Author - J. F Frøen et al Presented by: Carmen L. Trinidad

1. Adverse Effects of Nicotine and Interleukin-1ß on Autoresuscitation after Apnea in Piglets: Implications for Sudden Infant Death Syndrome Author - J. F Frøen et al Presented by: Carmen L. Trinidad

2. Objective • The affects of nicotine and IL-1ß on induced apnea to better understand the relationship between maternal smoking and infant death syndrome

3. What is Sudden Infant Death Syndrome? • SIDS - also called crib or cot death • Unexplained sudden death, during sleep of an apparently healthy infant • In the U.S, SIDS is the leading cause of death in infants between 1 - 12 months of age • Rate of 1 of every 1,000 live births

4. Risk Factors • Infants with low birth weights < 3.5 lbs • Inadequate prenatal care • Mothers (non-smoker) who do not breast feed • Sleeping position • Insufficient exchange of oxygen - Apnea • Prenatal, Postnatal, & Passive smoking

5. Smoking- Major risk factor • Case control studies have shown clear, dose-related associations between maternal smoking and infant death • Strongest relationship found when mother smoked during pregnancy & Postnatally • Exposure to environmental tobacco smoke increases risk of having night cough & respiratory infections

6. Smoking- Major risk factor • SIDS victims have a slight infection & triggered immune system before their death • Release cytokines • a large group of molecules involved in signaling between cells during immune responses • interleukin 1ß (IL-1ß) - may depress respiration

7. Apnea • Apneas - associated with SIDS in infants • brief suspension of breathing occurring repeatedly during sleep • Postnatal exposure to tobacco and infections adversely affect ability to cope with an apneic episode

8. Purpose of Investigation • Investigate the acute effects of nicotine and IL-1ß on apnea by laryngeal reflex stimulation and the subsequent autoresuscitation

9. Methods • 30 - 1 week old piglets were sedated with butyrophenone azaperone • Catheter was inserted into immediate subglottic space & in left femoral artery • Heart rate monitored • Blood pressure recorded • Airflow monitored

10. Methods • Blood samples tested for analysis of glucose, blood gas, & hematology • Piglets were allowed 30 min. stabilization before recording of baseline values

11. Method • 1) Immediate infusion of IL-1ß intravenously • 2) Slow infusion of nicotine intravenously-5min. Later • 3) Both IL-1ß and nicotine (NIC) • 4) Placebo by infusion of .9% NaCl (CTR)

12. Inducing Apnea • 15 min. later apnea was induced by insufflation of .1ml .9% NaCl acidified with HCl through tracheal catheter • Apnea induced 5 times with 5 min intervals • *apnea - defined as no airflow for >5 seconds • end of apnea - defined as the start of a respiratory movement producing airflow >5 seconds

13. Results: Pretreatment with nicotine • Caused more spontaneous apneas • repeated spontaneous apneas caused an inability to increase respiratory rate

14. Addition of IL-1ß • Prolonged apneas • inability to hyperventilate

15. Addition of IL-1ß + NIC • More spontaneous apneas • Apneas were prolonged • Inability to hyperventilate normally after apnea • decrease in respiratory rate

16. Insufflation of acidified saline (CTR)-Placebo • Insufflation of saline produced apneas • followed by decrease in heart rate • fall in blood pressure • swallowing • occasional coughs • finally autoresuscitation with gasping

17. Before During BP HR BP After HR BP HR

18. Table 1 Results • Heart rate of piglets was higher after the apnea attack • Heart rate was lowest during the apnea attack • Results for the blood pressure were similar to that of the heart rate

19. Fig. 1. Change in respiratory rate (in percent) after end of induced apnea versus baseline values.

20. Change in Respiratory Rate • The control group had a significantly higher respiratory rate than that of the Nicotine and IL-1ß groups

21. Spontaneous Apneas: 5min. before and after

22. Spontaneous Apneas Results • The amount and duration of the spontaneous apneas were higher in the IL-1ß groups comparing to the control, nicotine and IL-1ß groups alone

23. Oxygen saturation at start of Apnea, and end of apnea

24. Oxygen Saturation Results • The oxygen saturation of the experimental groups were below that of the control group

25. Characteristics which enhance, produce, & prolong apneas • interfere with normal autoresuscitation after apnea • vomiting • low gestational age • overheating • hypoxia • infection - release of interleukines

26. Conclusions • Apnea by laryngeal reflex plays an important role in apnea associated with SIDS • Nicotine combined with IL-1ß has an adverse effect on apnea and autorescscitation

27. References • Frøen J.F et al. 2000. Adverse Effects of Nicotine and Interleukin-1ß on Autoresuscitation after Apnea in Piglets: Implications for Sudden Infant Death Syndrome. Pediatrics 105: 52 • Haslam R. 2000. Smoking and Sleep position are only pieces of the puzzle resulting in the sudden infant death syndrome. Pediatric Research 48: 715. • Schoendorf K, Kiely J. 1996. Relationship of sudden infant death syndrome to maternal smoking during and after pregnancy. Pediatrics 90: 905-908. • Wisborg K, et al. 2000. A prospective study of smoking during pregnancy and SIDS. Arch Dis Child 83: 203-206.