Yasutomo Azumi

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.

Study of 16,16-Dimethyl Prostaglandin E2 for Prevention of Stress Ulcer after Hepatectomy of Experimental Cirrhotic Liver and Its Influence on Hepatic Regeneration

The influence of 16,16-dimethyl prostaglandin E2 (16,16-dm PGE2; an agent used for the prevention of stress ulcer after hepatectomy of the cirrhotic liver) on liver regeneration after hepatectomy was studied in rats. The following results were obtained. Ulceration after the stress of 6 h of water immersion was markedly suppressed in rats treated with 30 r/kg of 16,16-dmPGE2 as compared with the untreated controls. In animals that received hepatectomy alone, the gastric pH and gastric mucosal blood flow showed significant reduction from the preoperative levels. In animals that received hepatectomy plus 16,16-dmPGE2 treatment the postoperative reduction in the gastric pH and gastric mucosal blood flow was suppressed, suggesting the effectiveness of 16,16-dmPGE2 treatment in the prevention of stress ulcer after hepatectomy of the cirrhotic liver. The 3H-thymidine uptake percentage and thymidine activity 24 h after hepatectomy and the DNA content 30 h after hepatectomy were significantly higher in animals treated with 16,16-dmPGE2 than in the untreated controls. In animals that were treated intraperitoneally with 50 mg/kg of indomethacin 6 h before hepatectomy the mitotic index 30 h after hepatectomy was markedly lower than that in untreated controls. This indomethacin-induced reduction in the mitotic index tended to be normalized by treatment with 16,16-dmPGE2. These results suggest that 16,16-dmPGE2 treatment effectively prevents stress ulcer and favorably affects hepatic regeneration after hepatectomy of the cirrhotic liver.

The mechanism of acute gastric ulcer after induced hemorrhagic shock.

Changes in gastric mucosal blood flow were investigated for their relationship to gastric mucosal prostaglandin E2 (PGE2) and noradrenaline (NA) in rats with hemorrhagic shock. The results were as follows: 1) Gastric mucosal blood flow and NA decreased after hemorrhage. Gastric mucosal PGE2 initially increased after exsanguination and then markedly decreased. 2) Administration of NA before hemorrhage resulted in an increase of PGE2. However, the PGE2 value for animals receiving NA after hemorrhage was not different from that of non-NA-treated group. 3) Pre-treatment with PGE2 suppressed the reduction in both gastric mucosal blood flow and NA and the development of ulcer. These results suggest that the increase in gastric mucosal PGE2 in the early stage of shock might represent a phenomenon of adaptation by the adrenergic activation, and the decrease in PGE2 in the late stage might result from impaired synthesis of PGE2 due to persistent hypoxia and might be one of the possible factors in ulcer formation.

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.

Incidence of esophageal injury after pulmonary vein isolation in patients with a low body mass index and esophageal temperature monitoring at a 39 °C setting

Esophageal injury following catheter ablation of atrial fibrillation (AF) is reported to occur in 35% of patients. Even with a low energy setting (20–25 W), lesions develop in 10% of patients. Body mass index (BMI) has been reported to be a predictor of esophageal injury, indicating that patients with a low BMI (<24.9 kg/m2) are at a higher risk. We hypothesized that catheter ablation with a lower energy setting of 20 W controlled by esophageal temperature monitoring (ETM) at 39 °C could prevent esophageal injury even in patients with a BMI <24.9 kg/m2.

Elderly case of Dieulafoy's lesion in the jejunum presenting with repeated hemorrhagic shocks

A 72-year-old man with hypertension was admitted to our hospital because of temporary stupor. On admission, neurological examination and brain magnetic resonance imaging showed no remarkable findings. Hemoglobin concentration of the blood was 14.4 g/dL. He developed shock following melena (day 1). Hematological examination after the shock revealed hemoglobin of 7.6 g/dL. Blood transfusion was performed. Initial gastrointestinal endoscopy and colonoscopy performed 4 h after the shock revealed blood in the colon, but did not reveal mucosal changes and the bleeding source. A second gastrointestinal endoscopy performed after a second shock revealed faint backward flow of the intestinal bleeding from the jejunum and did not show bleeding source in the esophagus, stomach and duodenum (day 2). Computed tomography (CT) and angiography performed on day 2 revealed the bleeding source (Fig. 1a– d). Although radiologists performed transcatheter arterial embolization (Fig. 1e), the patient developed a third shock following melena (day 4). A third gastrointestinal endoscopy showed a Dieulafoy’s lesion (DL) in the jejunum (Fig. 1f,g). We applied two clips and an endoscopic local injection of hypertonic saline– epinephrine solution. The hemostasis was successful. We could not perform gastrointestinal endoscopy after the treatment because of disappearance of melena and patient refusal. As in a similar previous report, we speculate that the DL in our case healed and disappeared. However, this could not be proven. Dieulafoy’s lesion is a vascular malformation and a rare but potentially life-threatening disease that is responsible for 7% of upper gastrointestinal hemorrhage. DL in the small intestine is extremely rare, and the diagnosis is difficult. In addition, elderly patients with DL can have several complications such as cardiovascular disease, chronic renal disease and dementia. Repeated hemorrhagic shocks can cause anemia and malnutrition, and worsen the general condition of elderly patients. Malnutrition among elderly patients leads to poor outcomes such as functional decline, frailty, the decline in quality of life and higher mortality. Nevertheless, DL located in the jejunum is beyond conventional gastrointestinal endoscopy. Angiography is useful for defining the lesion. Therefore, early detection of the bleeding source by repeated endoscopy, CT and angiography is necessary, and appropriate treatment is more important in elderly than young patients. Aging may be a risk factor for DL. The findings of DL in elderly patients suggest that atherosclerosis is associated with DL. DL also may be caused by an aneurysm in one of the vessels, perhaps in combination with atherosclerosis. Meanwhile, congenital or acquired vascular malformation might be an underlying cause in young patients. Although surgery had been performed in patients presenting with DL in the jejunum, endoscopic therapy is effective and safe in most cases. Endoscopic hemostasis is less invasive than surgery, especially for elderly patients. Although balloon-assisted enteroscopy recently has become practicable, this method was unavailable in our case. Transoral endoscopy accomplished by colonoscopy could be an alternative in emergency cases. This case highlights the unusual gastrointestinal hemorrhage that can induce repeated hemorrhagic shocks and malnutrition. The possibility of underlying causes in the small intestine should be kept in mind in patients with unusual gastrointestinal hemorrhage. Careful evaluation of the clinical and laboratory findings, and early treatment is important, especially in elderly patients. Geriatr Gerontol Int 2010; 10: 267–268

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. SinceHelicobacter pylori is considered to be one of the most important pathogenetic factors in gastritis, the association betweenH. 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 forH. pylori infection. Fifty-two patients (36%) demonstratedH. pylori infection. The prevalence ofH. 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 withH. 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 ofH. pylori is suspected in the pathogenesis of “nonreflux” gastritis after gastrectomy.

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 into 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.

Experimental Study of Vagotomy for Prevention of Stress Ulcer after Hepatectomy of Cirrhotic Livers Its Influence on Hepatic Regeneration

We experimentally studied the influence of vagotomy on hepatic regeneration in rats after hepatectomy of cirrhotic livers. In animals that underwent hepatectomy plus vagotomy the reduction in gastric pH was suppressed, but gastric mucosal blood flow was less than that in control animals that received hepatectomy alone. The suppression of 3H-thymidine uptake percentage and thymidine kinase activity after hepatectomy was more marked in animals treated with hepatectomy plus vagotomy than in controls treated with hepatectomy alone. Hepatic DNA level tended to be lower in animals treated with hepatectomy plus vagotomy than in controls. In animals treated with hepatectomy plus vagotomy, the peak level of the mitotic index was lower and the hepatic regeneration rate was evidently suppressed. These results suggest that it is not appropriate to apply vagotomy, during hepatectomy of cirrhotic livers, for the prevention of postoperative stress ulcer because it causes a marked reduction in gastric mucosal blood flow and suppresses hepatic regeneration.

A Rare Case of Bile Duct Cancer Associated with Pancreaticobiliary Maljunction without Bile Duct Dilatation Diagnosed by MRCP.

膵・胆管合流異常の診断にMRCPが有用であった胆管非拡張型合流異常に合併した胆管癌の1例を経験したので報告する. 症例は70歳の女性. 一過性の右季肋部痛あり, その6か月後黄疸が出現した. 全身状態は暦年齢以上に不良であった. MRCPでは中部胆管に縦径2cmの腫瘍像, 胆管の完全閉塞がみられたが, 腫瘍より下流の胆管に拡張はなく, 共通管が1.5cmの胆管合流型の膵・胆管合流異常を認めた. 高齢で低栄養であるため, 胆管切除術を施行した. 手術診断はEM1, DM0, HM0, Surgical Stage I, Cur Bであったが, 病理組織学的所見は高分化型管状腺癌, hm2, em2, comprehensive stage II, cur Cであり癌の遺残を認めた. 本例は非拡張型合流異常における積極的分流手術の必要性を示唆する1例と考えられた.