Studies were carried out, after laparotomy, in vivo and in vitro on the stomach and small intestine of a patient with severe idiopathic intestinal pseudoobstruction. Gastrointestinal electrical activities were recorded in vivo for 7 days postoperatively by 10 sets of bipolar electrodes implanted seromuscularly in the jejunum on both sides of an anastomosis, and in the stomach. The jejunal electrical control activity (ECA) frequency was very low (4.75 ± 5.34 SD cycles per min) and highly irregular immediately postoperatively, but its frequency and regularity improved over the next hour. Then ECA disappeared except during the occurrence of a migrating myoelectrical complex (MMC) at the recording sites. The mean duration of 28 MMC's was 5.91 ± 2.79 sd min. The mean interval between successive MMC's was 34.7 ± 18.9 sd min. Drugs like meperidine as well as small doses (2.5 μg per min) of prostaglandin F2α initiated MMC's, whereas morphine, pentagastrin, and larger doses of prostaglandin F2α initiated ECA with electrical response activity simultaneously at all the electrodes. Feeding ice cubes or a cup of tea also induced irregular ECA with electric response activity superimposed on it. Electrical stimulation during the absence of ECA could not restore it. When ECA was present, electrical stimulation could decrease but not increase the frequency of ECA, presumably because it was maximal. In vitro studies on longitudinal and circular muscle strips from a segment of jejunum removed from the patient during operation showed that the responses to transmural stimulation of intrinsic cholinergic or nonadrenergic inhibitory nerves and to drugs like acetylcholine, carbamoylcholine, physostigmine, serotonin, catecholamines, and ATP differed only quantitatively from responses to similar strips from normal small intestine. In conclusion, the total absence of ECA except during a MMC may be responsible for the motility disorder in this patient. Vagal activity may be essential for initiation of MMC's; if so, the efferent cholinergic system appeared to function. Idiopathic intestinal pseudoobstruction in this patient did not result from primary impairment of muscle contractile function, or of receptors to nerve mediator function of intrinsic cholinergic or nonadrenergic inhibitory nerves. We suggest hyperpolarization of intestinal smooth muscle may explain the absence of ECA and most other motility abnormalities in this patient.
ASJC Scopus subject areas