We investigated the contractile mechanisms of action of three putative gastroprokinetic agents (cisapride, metoclopramide, and domperidone) on the linear phase of gastroduodenal emptying of solid meals in six healthy conscious dogs. The spatial and temporal parameters of gastric, pyloric, and duodenal contractions during the entire period of gastroduodenal emptying, during the 60-min period of drug infusion (ti), and during the postdrug infusion period (tpi) were analyzed by a computer method. Cisapride accelerated the total gastroduodenal emptying time (tfull), metoclopramide had no significant effect, and domperidone delayed the tfull. None of the drugs had a significant effect on gastroduodenal emptying during ti. Both cisapride and metoclopramide enhanced the rate of gastroduodenal emptying during tpi. Cisapride enhanced pyloric and duodenal motor activity but had no significant effect on antropyloroduodenal coordination during tfull and ti. During tpi, cisapride significantly enhanced both the pyloric and duodenal motor activity and antropyloroduodenal coordination. Metoclopramide exhibited only a few significant effects on the frequency, amplitude, duration, and area under contractions in the antrum, pylorus, and duodenum, but it enhanced antropyloroduodenal coordination during tfull and tpi. Domperidone decreased the frequency of corporeal, pyloric, and duodenal contractions and deteriorated antropyloroduodenal coordination by decreasing the frequency of contractions propagating from the antrum or the pylorus to the duodenum. Cisapride and metoclopramide, but not domperidone, increased the mean distance of propagation of duodenal contractions during tfull, ti, and tpi. We conclude that cisapride is more effective in accelerating gastroduodenal emptying because it stimulates the largest number of parameters of gastropyloroduodenal contractions that enhance gastric emptying. Most enhancement of gastric emptying rate with both cisapride and metoclopramide occurs during tpi.
The effect of nitric oxide (NO) synthase inhibition on the gastric emptying of nutrient and nonnutrient meals was investigated in nine dogs. The inhibition of NO synthase delayed the gastric emptying time of both nutrient and nonnutrient meals, but the percentage delay of nutrient meals was significantly greater than that of nonnutrient meals. The inhibition of NO synthase during the emptying of nonnutrient meals enhanced mainly the amplitude of antral, pyloric, and distal duodenal contractions. However, NO synthase inhibition during the emptying of nutrient meals stimulated several spatial and temporal parameters of gastropyloroduodenal contractions. We conclude that NO is one of the neurotransmitters of intestinal feedback that regulates the gastric emptying of both nutrient and nonnutrient meals. The nature and intensity of intestinal feedback by the stimulation of both chemo- and mechanoreceptors by nutrient meals is different from that by the stimulation of mechanoreceptors only by the nonnutrient meals.
We herein present the case of a-58-year-old female with a metastasis of breast cancer to the appendix, which caused acute appendicitis. She had undergone a bilateral partial mastectomy with sentinel lymph node biopsy ten years earlier at another hospital. She had subsequently received radiation therapy, chemotherapy and endocrine therapy. There had been no sign of recurrence for five years after the surgical procedure. She was admitted to our hospital because of abdominal pain lately. Abdominal computed tomography showed a dilated and thickened wall of the appendix. She was diagnosed with acute appendicitis and underwent appendectomy. A histopathological examination revealed metastatic breast cancer of the appendix, and the patient received endocrine therapy using an aromatase inhibitor. Metastatic involvement of the appendix should be suspected in any patient with a previous history of breast cancer presenting with acute appendicitis, even if many years have passed after initial therapy.
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