Gastric stasis of solids after Roux gastrectomy: is the jejunal transection important?

To investigate the effect of jejunal transection on the rate of gastric emptying after Roux gastrectomy, a two-part study was conducted. First, we investigated the relationship between Roux limb slow wave frequency and gastric emptying of solids. Six dogs underwent Roux-en-Y gastrectomy with vagal preservation and placement of intestinal electrodes. Gastric emptying studies were performed on each animal with simultaneous pacing of the Roux limb, either at the slowest rate (Pmin) or the fastest rate (Pmax) at which entrainment could be achieved. Gastric emptying studies were also performed in the unpaced (control) condition. Gastric half-emptying times (X +/- SEM minutes) and slow wave frequencies (X +/- SEM cycles per minute), respectively, were Pmin 117 +/- 26 min, 15.7 +/- 0.1 cpm; Pmax 97 +/- 18 min, 19.0 +/- 0.3 cpm; and unpaced 127 +/- 16 min, 15.1 +/- 0.3 cpm. The gastric half-emptying time during Pmax was significantly lower than unpaced controls (P = 0.01). The second part of the study sought to determine if transecting the intestine at 10 cm distal to the pylorus rather than at 20 cm distal to the ligament of Treitz would improve gastric emptying in animals with a truncal vagotomy and Roux-en-Y gastrectomy. Gastric half-emptying times were 149 +/- 21 and 164 +/- 24 min (ns), respectively. Slow wave frequencies were 17.01 +/- 0.06 and 15.7 +/- 0.17 cpm (P < 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Migrating myoelectric complex and jejunal slow-wave propagation after Roux gastrectomy in dogs.

Roux-en-Y gastrectomy is associated with a high incidence of symptoms of gastric stasis. Retrograde propagation of jejunal electrical slow waves and spike bursts has been implicated in the Roux Y stasis syndrome. Since the fasted state may persist after feeding, this study examined the extent of retrograde slow-wave propagation in the fasted state, particularly during aboral migration of phase III. Six dogs underwent Roux gastrectomy and placement of bipolar electrodes along the Roux limb. Four normal dogs with electrodes acted as controls. Thirty-five migrating myoelectric complexes were recorded in Roux dogs and 13 in controls. In Roux dogs, the incidences of retrograde propagation of slow waves during the migrating myoelectric complex were phase I 56 +/- 13%, phase II 60 +/- 12% and phase III 58 +/- 14% (not significant). For controls, the incidences were 0%, 0%, and 1%, respectively (P < 0.006 versus Roux dogs). In the Roux limb, retrograde propagation of slow waves, and hence spike bursts, occurs even during aboral migration of phase III. This abnormality may contribute to the Roux Y stasis syndrome.

Postprandial changes in intestinal slow-wave propagation reflect a decrease in cell coupling.

The purpose of these studies was to determine the effects of feeding on jejunal slow-wave propagation velocity (SWPV). Nine cats were instrumented with six pairs of electrodes implanted 4 cm apart on the jejunum. Electrical activity was recorded at the end of an 18-h fast after which each animal was fed 60 g of canned cat food. Recordings were continued during feeding and for several hours thereafter. This procedure was repeated at least twice for each cat. Average SWPV (cm/s) decreased from a fasting level of 2.28 +/- 0.20 (mean of means +/- SE) to 1.93 +/- 0.16 at 10-20 min, 1.51 +/- 0.11 at 1 h, and 1.37 +/- 0.10 at 3 h postprandially. Corresponding SW frequencies (SWFs) were 19.6 +/- 0.3, 18.7 +/- 0.2, 19.2 +/- 0.2, and 19.0 +/- 0.2 cycles/min, respectively. The differences between the fasting SWPV and that at 1 and 3 h were significant (P less than 0.05). When SWPV was plotted as a function of SWF, the slopes of the corresponding curves were also found to decrease postprandially (P less than 0.05, fasting vs. 1 and 3 h). There was no apparent change in SW amplitude, maximum rate of SW depolarization, or threshold. In the absence of changes in these parameters, the divergence of the slopes at lower SWFs indicates that the decrease in SWPV is because of increased internal resistance, probably the result of uncoupling of intestinal muscle cells. The change is rapid in onset and long in duration, suggesting that an uncoupling factor is released during ingestion of a meal, and that its effect persists for several hours.

Changes in intercellular electrical coupling of smooth muscle accompanying atrophy and hypertrophy.

Longitudinal tissue impedance was determined for cat circular intestinal muscle that was either hypertrophied due to volume overloading or atrophied due to defunctionalization. These conditions were produced by bypassing 50 cm of jejuno-ileum in six cats and, 2-6 mo later, removing segments from the proximal jejunum of the hypertrophied functional gut and from the atrophied proximal end of the bypassed loop. Impedances were compared with those of jejunal circular muscle from 15 normal cats. Specific tissue impedance was determined by a modification of the method of Tomita (J. Physiol. Lond. 201: 145-159, 1969), which employs Krebs and Krebs-sucrose solutions; a tissue shrinkage of 5%, empirically found to occur in Krebs-sucrose solution, was corrected for. Impedance values were determined at 20 frequencies between 30 Hz and 30 kHz. The value at 30 kHz was taken to represent the specific myoplasmic resistance (Rmyo) of each tissue, while the difference between the value of 30 Hz and 30 kHz was taken to represent the specific junctional resistance (Rj). Values (in omega X cm) for Rmyo were control 134 +/- 2, functional 128 +/- 5, bypassed 151 +/- 6 (mean of means +/- SE). Corresponding values for Rj were control 173 +/- 15, functional 96 +/- 27, bypassed 340 +/- 75. Calculated values (in microF/cm) for junctional capacitance were control 2.66, functional 6.10, bypassed 1.97. Acid uncoupling by saturating the bathing solutions with 100% CO2 revealed a pH-sensitive resistive component of Rj, assumed to be attributable to gap junctions.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrical coupling of longitudinal and circular intestinal muscle.

Space constants (lambda) were determined for longitudinal-circular muscle strips of cat jejunum by the partition method. Pulses of hyperpolarizing current spread along the major axes of circular muscle cells. In the absence of electrical coupling lambda measured from the longitudinal side of the strips should have been approximately 20 times shorter than lambda measured from the circular side. Median values were found to be statistically the same, 2.4 mm for the longitudinal side (n = 13) and 2.9 mm for the circular (n = 25). Methyl blue, iontophoretically injected into cells on the longitudinal side after recording large hyperpolarizing responses, was found in muscle cells located superficially in the longitudinal layer. The radial lambda for longitudinal muscle, determined from the change in magnitude of the hyperpolarizing response as the microelectrode was advanced through the layer, was 0.27 mm. This is too large to cause differences in depth of recording to significantly affect the circumferential lambda in this layer. These data provide evidence for a high degree of electrical coupling between the two muscle layers of cat jejunum.

Chronic electrical activity of cat intestine.

Spontaneous electrical activity was recorded with bipolar electrodes from the gastrointestinal tracts of unanesthetized fasted cats (upper and lower cut-off frequencies: 35 and 3 Hz). In addition to slow waves (SWs) and spike potentials (SPs), the following three patterns of activity were recorded that are not observed in vitro. 1) Intense bursts of SPs (migrating spike complexes, MSCs) migrate caudally at a velocity of approximately 1 mm/s. MSCs resemble migrating myoelectric complexes (MMCs) in their velocity and by their traversal of intestinal anastomoses. SWs are usually suppressed during and immediately after the MSC, and, on their return, propagate at a higher velocity than they do prior to the MSC. Unlike its effect on MMCs, motilin does not appear to elicit MSCs, a finding consistent with the fact that MSCs occur infrequently in the duodenum and not at all in the antrum. 2) Bursts of SPs are found in the absence of recorded SWs. The SP bursts are of variable duration and occur virtually simultaneously at several recording sites, or propagate at 1-2 cm/s in either direction along the jejunum. The more usual caudally propagating SPs occur when SWs reappear. 3) "Minute rhythms," periods of spiking SWs, occur simultaneously over long lengths of upper bowel, sometimes including antrum, at intervals of about 1-2 min. It is proposed that, despite their differences, the cat MSC may be the functional counterpart of the MMC, that cat SWs are not omnipresent, and that the minute rhythms described here are of central origin.

Gastric and small intestinal myoelectric dysrhythmia associated with chronic intractable nausea and vomiting.

We describe a patient with symptoms of severe nausea, vomiting, epigastric bloating and pain, and marked weight loss due to a gastrointestinal motility disturbance. Motility abnormalities were characterized by uncoordinated high pressure (as high as 300 mm Hg) contractions and uncoordinated interdigestive motor complexes in the duodenum and small intestine, and tachygastria often associated with tachyarrhythmia in the gastric myoelectric activity recordings. Uncoordinated interdigestive myoelectric complexes again were found in the duodenum and small intestine. These abnormal myoelectric activities observed in the in-vivo study were confirmed in the in-vitro study. After distal hemigastrectomy and gastrojejunostomy, the symptoms of nausea, vomiting, and epigastric pain decreased considerably. Thus, the motility abnormality found in the study appears to be responsible for the symptoms described. This is probably a new clinical entity. The importance of manometric and myoelectric study of a gastrointestinal motility for unexplained nausea and vomiting is emphasized.

Dominance of longitudinal muscle in propagation of intestinal slow waves.

The purpose of these experiments was to test the hypothesis that circular muscle plays an active role in the propagation of intestinal slow waves, specifically be providing excitatory current through a process of regenerative amplification. With volume-recording techniques and microelectrode recordings we obtained the following results that are not consistent with such a mechanism: 1) slow waves propagated without delay or decrease in amplitude along segments of cat jejunum devoid of a ring of circular muscle up to 3 mm wide, i.e., across a longitudinal muscle bridge more than 4 space constants long (9 of 11 preparations) but did not propagate across a circumferential cut through the longitudinal muscle layer (14 of 14 preparations); 2) the membrane current associated with the slow wave had a pronounced inward component when recorded from either the serosal or the mucosal side of the longitudinal muscle bridge but was entirely outward when recorded from either the mucosal or the serosal side of exposed circular muscle, including those preparations in which various thicknesses of circular muscle were removed from the mucosal side of the recording area; 3) slow-wave amplitudes recorded intracellularly from intact (n = 9) and isolated (n = 8) longitudinal muscle preparations were not significantly different (27.0 +/- 4.3 vs. 25.4 +/- 5.3 (SD) mV); 4) after 30 min in 4.4 X 10(-6) M verapamil, slow-wave amplitude did not significantly decrease, although contractile activity had long since terminated. These results are more consistent with the hypothesis that longitudinal muscle provides most, if not all, of the current required for slow-wave propagation in the small intestine.

Stimulation of intestinal smooth muscle by atropine, procaine, and tetrodotoxin.

In order to determine whether or not atropine, procaine, and tetrodotoxin (TTX) can stimulate intestinal smooth muscle directly, we examined the effects of these drugs on the mechanical and electrical activities of several types of cat intestinal smooth muscle preparations. The preparations consisted of isolated rings of 1) intact intestinal wall, 2) intact longitudinal and circular muscle, 3) ganglion-free circular muscle, and 4) ganglion-free circular muscle devoid of its dense layer and plexus muscularis profundus. Atropine and procaine (greater than 10(-4) M) stimulated all four types of preparation. On the other hand, TTX (up to 5 X 10(-6) M) stimulated only preparations 1 and 2. It is concluded that whereas atropine and procaine can directly stimulate intestinal smooth muscle, the excitatory effect of TTX is neurally mediated.