Supplemental oxygen, but not supplemental crystalloid fluid, increases tissue oxygen tension in healthy and anastomotic colon in pigs

BACKGROUND: Low tissue oxygen tension is an important factor leading to the development of wound dehiscence and anastomotic leakage after colon surgery. We tested whether supplemental fluid and supplemental oxygen can increase tissue oxygen tension in healthy and injured, perianastomotic, and anastomotic colon in an acutely instrumented pig model of anastomosis surgery. METHODS: Sixteen Swiss Landrace pigs were anesthetized (isoflurane 0.8%-1%) and their lungs ventilated. The animals were randomly assigned to low fluid treatment ("low" group, 3 mL x kg(-1) x h(-1) lactated Ringer's solution) or high fluid treatment ("high" group, 10 mL/kg bolus, 18 mL x kg(-1) x h(-1) lactated Ringer's solution) during colon anastomosis surgery and a subsequent measurement period (4 h). Two-and-half hours after surgery, tissue oxygen tension was recorded for 30 min during ventilation with 30% oxygen. Three hours after surgery, the animals' lungs were ventilated with 100% oxygen for 60 min. Tissue oxygen tension was recorded in the last 30 min. Tissue oxygen tension was measured with polarographic Clark-type electrodes, positioned in healthy colonic wall, close (2 cm) to the anastomosis, and in the anastomosis. RESULTS: In every group, tissue oxygen tension during ventilation with 100% oxygen was approximately twice as high as during ventilation with 30% oxygen, a statistically significant result. High or low volume crystalloid fluid treatment had no effect on colon tissue oxygen tension. CONCLUSIONS: Supplemental oxygen, but not supplemental crystalloid fluid, increased tissue oxygen tension in healthy, perianastomotic, and anastomotic colon tissue

La mort subite du nourrisson(MSN) Données récentes en physiologie

Prevention campaigns to avoid risk factors for the occurrence of sudden infant death syndrome (SIDS) during sieep have ied to a significant decrease in the number of infants dying suddeniy and unexpectedly during sieep. Despite a growing amount of evidence, the understanding of the mechanisms responsible for SIDS is stilt iargeiy incomplete. We will review the most recent epidemiotogicai, electrophysiologicai, genetic and pathological research on this topic. From these data, a comprehensive model for SIDS has been proposed: the death wouid resuit from the combination of three factors (a prenatal vulnerability, a critical developmental period and an exogenous postnatal stress) and three potential mecbanisms (deficiencies in breathing, autonomie and sleep-wake controis). As arousal represents the last chance of survival when an infant is exposed to a life-threatening challenge during sleep, failure to arouse could be involved in the final pathway of SIDS. An infant could be vulnerable to SIDS because of a deficiency in cardio-respiratory or in sleep/wake behaviour controis during sleep. Genetic, metaboiic, nutritbnal or toxic prenatal brainstem injury could be responsible for these deficits. The infant's vulnerability lies latent until he/she enfers the critical developmental period from 2 to 6 months when significant changes in sleep-wake, breathing and autonomie controls occur. The accident has a greater probability of occurring when the infant is exposed to an infection, or an unfavourable environmental factor which enhances the immature cardio respiratory and sleep/wake behaviours of the infant. © 2005 Elsevier Masson SAS. All rights reserved.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Sudden infant death syndrome from epidemiology to pathophysiology

SCOPUS: re.jinfo:eu-repo/semantics/publishe

QT interval prolongation in future SIDS victims: a polysomnographic study.: QT intervals in future SIDS victims

International audienceOBJECTIVE: Previous data have suggested that a prolonged QTc interval during the first days of life can be associated with some cases of sudden infant death syndrome (SIDS). Analysis of heart rate variability during sleep in future SIDS victims has shown findings compatible with an imbalance in autonomic tone. We hypothesized that some future SIDS infants could have longer QTc intervals during sleep, compared with healthy control infants, and that this difference would correlate with the autonomic imbalance already found in these infants. METHODS: QTc intervals and a heart rate autoregressive power spectral analysis were calculated during the same periods in the polysomnographic sleep recordings of 18 infants who eventually died of SIDS and of 18 control infants. The control infants were matched for sex, gestational age, postnatal age, birth weight, and sleep position. The median postnatal age was 8 weeks. RESULTS: Compared with control infants, future SIDS victims were characterized by having longer QTc intervals during total sleep (P = 0.019), rapid eye movement sleep (P = 0.045) and non-rapid eye movement sleep (P = 0.029). When the night was divided into 3 equal parts, this difference was always present but was most marked during the last part of the night. There was, respectively, a negative and a positive correlation between parasympathetic activity and sympathovagal balance and median and maximum QTc interval values. CONCLUSION: Compared with QTc intervals in matched control infants, QTc intervals were increased in future SIDS victims. Such a prolongation could be related to the autonomic dysfunction already reported in these patients

QT interval prolongation in future SIDS victims: A polysomnographic study

SCOPUS: ar.jinfo:eu-repo/semantics/publishe