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Biomedical subjects

C Navarro

Publications and source records attributed to C Navarro.

At least 163 records · Page 9Linked to original sources
PubMed1990

Zinc acexamate inhibits gastric acid and pepsinogen secretion in the rat.

Pretreatment with zinc acexamate (25-100 mg kg-1 i.p.) inhibited acid and pepsinogen secretion in the pylorus-ligated rat. Zinc acexamate (5-50 mg kg-1 p.o.) also inhibited the increases in acid secretion induced by carbachol (10 micrograms kg-1) and 2-deoxy-D-glucose (200 mg kg-1) in the perfused stomach of the anaesthetized rat. A delayed antisecretory effect was observed with this drug on histamine induced responses. High concentrations of zinc acexamate (10(-5) - 10(-2) M) did not modify the in-vitro activity of pepsin. Administration of zinc acexamate resulted in an increase in the presence of pepsinogen at the mucosal level. A morphological examination of the gastric mucosa confirmed an accumulation of zymogen-containing granules in the gastric chief cells of zinc acexamate-treated rats (50 mg kg-1 p.o.). These results indicate that zinc acexamate decreases acid and pepsinogen secretion in-vivo, and this may explain its antiulcer activity.

Aminocaproates↗
PubMed1990

Effect of zinc acexamate and ranitidine on chronic gastric lesions in the rat.

Using the rat as an experimental model we have studied the healing of chronic gastric lesions and the modifications of these lesions by antiulcer agents. Gastric injuries were induced by submucosal injection of 0.05 ml of 5% acetic acid. Placebo, ranitidine (RNT) or zinc acexamate (ZAC) were administered orally. The evolution of gastric injuries was macro- and microscopically evaluated at 6, 12 and 21 days after acetic acid injection. The administration of either RNT (30 mg/kg) or ZAC (200 mg/kg) was followed by a marked improvement of the healing process with respect to control groups. The size of experimental ulcers at 21 days was 3.1 +/- 0.8 mm2 for the control group, 1.8 +/- 1.1 mm2 for RNT-treated animals and 0.3 +/- 0.6 mm2 for ZAC-treated rats (p less than 0.05, vs. control). A similar tendency was observed when lesions were microscopically analyzed. Indices of microscopical lesions (0-6) at 21 days were 3.8 +/- 0.8 for the control group, 3.0 +/- 0.8 for rats receiving RNT and 2.3 +/- 0.4 for rats receiving ZAC (p less than 0.05, vs. control). The statistical analysis of the distribution of microscopical indices of lesions showed significant differences in favour of ZAC at days 6 (p less than 0.01) and 21 (p less than 0.05). Our study indicates that the evolution of gastric damage induced by acid acetic injection was consistently better in rats treated with ZAC than in those receiving RNT. Data obtained in our experiments suggest that the blockade of H2 receptors does not guarantee the optimal healing of chronic gastric lesions induced in rats.

Acetates↗
PubMed1990

Chlorpromazine and clothiapine actions at the level of the CNS and vas deferens.

CNS-level changes caused by chlorpromazine and clothiapine, a structural analogue, were studied with a battery of behavioral tests in rats, along with the ability of these two drugs to antagonize electrically and alpha-stimulator (phenylephrine-)induced contractions in the rat vas deferens. The findings indicated that clothiapine, while less effective as an alpha-receptor antagonist, was a much more active CNS-depressant than chlorpromazine.

Animals↗
PubMed1989

Effects of zinc acexamate on blood flow and prostanoid levels in the gastric mucosa of the rat.

The effects of the new antiulcer compound zinc acexamate on blood flow and prostanoid levels in the gastric mucosa have been studied. Zinc acexamate (30 and 300 mg/kg) dose-dependently prevents the reduction induced by the perfusion of noradrenaline (3.5 micrograms/kg.min, 30 min) in gastric mucosal blood flow, as measured by 3H-aniline clearance. Zinc acexamate pretreatment also increases the levels of prostaglandin E2 in the gastric mucosa of the rat, both under control conditions and after infusion with noradrenaline. The levels of thromboxane A2 and prostacyclin were not modified by zinc acexamate. These results confirm the importance of microcirculation in pathogenesis and the idea that the antiulcer activity of zinc acexamate is due in part to its action in increasing the mechanism which defend the gastric mucosa against aggression.

Aminocaproates↗
PubMed1989

Zinc acexamate reduces gastric damage induced by platelet-activating factor.

We have tested the ability of zinc acexamate (ZAC) to prevent platelet-activating-factor (Paf) induced gastric damage in rats. Lesions were characterized by a vascular congestion affecting the entire mucosa, oedema, haemorrhage and frequent necrosis of the more superficial areas. The gastric damage appearing after Paf was accompanied by degranulation of gastric mast cells. Leukocytes were often seen at the submucosal level. Oral pretreatment with ZAC reduced in a dose-dependent manner both gastric damage and mast cell degranulation observed after Paf. ZAC administered orally at a dose of 100 mg kg-1 statistically inhibited (p less than 0.01) gastric damage and mast cell degranulation. ZAC did not affect the hypotension induced by Paf confirming that gastric damage and hypotension appearing in rats after Paf administration are two independent phenomena. The present findings indicate that the inhibitory effect of ZAC upon gastric lesions induced by Paf may be related to the different protective actions exhibited by this zinc compound in a wide variety of experimental models of gastric ulcer.

Aminocaproates↗
PubMed1989

Changes in chlorpromazine induced CNS effects when associated with other neuroleptics and anxiolytics.

A set of test (General behavior, traction, chimney, rotarod, conditioned reflexes, curiosity and potentiation of barbiturate sleep) were given in addition to studying the hypothermia of associations of chlorpromazine with various neuroleptic and one anxiolytic (Perphenazine, clothiapine, haloperidol and diazepam), which demonstrated an evident enhancement of the depressant effects of chlorpromazine when combined with clothiapine and haloperidol.

Animals↗
PubMed1989

Dilated cardiomyopathy associated with chylous ascites.

Chylous ascites is a well-documented sequelae of traumatic rupture of the thoracic duct and mechanical obstruction of the lymphatic system due to neoplastic, inflammatory, or congenital anomalies. Less commonly, chylous ascites results from altered hemodynamics and lymphatic flow, as seen in cirrhosis and constrictive pericarditis. Rarely, severe right-sided heart failure from a variety of causes has also resulted in chylous ascites or a protein-losing enteropathy. We report a case of chylous ascites due to dilated cardiomyopathy with autopsy findings. The pathophysiology of chylous ascites formation in right heart failure will be discussed, with a review of the literature.

Aged↗
PubMed1988

Peripheral neuropathy in essential mixed cryoglobulinemia.

Sixteen patients with essential mixed cryoglobulinemia were studied and followed up clinically and electrophysiologically for 4.2 years. Peripheral neuropathy was diagnosed in seven cases. Five of these patients had distal symmetrical sensorimotor polyneuropathy. Nerve conduction velocities were normal and therefore indicative of pure axonal neuropathy. Sural nerve biopsy showed moderate loss of myelinated axons in two patients and severe loss in one. This patient also had necrotizing arteritis. The remaining two had both clinical and electrophysiologic signs of overlapping mononeuritis multiplex with severe denervation in the territory of the involved nerves, but normal conduction velocities. Sural nerve biopsy in one of these two patients showed marked loss of myelinated fibers and signs of vasculitis. Two types of neuropathy were noted: (1) a mild distal neuropathy with relatively minor neurologic deficit, probably due to vasa nervorum microcirculation occlusion caused by intravascular deposits of cryoglobulins and (2) a severe distal symmetrical sensorimotor neuropathy or overlapping mononeuritis multiplex, associated with necrotizing vasculitis.

Adult↗
PubMed1988

Gliomatosis cerebri with formation of a glioblastoma multiform. Study and follow-up by magnetic resonance and computed tomography.

A case of gliomatosis cerebri studied by computed tomography (CT) and magnetic resonance imaging (MRI) is reported. Follow-up by serial CT revealed a right parieto-occipital glioblastoma. Gliomatosis cerebri and multiform glioblastoma were demonstrated by histologic study. Anatomic and CT data were correlated. The role of CT and MRI in the diagnosis of this disease was evaluated and case studies of CT published in the literature were reviewed.

Adult↗
PubMed1988

Effects of zinc acexamate on gastric mucosal production of prostaglandin E2 in normal and stressed rats.

Changes in PGE2 levels induced by zinc acexamate (ZAC) at gastricmucosal level were assessed in a rat model. Experiments were performed in normal rats and rats subjected to cold-restraint stress and in experimental conditions in which prostaglandins (PGs) synthesis was inhibited by prior administration of indomethacin. Gastric injuries after different treatments were quantified macro and microscopically. Total amount of PGE2 and mucus material recovered from gastric mucosa were increased after ZAC treatment. Indomethacin aggravated gastric damage secondary to stress and inhibited PGE2 and mucus increase appearing after ZAC treatment. These data confirm the relation between PGE2, mucus production and gastric protection. ZAC 200 mg/kg was able to reduce the gastric damage induced by stress. This decrease was also evident in the group receiving indomethacin before ZAC administration. These experiments indicate that ZAC exhibits its antiulcer action by increasing prostaglandins but other mechanisms independent of PGs synthesis are also involved.

Aminocaproates↗