Characterization of anorectal pressure and the anorectal inhibitory reflex in healthy preterm and term infants.

OBJECTIVES: To evaluate anorectal motor function in healthy premature and term infants with the use of micromanometric techniques. STUDY DESIGN: Anorectal manometry was performed in 22 healthy neonates (9 female) with a mean postmenstrual age of 32 weeks (range, 30 to 38 weeks) with a micromanometric anorectal assembly (od 2.0 mm). The assembly incorporated a 2-cm-long sleeve sensor for measurement of resting anal sphincter pressures and relaxation, and 4 sideholes recorded anal and rectal pressures. Rectal distension was performed with a latex balloon or direct air insufflation to elicit the anorectal inhibitory reflex (AR). RESULTS: The mean anal sphincter pressure, rectal pressure, and rhythmic wave frequency were 40 mm Hg (range, 7 to 65 mm Hg), 11 mm Hg (range, 1 to 27 mm Hg), and 10/min (range, 8 to 14/min), respectively. A normal AR could be elicited in 21 of the 22 infants studied. CONCLUSION: An anorectal micromanometric sleeve catheter is suitable for use in evaluating anorectal pressures in preterm and term neonates. Insufflation of air without the use of a balloon to elicit the AR is reliable and suitable for use in infants <34 weeks. Premature infants older than 30 weeks' postmenstrual age have normal anorectal pressures and a normal AR.

Characterization of esophageal body and lower esophageal sphincter motor function in the very premature neonate.

OBJECTIVES: To characterize esophageal body and lower esophageal sphincter (LES) motor function in very premature infants. STUDY DESIGN: Esophageal manometry was performed in 12 very premature infants of 26 to 33 weeks' postmenstrual age (PMA) (body weights of 610-1360 g). Esophageal motor patterns were recorded for 30 minutes with a perfused micromanometric sleeve assembly (outer diameter, 2.0 mm). RESULTS: Esophageal pressure waves triggered by dry swallows were predominantly (84%) peristaltic in propagation sequence. All infants showed tonic LES contraction; the mean resting LES pressure (LESP) for individual infants ranged from 5.0 +/- 4.1 mm Hg to 20.0 +/- 4.8 mm Hg. In all infants the LES relaxed (duration, 5.8 +/- 3.0 seconds; nadir pressure, 1.8 +/- 2.6 mm Hg) in response to pharyngeal swallows. Transient LES relaxations (TLESRs) (duration, 21.7 +/- 8.7 seconds; nadir pressure, 0.1 +/- 1.8 mm Hg) occurred on average 2.6 +/- 1.6 times per study; 86% of these relaxations triggered esophageal body common cavity events known to be associated with gastroesophageal reflux. CONCLUSIONS: Esophageal motor function is well developed in very premature infants. Our data also suggest that TLESR is the predominant mechanism of reflux in these babies.

Lower esophageal sphincter position in premature infants cannot be correctly estimated with current formulas.

OBJECTIVES: Strobel's formula (Esophageal length = 5 + 0.252 x Height) is frequently used as a guide for determining the distance from the nares to the lower esophageal sphincter (LES) in term infants. The aim of this study was to examine this relationship in premature infants. STUDY DESIGN: The distance from nares to LES was manometrically determined in 156 premature infants (26-40 weeks' postmenstrual age; body weights of 610-3050 g). The ability of body weight, height (body length), head circumference, and postmenstrual age to predict the manometrically determined LES position was evaluated with linear and non-linear regression analyses. RESULTS: Body weight and body length were the most predictive of distance from nares to LES (r(2) = 0.848 and 0.802, respectively). These relationships were non-linear and, in the case of body length, deviated substantially from Strobel's model. CONCLUSIONS: In premature neonates, a different formula is needed for prediction of the distance between nares and LES than that applied to term infants and children.

Mechanisms of gastroesophageal reflux in healthy premature infants.

OBJECTIVES: The aim of this study was to characterize the motor events responsible for gastroesophageal reflux (GER) and esophageal acid clearance in a cohort of healthy preterm infants. STUDY DESIGN: Esophageal motility was recorded for 2 to 3 hours after a feeding in 24 preterm infants, 31 to 38 weeks' postmenstrual age, by using a sleeveside hole micromanometric assembly incorporating a pH probe. RESULTS: Sixty acid GER episodes were recorded by pH probe, and 133 non-acid GER episodes were recorded manometrically by the presence of esophageal common cavities. Of the 193 GER episodes, 159 (82%) were associated with transient lower esophageal sphincter relaxation (TLESR). TLESRs were significantly longer in duration than single swallows (15.1 seconds vs 5.6 seconds, P < .001) and had lower nadir pressures (0.8 mm Hg vs 2.3 mm Hg, P < .001). A total of 3216 esophageal body pressure waves were analyzed; 70% of swallow-induced pressure waves were peristaltic in sequence compared with 5% of swallow-unrelated pressure waves. During periods of esophageal acidification (pH below 4), peristaltic esophageal body pressure wave sequences cleared acid refluxate more effectively than nonperistaltic pressure wave sequences. CONCLUSIONS: In healthy preterm infants, TLESRs are the predominant mechanism underlying GER, and esophageal clearance mechanisms are well developed by at least 31 weeks' postmenstrual age.

Methoxyflurane enhances allyl alcohol hepatotoxicity in rats. Possible involvement of increased acrolein formation.

The effect of methoxyflurane anesthesia on allyl alcohol-induced hepatotoxicity and the metabolism of allyl alcohol was studied in male rats. Hepatotoxicity was assessed by the measurement of serum alanine aminotransferase activity and histopathological examination. Allyl alcohol-induced hepatotoxicity was enhanced when allyl alcohol (32 mg/kg) was administered 4 hr before or up to 8 days after a single 10-min exposure to methoxyflurane vapors. The possibility that methoxyflurane increases alcohol dehydrogenase-dependent oxidation of allyl alcohol to acrolein, the proposed toxic metabolite, was evaluated by measuring the rate of acrolein formation in the presence of allyl alcohol and liver cytosol. The effect of methoxyflurane on alcohol dehydrogenase activity in liver cytosol was also assessed by measuring the rate of NAD+ utilization in the presence of ethyl alcohol or allyl alcohol. Alcohol dehydrogenase activity and rate of acrolein formation were elevated in methoxyflurane-pretreated rats. The results suggest that a modest increase in alcohol dehydrogenase activity and rate of acrolein formation markedly enhances allyl alcohol-induced hepatotoxicity.