QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online August 4, 2005
Journal of Experimental Biology 208, 3047-3053 (2005)
Published by The Company of Biologists 2005
doi: 10.1242/jeb.01746

This Article Summary Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Uriona, T. J. Articles by Moore, J. Search for Related Content PubMed PubMed Citation Articles by Uriona, T. J. Articles by Moore, J.

Structure and function of the esophagus of the American alligator (Alligator mississippiensis)

T. J. Uriona^1,*, C. G. Farmer¹, J. Dazely¹, F. Clayton² and J. Moore²

¹ Department of Biology, 257 South 1400 East, University of Utah, Salt Lake City, UT 84112, USA
² Department of Medicine and Pathology, Salt Lake City Veteran's Hospital, 500 Foothill Blvd, Salt Lake City, UT 84148, USA

View larger version (87K): [in a new window]   Fig. 1. Longitudinal-section at the mid-esophageal level. The crocodilian esophagus exhibits three muscle layers: muscularis mucosa (MM), circular muscle (CM) and outer longitudinal muscle (LM) layer of the muscularis propia.

View larger version (145K): [in a new window]   Fig. 2. Longitudinal-section at the distal esophageal level in the region of the high-pressure zone. Note the increased muscle thickness in all layers when compared with the mid-esophagus (Fig. 1).

View larger version (137K): [in a new window]   Fig. 3. Section of the inner mucosa at the mid-esophagus level. Note the ciliated columnar epithelium at the surface as well as two large mucous cells. In addition, a nucleated red blood cell can be seen on the left margin, mid-section.

View larger version (13K): [in a new window]   Fig. 4. A sample of data from one animal. The esophageal peristaltic wave was stimulated with a bolus of water.

View larger version (20K): [in a new window]   Fig. 5. Sample of data collected when both pressure probes were placed within the lower esophageal sphincter (LES). The top and second trace are recordings of the pH and ventilation, respectively. Ventilation begins with an exhalation (positive voltage) and ends with an inspiration. Thus, the apnea consists of a breath-hold. The third and fourth traces give the pressure from the most proximal (cranial) probe with a gross and fine pressure scale, respectively. Note that peak pressures during ventilation increased dramatically, in this case from a baseline of 1.3 kPa to a peak of nearly 26.7 kPa. The small regular spikes in pressure seen in the fine scale are caused by the heartbeat. The fifth and sixth traces are the pressure recordings from the distal (caudal) probe with two pressure scales. The expanded pressure scale of the sixth trace shows most clearly the relaxation in pressure that occurred in the LES during a wet swallow (the arrow indicates the time a 2 ml bolus of water was given). This response to wet swallows was observed in all animals studied (N=5).

View larger version (20K): [in a new window]   Fig. 6. Sample of data collected when the proximal (cranial) and distal (caudal) transducers were located within the lower esophageal sphincter (LES) and stomach, respectively. The top portion of the graph shows a time span of approximately 15 min and illustrates large rises in LES (proximal) pressure with ventilation. The two spikes in pressure marked with an asterisk were due to vocalization and a general elevation of pressure in the thoraco-abdominal cavity. These spikes demonstrate that the increase in LES pressure associated with ventilation is independent of any thoraco-abdominal pressure changes and is intrinsic to the LES. Fluctuations in the ventilatory trace that are marked with daggers are caused by gular flutter, where air is taken in and out of the gular cavity. This serves an olfactory but not a gas exchange function (Farmer and Carrier, 2000b). Note that there is no rise in LES pressure associated with the gular flutter. The bottom part of the figure shows panels 1, 2 and 3 in more detail. Note that the scale for the gastric pressure on panel 2 is also expanded. Although ventilation generally caused LES pressure to increase, it caused gastric pressures to decrease. This is because the glottis is closed during apnea and the respiratory muscles are relaxed, thus elevating thoraco-abdominal pressure (Farmer and Carrier, 2000a). Panel 3 shows a bout of ventilation that was interrupted by a 2 ml bolus of water (indicated by arrow). Note that the wet-swallow reflex predominated over the LES pressure increase.