concluded that GD only resulted in GDV if the stomach was already malpositioned. This obser-vation has led many investigators to consider otherfactors such as the influence of the spleen, exercise,and concurrent inflammatory GI disease as well asmeal size and frequency. The fact that GDV can oc-cur in splenectomized dogs
suggests that it is not es-sential in the pathogenesis of GDV in all dogs.Similarly, meal type and feeding frequency are notconsistent among GDV patients, ruling out diet as acommon etiologic factor. Some dogs clearly tolerategastric volvulus (without dilation) for extended peri-ods.
Consequently, if the stomach is rotated, itsmalposition could influence both eructation and py-loric function and thereby lead to dilation. I
ncom-plete GES and pyloric dysfunction in some volvuluspatients may permit gas to escape through eructation,gastric emptying, or absorption.
The initiation of eructation and the vomiting reflexoccurs at intragastric pressures lower than those record-ed from spontaneous cases of GDV.
Factors that canindependently influence the eructation mechanism in-clude sleep, certain anesthetic drugs, and damage or in-filtration of the vagus nerve or gastric cardia.
Transient relaxation of the GES following gastric fun-dus distention is an important mechanism for eructa-tion in dogs.
Presumably, gastric volvulus mechanical-ly interferes with eructation. If gastric volvulus alwayspreceded GDV, disordered eructation could be easily explained. In situations in which GD precedes GDV,the question of what prevents gastric decompression
either eructation of gas or vomiting of solids
remains. When dogs were gorge-fed in an attempt to createGDV, gastric decompression was achieved rapidly by opening the pyloric canal, vomiting, or both.
Even if the eructation mechanisms were defective, given thatgastric decompression can also be achieved by openingthe pyloric canal, failure to eructate or vomit aloneshould not necessarily initiate GD. Acute failure of theeructation and vomiting mechanism must occur inGDV-affected dogs, perhaps with simultaneous pyloricdysfunction; therefore, disorders of eructation andvomiting most likely contribute to the initiation of GDV.
Gastric Rhythm, Motility, and Emptying
Funkquist and Garmer
demonstrated that the gas-tric emptying of a liquid barium meal was delayed inanimals recovering from GDV. This study was prompt-ed by the observation that several of the animals thatpresented with GDV had historical evidence of chronicvomiting.
Together with the fact that some dogs hadrecurrent episodes of GD following otherwise success-ful therapy for GDV,
this evidence suggested the pres-ence of a primary gastric emptying disorder. In addi-tion,spontaneous gastric decompression normally occursat intragastric pressures far lower than those reportedfor naturally occurring GDV.
Gastric dysrhyth-mias, eructation disorders, and abnormal pyloric func-tion were suspected to be initiating factors. These fac-tors could influence gastric contents, degree of fill, andgastric position, thereby leading to GDV.Funkquist and Garmer
demonstrated delayed gas-tric emptying of a liquid barium sulfate suspension indogs recovering from GDV, suggesting that delayedgastric emptying played a role in the pathogenesis of this syndrome. A subsequent study that measured gas-tric emptying (using a radiolabeled test meal adminis-tered after recovery from GDV and tube gastropexy)failed to show a difference compared with nondiseasedcontrols.
Yet another study
using radiopaque mark-ers determined abnormalities of gastric emptyingamong dogs that had recovered from GDV and cir-cumcostal gastropexy. These experiments used differentmethods to evaluate gastric emptying; the timing of theevaluation relative to the acute episode of GDV varied.Typically, dogs with longstanding delayed gastricemptying are presented because of chronic vomiting, as was seen by Funkquist and Garmer.
Data from own-ers of dogs with GDV, however, have rarely indicated aclinical syndrome associated with chronic delayed gas-tric emptying before the acute GDV episode. In addi-tion, results of a clinical trial by Greenfield and col-leagues
suggested that pyloric modification, in anattempt to enhance pyloric outflow, caused increasedmorbidity without demonstrable enhancement of gas-tric emptying and could not be justified. These obser-vations suggest that the delayed gastric emptying that isseen experimentally may be the result
rather than theinitiator
of GDV and its treatment. Evidence forchronic gastric outflow obstruction in all GDV patientsis lacking, and pyloric modification cannot be recom-mended as routine. Acute pyloric dysfunction, however, is influential inGDV. The pyloric canal normally opens to allow aboralpassage of gastric contents at intragastric pressures of 8to 14 mm Hg,
far lower than intragastric pressurerecorded from clinical cases of GDV.
Stress, elec-trolyte disturbances, and certain anesthetic agents caninfluence pyloric function and delay gastric emptying.In a recent study,
stress associated with car rides orplacement in boarding kennels was calculated as a risk factor for GDV. Obversely, gastric malposition couldmechanically interfere with pyloric outflow. Therefore,