Abstract:In fasting human beings, the manometrically recorded duodenal contractions show, on the average, a significant time correlation with the contractions of the prepyloric antrum, for a length greater than 14 cm from the antrum. The number and average amplitude of duodenal contractions are increased for about 40 sec after the onset of the antral pressure wave, recorded with an open tip catheter in the prepyloric antrum. The propagation velocity for the pressure waves is estimated at 0.6–1 cm/sec from the prepylori… Show more
We examined the effect of intraesophageal acid (either spontaneous gastroesophageal reflux or infused) on airflow resistance in 15 sleeping asthmatic subjects. We observed no significant acute or sustained changes in airflow resistance relative to periods of intraesophageal acid. Overnight changes in spirometry and lower airway resistance also demonstrated similar nocturnal worsening of bronchoconstriction despite the occurrence of spontaneous or simulated gastroesophageal reflux. The presence or absence of clinical evidence of esophagitis (Bernstein test response) did not alter the observed lack of response to intraesophageal acid. We conclude that gastroesophageal reflux contributes little to the nocturnal worsening of asthma.
We examined the effect of intraesophageal acid (either spontaneous gastroesophageal reflux or infused) on airflow resistance in 15 sleeping asthmatic subjects. We observed no significant acute or sustained changes in airflow resistance relative to periods of intraesophageal acid. Overnight changes in spirometry and lower airway resistance also demonstrated similar nocturnal worsening of bronchoconstriction despite the occurrence of spontaneous or simulated gastroesophageal reflux. The presence or absence of clinical evidence of esophagitis (Bernstein test response) did not alter the observed lack of response to intraesophageal acid. We conclude that gastroesophageal reflux contributes little to the nocturnal worsening of asthma.
Our preliminary data obtained in a small group of selected patients with cirrhosis, portal hypertension, and hypoalbuminemia indicate that protein-losing enteropathy may represent an appreciable and underestimated cause of hypoproteinemia.
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