repair of truncus arteriosus (4), repair of total anomalous pulmonary venous return (3), pacemaker (2), repair of interrupted aortic arch and ventricular septal defect (VSD) (1), repair of coarctation/VSD (1), orthotopic heart transplant (1), repair of VSD (1), and patent ductus arteriosus ligation (1). Average age at discharge was 28 +/- 21 days. Four patients (6%) failed car safety seat testing secondary to a decrease in oxygen saturation. One of four passed on retesting after parental education; three of 4 (75%) were discharged home in a supine car safety seat. There was no relationship between the type of surgery and car safety seat test failure. It may be beneficial to extend the AAP recommendations for car safety seat testing to include this high-risk patient population.

Prehospital discharge car safety seat testing of infants after congenital heart surgery.

BACKGROUND: This study aimed to expand the American Academy of Pediatrics (AAP) car safety seat testing recommendation to include high-risk infants after cardiac surgery. METHODS: Car safety seat testing (< or =4 days before discharge), performed according to AAP guidelines, was retrospectively reviewed for 66 postoperative infants. Failure was defined as apnea, bradycardia, or oxygen desaturation. RESULTS: The average birth weight of the study infants was 3.1 +/- 0.5 kg. Two patients were born at less than 37 weeks gestation. Surgical procedures included modified Blalock-Taussig shunt technique (n = 15), arterial switch operation (n = 12), Norwood Sano modification (n = 11), coarctation repair (n = 8), repair of tetralogy of Fallot (n = 6), repair of truncus arteriosus (n = 4), repair of total anomalous pulmonary venous return (n = 3), pacemaker placement (n = 2), repair of interrupted aortic arch and ventriculoseptal defect (VSD) (n = 1), repair of coarctation and VSD (n = 1), orthotopic heart transplant (n = 1), repair of VSD (n = 1), and patent ductus arteriosus ligation (n = 1). The average age at discharge was 28 +/- 21 days. Four patients (6%) failed car safety seat testing because of a fall in oxygen saturation. One of the four patients passed on retesting after parental education, whereas three of the four (75%) were discharged home in a supine car safety seat. There was no relationship between the type of surgery and car safety seat test failure. CONCLUSION: It may be beneficial to extend the AAP recommendations for car safety seat testing to include high-risk infants after cardiac surgery.

Leptin production in adipocytes from morbidly obese subjects: stimulation by dexamethasone, inhibition with troglitazone, and influence of gender.

This study examined the regulation of leptin production by dexamethasone and troglitazone. Subcutaneous and omental adipose tissue was obtained during bariatric surgical procedures (30 women and 16 men; body mass index, 52.5 +/- 1.7 kg/m2, age, 39 +/- 2 yr), and adipocytes were cultured in suspension. Subcutaneous adipocytes from females released significantly more leptin than did omental cells from the same subject (P < 0.05), but basal leptin release was not different in adipocytes from these depots in males. Dexamethasone (0.1 micromol/L) significantly increased leptin release within 24 h from sc (135 +/- 13% of control) and omental (227 +/- 53%) adipocytes of females, but not males. Dexamethasone-stimulated leptin production at 48 h was significantly greater in the omental adipocytes of females (398 +/- 64% of control) than in sc adipocytes of females (207 +/- 21%) or the omental (211 +/- 33%) and sc (180 +/- 23%) adipocytes of males. Troglitazone (10 micromol/L; 48 h) significantly inhibited dexamethasone-stimulated leptin release in sc (57 +/- 10.7% inhibition) and omental adipocytes (134 +/- 26% inhibition). There was no gender-related difference in the effect of troglitazone to inhibit dexamethasone-stimulated leptin release. Troglitazone significantly inhibited basal leptin production from omental adipocytes by 15.0 +/- 5.2%. The effect of dexamethasone and troglitazone to regulate leptin release was mediated through changes in ob gene expression, but did not involve changes in glucose uptake or metabolism to lactate. The data suggest that adipocytes from females are more responsive to the stimulatory effect of dexamethasone in vitro than are adipocytes from males. If adipocytes from females are more responsive to relevant in vivo stimuli for leptin secretion such as insulin or glucose, this could contribute to the gender difference in serum leptin. The data also suggest that leptin release from omental adipocytes may be more responsive to hormonal and nutrient regulation in vivo than are sc adipocytes.