Laparoscopic lower anterior resection is equivalent to laparotomy for lower rectal cancer at the distal line of resection.

BACKGROUND: Procedures that involve resection of the distal rectum challenge the current limitations of laparoscopic technology, because of lack of compact articulating stapling instruments. METHOD: We improve the procedure with the aid of a Lap disk, an abdominal wall sealing device that was developed for hand-assisted manipulation. A linear stapler capable of changing its stop angle is inserted through the disk, and the rectum is transected by the disk during a second pneumoperitoneum. RESULTS: The transection line becomes equivalent to that obtained with laparotomy. CONCLUSION: This new technique made laparoscopic lower anterior resection possible to transect the lower rectum in the same way as is done with laparotomy.

Role of platelet activating factor on severity of ischemic colitis.

PURPOSE: Ischemic colitis develops after a sudden decrease in colonic blood supply and has a variety of clinical manifestations. The aim of this study was to assess the role of platelet activating factor in the pathogenesis of ischemic colitis with use of the platelet activating factor antagonist TCV-309. METHODS: Rats were randomly divided into four groups. Rats in Group RV underwent ring attachment around the rectum to induce partial obstruction and ligation of the marginal vessels of the left colon. As control, rats in Group R underwent the ring attachment and rats in Group V underwent the vascular ligation. Rat in Group C underwent sham operation. The effects of TCV-309 on lesion formation in the colon were evaluated. Thiobarbituric acid reactant level was determined in colonic mucosa, and the incidence and severity of ischemic lesions were also determined. RESULTS: Lesions of colitis were frequently observed in Group RV. TCV-309 did not prevent lesion formation, nor did it suppress the increase in thiobarbituric acid reactant level in Group RV. However, TCV-309 mitigated the severity of the lesion. CONCLUSIONS: Partial obstruction of the colon tends to induce ischemic colitis, and additional ischemia completes lesion formation. Platelet activating factor may play a role in the progression of ischemic lesions.

Impaired response of gastric vessels to prostaglandin E2 in rats with persistent obstructive jaundice.

We investigated the response of gastric vessels to prostaglandin (PG) E2 after intra-duodenal release of bile in rats with obstructive jaundice. The animals were divided in four groups according to duration of bile duct obstruction (BDO): control and 1 week (W), 2W, and 3W groups. Prolonged BDO decreased gastric mucosal blood flow (BF) significantly. The BF recovered after the release of BDO in the 1W and 2W groups, but not in the 3W group. BDO decreased PGE2 content in gastric mucosa in the 1W, 2W, and 3W groups. PGE2 decreased vascular perfusion pressure of the isolated stomach in the control and 2W groups, but not in the 3W group. The response of gastric vessels to PGE2 was poor in the 3W group compared with the control and 2W groups. Decreased PGE2 in the gastric mucosa and decreased response of gastric vessels to PGE2 may affect gastric blood flow in obstructive jaundice.

Helicobacter pylori may cause "reflux" gastritis after gastrectomy.

Patients with "reflux" gastritis after gastrectomy suffer from a variety of symptoms, and this type of gastritis may sometimes compromise the quality of life of these patients. Since Helicobacter pylori is considered to be one of the most important pathogenetic factors in gastritis, the association between H. pylori and reflux gastritis was investigated in this study. A total of 145 patients with gastrectomy were entered into the study. Five biopsy specimens from the gastric remnant were taken at upper gastrointestinal endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. Fifty-two patients (36%) demonstrated H. pylori infection. The prevalence of H. pylori was significantly higher in patients who had a partial gastrectomy, and it was significantly lower in patients who had undergone gastrectomy more than 4 years previously. The histologic gastritis score in patients with H. pylori infection was significantly higher. Furthermore, H. pylori was eradicated in patients with some symptoms of gastritis and no bile reflux to the residual stomach at endoscopy; in these patients the symptoms were relieved and the histologic gastritis score decreased significantly. In conclusion, possible involvement of H. pylori is suspected in the pathogenesis of "nonreflux" gastritis after gastrectomy.

Etiological involvement of Helicobacter pylori in "reflux" gastritis after gastrectomy.

OBJECTIVES: "Reflux" gastritis after gastrectomy is associated with various symptoms that are often detrimental to the patients' quality of life. However, prevention of the reflux does not always bring relief from the symptoms of gastritis. Helicobacter pylori (H. pylori) is now considered one of the most important pathogenetic factors in gastritis. The association between H. pylori infection and reflux gastritis after gastrectomy was investigated in the present study. METHODS: In total, 115 patients who had undergone gastrectomy were entered in this study. Five biopsy specimens from the gastric remnant were taken during upper GI endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. The histological degree of gastritis was determined according to the score system of Rauws et al. RESULTS: Forty-six patients (40%) demonstrated H. pylori infection in their stomachs. The prevalence of the infection was significantly higher in patients with conventional gastrectomy than in those with subtotal gastrectomy. The prevalence of H. pylori infection was significantly lower in patients who had undergone gastrectomy more than 4 yr ago. The histological gastritis score in patients with H. pylori infection was significantly higher than in those without H. pylori infection. Furthermore, the eradication of H. pylori in patients with both serious gastritis symptoms and no bile reflux improved the symptoms and significantly decreased the histological gastritis score. CONCLUSIONS: The results suggest that H. pylori is a factor in the pathogenesis of reflux gastritis after gastrectomy.

[Role of platelet activating factor on the formation of ischemic colitis].

Role of platelet activating factor (PAF) on the formation of rat ischemic colitis was investigated. High incidence of the formation of ischemic colitis was observed after ligation of marginal vessels of the rat with stricture of the rectum, however, administration of PAF-inhibitor (TCV) decreased incidence of the lesion. Only the lesion in the mucosa occurred after clamping of the marginal vessels of the rat with stricture of the rectum and administration of TCV did not affect the incidence of the lesion. In conclusion, the etiological involvement of PAF on deterioration of the ischemic colitis was suspected.

Inhibitory effect of dopamine on gastric motility in rats.

BACKGROUND: There is disagreement with regard to the involvement of dopamine (DA) receptors in gastric motility. The mechanisms of the inhibitory effect of DA on rat gastric motility was investigated in association with acetylcholine (Ach) release in the present study. METHODS: In vivo vagotomized, splanchnicectomized rats and control rats were used, and gastric movement was determined as the gastric motility index after DA administration. In vitro study of Ach release from the circular muscle strips of the gastric corpus was investigated after administration of domperidone, SCH23390, phentolamine, or propranolol. RESULTS: In the in vivo study DA inhibited gastric motility in a dose-dependent manner. Vagotomy and splanchnicectomy had no effect on the inhibitory effect of DA. In vitro study DA inhibited [3H]-Ach release in a dose-dependent manner. The inhibitory effect of DA was antagonized by domperidone but not by phentolamine, propranolol, or SCH23390. CONCLUSIONS: Inhibition of gastric motility by dopamine is independent of extrinsic innervation and seems to be mediated by DA2 receptors in the gastric wall.

[A case of spontaneous mesenteric fibromatosis occurred from the mesentery of the small intestine].

The fibromatosis is benign tumor which is characterized by the remarkable proliferation and the invasive growth of fibrous tissue and no distant metastasis. It usually occurs from the abdominal wall or the extremities, and rarely from the mesentery. A 54-year-old male complained of an epigastralgia and emesis. He was diagnosed through imaging as the obstructive ileus by abdominal tumor. The laparotomy was performed and a round, egg sized tumor was found wear by dilated ileum. The tumor was considered to occur from the mesentery, and the iliectomy with the tumor was completed. It was suggested that ileus occurred in the early stage because the tumor was located just by the ileum.

[Residual gastritis after gastrectomy and Helicobacter pylori--its clinical significance].

Residual gastritis after gastrectomy brings the various symptoms such as abdominal pain, nausea, emesis and loss of appetite, and often hazards quality of life of the patient. Bile reflux to the stomach is believed as one of the important pathogenesis of residual gastritis, however the prevention for bile reflux cannot always heal the gastritis. Helicobacter pylori (H. pylori) is considered as one of the most important pathogenesis of gastroduodenal ulcer and gastritis, and H. pylori may possibly cause residual gastritis after gastrectomy. However, the association between infection with H. pylori and the residual gastritis has not revealed yet. In the present study, the association with H. pylori and the residual gastritis after gastrectomy was investigated in 56 patients who had undergone gastrectomy before. Twenty-four patients (42.9%) had H. pylori infection at their stomachs and the incidence of the infection in the patients with gastrectomy was significantly higher with subtotal gastrectomy. As for the histological gastritis score of Rauws (Rauws' score), Rauws' score of H. pylori positive group was significantly higher than H. pylori negative group. Furthermore, the eradication of H. pylori for the patients with serious symptoms of gastritis improved the symptoms and decreased significantly Rauws' score. These results suggest that H. pylori was associated with the pathogenesis of residual gastritis after gastrectomy.

Protein kinase C alpha-, beta- and gamma-subspecies in basal granulated cells of rat duodenal mucosa.

Protein kinase C [cPKC: alpha, beta (beta I, beta II), gamma], a Ca(2+)- and phospholipid-dependent enzyme, has been thought to play a critical role in the synthesis and secretion of gut hormones in gastrointestinal mucosa. However, the localization of PKC has not yet been clarified at the cellular level in the gastrointestinal epithelium. The present study was made to identify cPKC-containing cells immunohistochemically in the rat duodenal epithelium by light and electron microscopy and by confocal laser scanning microscopy. Special attention was paid to the demonstration of cPKC in basal granulated cells. By light microscopy, some duodenal epithelial cells were demonstrated to be immunopositive for PKC alpha-, beta- and gamma-subspecies. Their distribution and incidence were almost similar to those of cells stained by the silver impregnation method of Grimelius. By electron microscopy, profiles of secretory granules were found at the basal region of the PKC-immunopositive epithelial cells. When the cells were double-immunostained for gastrin, serotonin or somatostatin and for PKC alpha-, beta- or gamma-subspecies, these gut hormones and PKC subspecies were shown to colocalize as examined by confocal laser scanning microscopy. These findings show that cPKC (alpha, beta, gamma) is present in basal granulated cells such as G-, EC- and D-cells, presumably playing some important role in regulation of gut hormones, including their synthesis and/or secretion.

[The mechanism of development of acute gastric ulceration following biliary drainage in obstructive jaundice].

Upper gastrointestinal hemorrhage occurs occasionally in the time of surgery or biliary infection in patients with obstructive jaundice. In the present study, the influence of obstructive jaundice and biliary drainage on the rat gastric mucosa was examined. Serum t-Bil, GOT and Alp increased during obstructive jaundice, but decreased following biliary drainage. Hexose and fucose levels in gastric mucosa decreased during obstructive jaundice; both of them increased in the 1- and 2-week jaundiced groups, however, neither increased in the 3-week jaundiced group following biliary drainage. Prolonged obstructive jaundice demonstrated a marked increase of ulcer index (UI) and decrease of gastric mucosal blood flow (BF) following water immersion and restraint stress. Biliary drainage induced these changes in the 1- and 2-week jaundiced groups, but induced neither of these changes towards recovery in the 3-week jaundice group. Prostaglandin (PG) E2 induced significant decrease in isolated gastric vascular perfusion pressure in the 2-week jaundiced group; it did not, however, have this effect in the 3-week jaundiced group. In conclusion, it was speculated that differences between the 3-week and 2-week jaundiced groups were present in sensitivity to PGE2 in the gastric vascular system, and that different reactions of the gastric microcirculation resulted in different changes in the gastric mucosal state following biliary drainage.

Immunohistochemical study of dopamine in rat gastric mucosa with acute gastric ulcer.

Recent studies have shown the presence of dopamine (DA) in gastric and duodenal mucosa, and changes in gastric mucosal DA content have been observed in patient with acute ulcers. Immunohistochemical demonstration of the distribution of DA in gastric mucosa under stress was studied by light and electron microscopy. In the control group, DA was present in the gastric gland proper in the gastric corpus and antrum on light microscopy, and on the surface of mucous granules in chief cells, mucous neck cells, and surface epithelium on electron microscopy. In the stress group, DA in gastric mucosa was almost undetectable on light and electron microscopy. Further, in this group serum DA concentration was significantly higher in the portal vein than in the abdominal aorta. Endogenous DA in gastric mucosal cells may affect gastric mucosa differently from exogenous DA, and stress may release endogenous intracellular DA into extracellular spaces.

[A case report of allergic granulomatous angitis with the perforation of ileum].

A case of allergic granulomatous angitis (AGA) complicated with the perforation of the ileum was described. A 52-year-old male had suffered from bronchial asthma since 1990, and two years later he had severe attack of asthma and manifestation of systemic vasculitis. He was diagnosed a AGA with the symptom of vascultitis, history of asthma, and the abnormal hematological findings (WBC 13000/mm3, eosinophilia 11.1%, IgE 1290U/ml, RA 2+). The treatment with adrenal corticoid hormone was started. In April 1992, he complained of severe right lower abdominal pain. He was diagnosed the gastrointestinal perforation by the abdominal X-ray examination and emergency operation was performed. Two ileal perforations were found at the operation and the ileectomy was carried out. Only 11 cases of AGA complicated with the gastrointestinal perforation have ever been reported in Japan. The perforation occurred often at the small intestine and the poor prognosis was referred. The administration of adrenal corticoid hormone should be continued after operation.

An immunohistochemical study of glucagonoma conducted on the metastatic lymph nodes from a patient with recurrent metastatic glucagonoma: report of a case.

In this report, we briefly present the case of a 67-year-old woman who developed recurrent glucagonoma with lymph node metastasis. An immunohistochemical study of the metastatic tumor revealed immunoreactivity of glucagon and protein kinase C (PKC)-alpha, -beta, and -gamma in the tumor cells, two types of which were seen by electron microscopy. One type had abundant secretory granules and mitochondria, while the other had few granules and mitochondria. Some granules were similar to typical A cell granules and others were atypical. An immunoelectron microscopic demonstration revealed PKC-alpha, -beta, and -gamma immunostaining in the cytoplasm of all the tumor cells, while some secretory granules had PKC immunostaining, and others had no immunostaining. Thus, it appears that metastatic glucagonoma and its associated granules are composed of two types of mature and immature cells or granules. As immunoreactivity of PKC-alpha and -gamma was found in the tumor cells, but not in the normal A cells of the islets of Langerhans, the PKC subspecies alpha and gamma, which are not present in normal pancreatic A cells, may exist in human glucagonoma cells.

[Experimental study on the etiology of ischemic colitis].

A reliable experimental model for ischemic colitis in rat could be obtained by ligating the marginal vessels of the colon 3 days after attaching the ring to induce partial colon obstruction. This model has the advantage of enabling to observe the chronic progress and the organ of the sideration to clarify the cause of ischemic colitis. The decrease of blood flow within the colonic mucosa continued up to 7 days after ligation in rat with partial obstruction, while no apparent abnormal changes were observed, and the previous level for several hours in the rats with out attaching the ring. This fact proved that the RT group is in a state easily developing sideration due to the sustained partial colon obstruction. The reactant reacting with thiobarbituric acid (TBA) was found to increase, in particular, 6 or more hours after ligation of vessels. A superoxide scavenger, liposomal-encapsulated superoxide dismutase (1-SOD) suppressed development of the ischemic lesion. The change in free radicals is therefore, considered to be involved in the occurrence of ischemic colitis.

A case of benign schwannoma of the thoracic wall mimicking a malignant tumor.

A fist-sized tumor mainly locating in the right thoracic wall of a 73 year-old woman was found by ultrasonography and computed tomography, although a definitive diagnosis was not obtained because of the tumor extension to the abdominal cavity from the right internal thoracic wall, precluding biopsy. Angiography of the right eleventh intercostal artery demonstrated irregular tumor vessels, indicating malignant nature of the tumor. Therefore en-block resection of the tumor with the right eleventh rib was performed under a thoracotomy. Postoperative histopathological examination showed that the tumor was a benign schwannoma of Antoni type A. Since schwannoma is usually difficult to diagnose preoperatively without histopathological study, it is suggested that patients with schwannoma-like tumors, as represented by the present case, should be treated carefully to avoid excessive surgery including an extensive resection of the surrounding tissue.

Effect of pirenzepine on postoperative gastric secretion.

Post surgical stress ulcers of the upper digestive tract, once developed, is difficult to control depending on the primary disease and associated complications. As to the cause of postoperative stress ulcers, decreased defensive factors such as gastric mucosal blood flow and increased gastric secretions have been pointed out. Recently, pirenzepine hydrochloride has been shown to be a specific antagonist of muscarinic cholinergic M1 receptors and a suppressant of gastric acid secretion. Therefore we studied its effect on gastric secretions in postoperative patients. Twenty one patients admitted for abdominal surgery, excluding gastric surgery, were selected and randomly assigned to the pirenzepine group (10 cases) or control group (11 cases). Since the serum half life of pirenzepine is 10 hours, 20mg of pirenzepine was administered intravenously immediately after the operation and twice daily (9 a.m. and 9 p.m.) from postoperative day 1 until day 7. Gastric secretions and gastric pH were measured preoperatively and daily until day 7. In the control group, significant increases in the volume of secretion and significant decreases in gastric pH were observed after the operation. In contrast, the pirenzepine group had a significantly decreased amount of gastric secretion and the gastric pH was higher than those in the control group. Thus we conclude that pirenzepine decreases gastric secretion and increases gastric pH in postoperative patients. Pirenzepine can be regarded as an effective agent for the control of postoperative gastric hypersecretion and possibly a good prophylactic for postoperative stress ulcers.

The effect of dopamine on rat gastric motility.

The inhibitory mechanism of dopamine (DA) on rat gastric motility was investigated in association with DA receptors. Gastric movement was assessed according to the method of Jacoby et al and was expressed with the system of Ludwick et al. (1968). DA inhibited gastric movement in both the corpus and antrum in a dose-dependent manner. Domperidone, a specific antagonist of DA2 receptor, suppressed DA-induced inhibition of gastric movement in a dose-dependent manner. SCH23390, a specific antagonist of DA1 receptor did not affect DA-induced inhibition of gastric movement. LY171555, a specific agonist of DA2 receptor, inhibited gastric movement in both the corpus and antrum in a dose-dependent manner. SKF38393, a specific agonist of DA1 receptor, did not affect gastric movement. These results indicate that DA plays an important role in the inhibitory regulation of gastric motility, through DA2 receptor but not DA1 receptor.

[Inhibitory effect of peptide YY on gastric acid output in rats].

The purpose of this study was to elucidate the effect of Peptide YY (PYY) on gastric acid output in association with gastric mucosal blood flow (GMBF), acetylcholine (ACh) release in the gastric wall and gastric vascular perfusion pressure in rats. Baclofen stimulated the gastric acid output and GMBF in a dose-dependent manner. Both atropine sulfate and truncal vagotomy completely abolished the effect of baclofen. PYY caused inhibition of baclofen-stimulated gastric acid output and reduction in baclofen-stimulated GMBF in a dose-dependent manner, however PYY didn't cause inhibition of pentagastrin- and histamine-induced acid output completely. But PYY had no effect on bethanechol-induced acid output. PYY inhibited the [3H] ACh release from cholinergic nerve endings of gastric body evoked by electrical transmural stimulation. PYY had little effect on gastric vascular perfusion pressure in the basal state, and basal gastric acid output. In the present study, it was concluded that the mechanism of the inhibitory effect of PYY on gastric acid output seems to involve reduced ACh release from cholinergic nerves.

Effect of dopamine on prostaglandin E2 content in gastric mucosa.

The effects of dopamine (DA) on the prostaglandin (PG) E2 content of rat gastric mucosa was investigated. There was a 17.5% increase in gastric mucosal blood flow (BF) after administration of DA (5 micrograms/kg/min iv). After pretreatment with fusaric acid (FA), an antagonist of dopamine beta hydroxylase, DA increased BF by 27.8%. The PGE2 content in DA and DA + FA groups increased at rates of 45.8% and 42.4%, respectively. The PGE2 content in gastric mucosa after incubation following Basso's method, increased in the DA, DA + FA and noradrenaline (NA) groups to 3.32 +/- 0.40 micrograms/g, 3.30 +/- 0.39 micrograms/g and 3.37 +/- 0.42 micrograms/g respectively. It is concluded that there are no differences in PGE2 content among the DA, DA + FA and NA groups. The mechanism by which PGE2 content increases after administration of DA is the direct action of DA and/or increasing BF. It is suspected that DA directly affects PGE2 synthesis, however the possibility that DA is metabolized to NA, which secondarily results in increased PGE2 synthesis, cannot be excluded.