Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CINCHOPHEN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

Are epinephrine and gastrin accelerative factors of acute cinchophen ulcer?: Studies on gastric mucosal microcirculation and gastric secretion.

Measurements of serum epinephrine and gastrin, simultaneously, gastric mucosal blood flow and gastric secretion were carried out in cinchophen treated dogs. No significant changes in either serum concentrations of epinephrine and gastrin or fundic mucosal microcirculation after a single 100 mg/kg cinchophen administration were found while gastric secretion increased markedly after the medication. On the other hand, a significant increase in serum epinephrine and gastrin levels was observed while gastric secretion decreased significantly after large doses of cinchophen (300 mg/kg) were injected intravenously. Here gastric mucosal microcirculation is decreased. Repeated administration of 100 mg/kg cinchophen for 3 to 7 days brought about an increase in epinephrine and gastrin levels and caused an occurrence of fundic mucosal hemorrhage. Sympathetic discharge and gastrin release were not seen after a 3-week period of cinchophen administration. Cinchophen ulcers were produced, even when contact between the bile and the stomach mucosa was avoided. Vagotomy had no connection with ulceration and gastric secretion.

Animals↗
PubMed1977

Inhibitory effect of sulpiride on cinchophen gastric ulceration in dogs.

An intraventricular administration of sulpiride suppressed the experimental cinchophen ulcer, thereby the effect of repeated administration of the material on cinchophen ulcerogenesis is evident, whereas intermittent administration lacked this effect. Such an effect as reducing experimental cinchophen ulceration, which is due to central neurohumoral mechanism, following intraventricular infusion of sulpiride appears to be ascribable to a chemical blockage of the hypothalamic structure. It can thus be concluded that sulpiride acts principally at the level of hypothalamus. Its inhibitory action on cinchophen gastric ulcer development is probably exerted via the hypothalomo-pituitary-adrenal axis, which is essential to the occurrence of an ulcer, and may be regarded as favoring the central neurohumoral theory of cinchophen ulcerogenesis.

11-Hydroxycorticosteroids↗
PubMed1976

Changes in the antral mucosal pepsin in dogs with chronic ulcer: pathogenesis of cinchophen ulcer.

All of the dogs given continuous injection of 100 mg/kg sodium cinchophen for 21 days developed chronic ulcers in the pyloric portion of the stomach. Those dogs given cinchophen exhibited a definite increase in gastric pepsin secretion. Readings of gastric mucosal pepsinogen showed a significant high concentration both in the fundic and pyloric gland area in the cinchophen-treated animals. As the injections were continued, the gastric mucosa-juice peptic activity ratio (MJPR) in the fundic gland area become low. These results do not point to pathological changes in the fundic gland area. The mean pH value of the surface of antral mucosa varied greatly from dog to dog and was slightly higher than normal. In the dog which had chronic ulcers in the antral portion, the antral mucosal pepsinogen concentration become eight times higher than that seen in the control animals. The incidence and chronicity of the cinchophen gastric ulcers were related to the local pepsin increase adjacent to the lesions. The origin of pepsin which appeared in the antral mucosa and cinchophen ulcerogenesis were discussed.

Animals↗
PubMed1999

Healing process from cinchophen-induced acute gastric mucosal lesion in the rat: a scanning microscopic study.

The healing process in the microvasculature of cinchophen-induced acute gastric mucosal lesion was studied by the vascular corrosion casting method and conventional scanning electron microscopy. Thirty-six hours after cinchophen injection, prominent degeneration and exfoliation of surface mucous cells, along with exposure of the underlying connective tissue, were seen. The vascular casts showed leakage of resin and the occlusion of capillaries, which indicates breakage of the capillary network. One week after cinchophen injection, the denuded gastric mucosa was almost covered with surface mucous cells of irregular shape. The vascular casts showed signs of healing of the capillary network, including capillary neogenesis. The lesion was nearly healed by 2 to 3 weeks after cinchophen administration. Cinchophen induces the formation of acute gastric mucosal lesions that affect the surface mucous cells as well as the underlying vasculature. The subsequent healing process involves the regeneration of epithelial cells over the denuded areas and reconstruction of the underlying vascular network.

Journal Article↗
PubMed1977

New method of obtaining cinchophen ulcer in dogs.

Cinchophen injected into the cerebral ventricle reacted with the hypothalamus somewhere in the vicinity ventricle, and produced a release of ACTH as indicated by a rise in peripheral plasma 11-OHCS concentration in the dog. The amount of cinchophen injected into the ventricle corresponds to about 1/600 of the dose required to produce the same effect by the intravenous route. Repeated intraventricular injections of cinchophen were effective in producing gastric erosions and ulcers at smaller doses than the intravenous one (1/100 and 1/400). Damage to the gastric wall might be due to a mechanism involving a localized portion of the hypothalamus and/or via a cerebral ventricle. Bilateral truncal vagotomy did not have any effect on chronic ulcer production. The cinchophen ulcerations were accompanied by an increase in plasma corticosteroids. The new experimental technique for producing peptic ulcer in dogs via a central neurohumoral mechanism is described.

11-Hydroxycorticosteroids↗
PubMed1996

Ulcerogenic cinchophen induces c-Fos expression in CRH-secreting cells in the PVH of rat brain.

This study aimed at obtaining evidence that cinchophen, an ulcerogenic drug, stimulates the corticotropin-releasing hormone (CRH)-secreting cells in the paraventricular nucleus of the hypothalamus (PVH) to induce c-Fos expression. Without colchicine pretreatment, cinchophen was injected i.p. 60 min before the time of maximum CRH level in the hypothalamus, as decided by radioimmunoassay. Eighty percent of the c-Fos/CRH double-labelled cells were concentrated in the parvicellular subnuclei. In the medial and anterior parvicellular subnuclei, the double-labelled neurones of treated rats significantly outnumbered those of controls. The result shows that cinchophen induces excitation of the CRH-secreting cells.

Animals↗
PubMed1996

Effects of activated granulocytes and O2- on microcirculatory injury in acute gastric mucosal lesion in rats induced by sodium cinchophen.

The contribution of granulocytes and their byproducts to acute gastric mucosal lesion (AGML) is unclear. Our previous study showed that granulocytes produced O2- in the gastric mucosa of rats treated with 300 mg/kg of cinchophen (cinchophen ulcer, CU) and in rats subjected to 30 min-ischemia-reperfusion (IR). The present study investigated the effects of granulocytes and O2- on microcirculatory injury (MCI) in the gastric mucosa in both models. To evaluate MCI, we measured the amount of extravasated Evans blue, and monitored changes in blood flow and the formation of vascular casts in the gastric mucosa of rats with and without leukopenia. Mucosal levels of interleukin-8 (IL-8) were also measured, to determine granulocyte migration into the stomach. Our findings were: (1) IL-8 was decreased 30-45 min after CU injection (C-I) or after the start of occlusion (S-O), and levels had increased 90 min after either treatment. (2) Evans blue increased 120-150 min after C-I or S-O. These increases were lower in leukopenic than in non-leukopenic rats. (3) The blood flow decreased after C-I or reperfusion and continued at the same level during the 180-min measurement period. In CU leukopenic rats, the blood flow decreased slowly and was restored gradually. In IR leukopenic rats, the blood flow did not decrease. (4) There was a partial lack of capillary network, narrowing of capillaries, and extravasation of resin 90-120 min after C-I and S-O, and the disturbances were reduced in leukopenic rats in both models. (5) The extravasation of resin was reduced by the administration of superoxide dismutase (SOD) at the time O2- from granulocytes was being produced. (6) These reductions in the extravasation of resin due to leukopenia or SOD were smaller in CU than in IR rats. These findings indicate that granulocytes and O2- contribute to some extent to the MCI in CU rats.

Analysis of Variance↗
PubMed1994

Neuronal expression of Fos protein in the paraventricular nucleus of the hypothalamus after i.p. injection of ulcergenic cinchophen.

The purpose of this study was to identify the CNS neurons that express Fos protein after i.p. injection of ulcergenic drug cinchophen (300 mg/kg). This was done in unanesthetized Wistar rats with careful physiological controls. The population of Fos-immunoreactive (Fos-ir) neurons was the largest in the medial parvicellular part of the paraventricular nucleus of the hypothalamus (PVH). Distribution of Fos-ir neurons in the PVH corresponds with that of the parvicellular neurons in the PVH which secrete corticotropin-releasing hormone (CRH). This study strongly suggests that the cinchophen-induced peptic ulcer may originate in excitation of the CRH-secreting neurons in the parvicellular part of the PVH.

Animals↗
PubMed1983

Cinchophen analogues as potential CNS agents.

Several amides of cinchophen were prepared and evaluated as CNS agents. Compounds III, VII, XII, XIII, and XIV exhibited analgesic activity while I, III, and XIV acted as CNS depressants.

Analgesics↗