Clinical features and outcomes of delayed perforation after endoscopic submucosal dissection for early gastric cancer.

Perforation is a major complication of endoscopic submucosal dissection (ESD) for early gastric cancer (EGC). However, there have been no reports on delayed perforation after ESD for EGC. We aimed to elucidate the incidence and outcomes of delayed perforation after ESD. Clinical courses in 1159 consecutive patients with 1329 EGCs who underwent ESD were investigated. Delayed perforation occurred in six patients (0.45 %). All these patients had complete en bloc resection without intraoperative perforation during ESD. Five of six perforations were located in the upper third of the stomach, while one lesion was found in the middle third. Symptoms of peritoneal irritation with rebound tenderness presented within 24 h after ESD in all cases. One patient did not require surgery because the symptoms were localized, and recovered with conservative antibiotic therapy by nasogastric tube placement. The remaining five patients required emergency surgery. There was no mortality in this case series.

Prostaglandin E2-induced sensitization of the heat response of canine visceral polymodal receptors in vitro.

The sensitizing effect of prostaglandin (PG) E2 on the heat response of testicular polymodal receptors was studied in vitro by recording single polymodal receptor activities from the testis-spermatic nerve preparations excised from deeply anesthetized dogs. PG E2 at 10(-7) M had no significant influence on the heat response. PG E2 at 10(-6) and 10(-5) M did not induce substantial increases in discharge rates, yet it significantly augmented the heat response. The concentration necessary for augmenting the heat response is thus 100 times greater than that (10(-8) M) previously reported for bradykinin [Naunyn-Schmiedebergs Arch. Pharmacol., 344 (1991) 368-376].

Protective effects of ether, oxygen and their mixture for radiation in Drosophila melanogaster.

Protective effects of ether mixed with air or oxygen against ionizing radiation damages were demonstrated in adult flies of Drosophila melanogaster. The protective effects against knock-down on the 2nd day and lethality on the 8th day after irradiation were not affected by the radiation sensitivity and DNA repair capacity of the strains. Ether (4.2%) in oxygen was more effective than ether in air for both endpoints. The protective effects may be due to damages not involving cell division, since no mitotic cells are observed in adult flies except in gonadal glands. A change in the orderliness of the cell membrane by ether is suggested to be the cause of the protective effects.

A trial of quantitative estimation of Al-corrosion detected by neutron radiography.

Comparing the hydrogen content in aluminum hydroxides, one of the main components of Al-corrosion, with that in polyethylene sheets, corroded degree of practical Al-corrosions were estimated quantitatively by neutron radiography.

Sensitizing effects of bradykinin on the heat responses of the visceral nociceptor.

1. Whether bradykinin (BK), which is known as an endogenous pain-producing substance, induces augmentation of the discharges of polymodal receptors evoked by heat stimulation was investigated in in vitro canine testis-superior spermatic nerve preparations. 2. The heat response was significantly augmented by pretreatments with BK at concentrations greater than 0.094 nM, whereas BK induced significant increases in the mean discharge rates at concentrations above 9.4 nM. Both effects increased in a concentration-dependent manner. The augmenting effect of BK on the heat response diminished within 10 min after application of BK, regardless of concentration. 3. When 9.4 nM BK was applied in a mixture with 940 nM NPC349, a B2 receptor antagonist, the averaged mean discharge rate evoked by BK and the averaged augmenting effect were both significantly suppressed compared with those induced by BK given alone. 4. The augmenting effect of BK on the heat response of polymodal receptors could be observed even in the absence of BK-evoked discharges per se in several cases in which low concentrations of BK or BK plus B2 antagonists were given. 5. These findings suggest that the augmenting effects of BK on the heat response depend on B2 receptor-mediated intracellular processes acting in parallel to, but not directly on, the impulse-generation mechanism of the heat response of the polymodal receptor.

Sympathetically induced paradoxical increases of the cutaneous blood flow in chronically inflamed rats.

In adjuvant arthritic (AA) rats, an abnormal responsiveness of nociceptors (C-fibre polymodal receptors) to sympathetic activities, i.e., alpha 2-adrenoceptor mediated activation of C-fibre polymodal receptors (CPRs), has been observed. The present investigations were undertaken to determine if a similar plastic change would occur in the cutaneous vascular system in the rat chronic inflammation model. The vascular responses were measured by a laser-Doppler flowmeter in the hindpaw skin of the AA rats after electrical stimulation of lumbar sympathetic trunk (sympathetic stimulation). In control non-arthritic rats, the sympathetic stimulation caused decrease in blood flow of the skin (SkBF) in all animals tested (n = 7). On the other hand, the sympathetic stimulation in the AA rats caused both increase (n = 15) as well as decrease (n = 11) in SkBF. In contrast to the abnormal responsiveness of CPRs, the intra-arterial injection of noradrenaline caused the expected decrease in SkBF in all animals tested, and in no instances increases in SkBF were observed. To determine whether activation of nitric oxide (NO), which is known to be a potent endogenous vasodilatation substance, was involved in the vasodilating effect to sympathetic stimulation, an inhibitor of NO synthase, NG-monomethyl-L-arginine (L-NMMA), was applied systemically. L-NMMA significantly increased baseline blood pressure in the control and the AA rats, but it did not significantly alter the SkBF in the control or the AA rats after the sympathetic stimulation, suggesting that NO is not a mediator in the vasoactive responses. The results of the current studies showed for the first time that electrical stimulation of the lumbar sympathetic trunk causes vasodilatation in the skin of the AA rats. This abnormal responsiveness of regional SkBF after sympathetic stimulation was not mediated by adrenergic or NO system.