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Biomedical subjects

A Robert

Publications and source records attributed to A Robert.

At least 361 records · Page 20Linked to original sources
PubMed1982

[Budd-Chiari syndrome with massive thrombosis of the subdiaphragmatic venous system and major fibrinopenia (author's transl)].

A 32-year-old patient without previous medical history died within three weeks of acute Budd-Chiari syndrome with massive thrombosis of the subdiaphragmatic venous system. No definite cause could be elicited. The course of the disease was complicated by anuria attributed to hepotorenal syndrome. Laboratory tests demonstrated major fibrinopenia. Detailed study of the haemostatic system was suggestive of hepatic failure associated with consumption coagulopathy of obscure origin.

Adult↗
PubMed1982

Cytoprotection of canine gastric mucosa by prostacyclin: possible mediation by increased mucosal blood flow.

UNLABELLED: This study examined the role of the gastric mucosal blood flow (MBF) in the gastric cytoprotection produced by prostacyclin (PGI2) and prostaglandin E2 (PGE2) in dogs. An acidified solution of saline was applied topically on the canine gastric mucosa with and without ethanol at various concentrations. Ethanol applied to the mucosa of a stomach flap preparation, in concentrations ranging from 5 to 80%, gradually decreased the transmucosal potential difference (PD) from -58 to -5 mV and increased net ionic fluxes. MBF gradually increased at lower concentrations of ethanol, reaching the peak of about 50% above basal at 20% ethanol and then declining at 40 and 80% ethanol. PGI2 (10 micrograms/kg/h) prevented the changes in PD and ion fluxes produced by lower but not higher concentrations of ethanol and this was accompanied by a marked increase in the MBF above the level produced by ethanol alone. The instillation of acidified 15% ethanol into Heidenhain pouch (HP) reduced the PD from -57 to -40 mV and elicited large net H+ and Na+ fluxes. MBF was increased by 30%. PGI2 (10 micrograms/kg/h) completely prevented ethanol-induced changes in PD, reduced ionic fluxes, and raised the MBF twofold. On the contrary PGE2 (80 micrograms/kg/h) did not affect ethanol-induced alterations in PD, ion fluxes, and MBF. CONCLUSIONS: PGI2, but not PGE2, effectively protects the canine gastric mucosa against the damage produced by ethanol. This cytoprotection may be due to increased mucosal circulation, which by an unknown mechanism interferes with the mucosal damage caused by ethanol.

Action Potentials↗
PubMed1982

Effect of 15(R)-15-methyl prostaglandin E2 (arbaprostil) on the healing of duodenal ulcer: a double-blind multicenter study.

A multicenter study was conducted on 173 patients with active, endoscopically proven duodenal ulcers (158 men, 15 women). They were randomly assigned, in a double-blind manner, to two groups: those receiving placebo capsules (91 patients) and those receiving capsules containing 100 microgram of 15(R)-15-methyl prostaglandin E2 (arbaprostil) (82 patients). Each drug was ingested four times a day (1 h before meals and at bedtime) for 28 days. Endoscopy was performed on days 0, 14, and 28 after the trial began. At each examination, the ulcer size was measured and whether the ulcer had healed was recorded. Arbaprostil increased the incidence of ulcer healing to approximately the same degree as reported in most extensive studies with cimetidine. At 14 days, three times as many patients were totally healed in the arbaprostil-treated as in the placebo-treated group (37% vs. 12%, p less than 0.001). At 28 days, 67% of patients receiving arbaprostil were healed compared with 39% in the group receiving placebo (p less than 0.001). Similarly, the ulcer size, measured endoscopically, was much smaller after arbaprostil administration than in the group receiving placebo after both 14 and 28 days (p less than 0.001). Side effects attributable to treatment consisted primarily of loose stools and diarrhea (34%). Smoking retarded healing in the placebo-treated group (p less than 0.05), but did not significantly retard healing in patients treated with arbaprostil. We conclude that arbaprostil markedly accelerates the healing rate of active duodenal ulcers. This effect may be due to inhibition of acid secretion as well as gastric cytoprotection.

Adolescent↗
PubMed1982

[Importance of synoviorthesis using osmic acid in the treatment of hemophilic arthropathy. Apropos of 19 cases].

While getting synovial sclerosis and articular drying, the synoviorthesis breaks the circulus vicious which comes from iterative hemarthrosis to articular destruction. With 25 cases and a follow up of 6 years, we have got 39% of good results, 35% of medium and 26% of bad ones. The therapeutic efficiency requires a certain latent time (0 to 15 days for isotopical synoviorthesis, 2 to 3 months for those ones with osmical acid.) A new synoviorthesis can be made if needed. Neither age nor radiological stage are of any influence. The radiological worsening uses to go on unchanged. The synoviorthesis should be performed at an early stage, previous to the cartilage and bone destructions.

Adolescent↗
PubMed1982

Coulter Counter studies of hypotonic-induced macrothrombocytosis in normal subjects and in idiopathic thrombocytopenic purpura patients.

The addition of distilled water to platelet rich plasma converts the platelets into large spherocytes without lysis. This phenomenon implies an evagination of the platelet membrane which participates in the surface connecting system. An adaptation of the direct microscopic method (Milton & Frojmovic, 1979) to the Coulter Counter is reported. The maximum increase in platelet volume without platelet lysis was obtained for 120 mOsm. These volume changes are a consequence of a shift in the platelet volume distribution curve towards higher values without loss of log normality, while the volume dispersion is only slightly modified. This suggests that the amount of evaginable platelet membrane is correlated to the size of the platelet. The size parameters (volume, surface, diameter) of hypotonic-induced spherocytes closely agree with those reported in the original microscopic method. Application of this technique to ITP-platelets suggests a reduced evaginable platelet membrane; this fact probably reflects the abnormal demarcation of platelet territories at the megakaryocytic level.

Blood Platelets↗
PubMed1981

[Ultrastructural visualization of binding and internalization of cholera and tetanuts toxins].

In monolayer cultures of a liver line, a population of non-coated membrane microinvaginations is preferentially involved in both the initial binding and subsequent internalization of colloidal gold-labelled cholera and tetanus toxins. These two toxins thus appear to be internalized via another pathway than most other polypeptide ligands studied, which enter cells via coated plasma membrane invaginations.

Animals↗
PubMed1981

Gastric cytoprotection by sodium salicylate.

Sodium salicylate (SA), contrary to acetylsalicylic acid (ASA, aspirin), was not ulcerogenic in rats. SA was also found to be cytoprotective: it prevented formation of gastric mucosal necrosis produced by either absolute ethanol or 0.6 M HCl, and formation of gastric ulcers produced by acidified ASA. The degree of protection was dose dependent. The mechanism of this cytoprotection is unknown, but unlike cytoprotection elicited by mild irritants, e.g., 20% ethanol or 0.35 M HCl, whose effects appear to be due to endogenous formation of PG by the stomach, SA acts through a different mechanisms, since its protective effect was not blocked by indomethacin.

Animals↗
PubMed1981

Dose response inhibition in man of meal-stimulated gastric acid secretion by 15(R)-15-methyl prostaglandin E2, given orally.

15(R)-15-methyl prostaglandin E2 was given orally to healthy male volunteers. Thirty minutes later a 10% peptone meal was introduced into the stomach, and the acid response was measured by continuous intragastric titration with 0.5 N NaOH for the next two hours. The prostaglandin inhibited acid output in a dose dependent manner; the ED50 (dose inhibiting acid output by 50%) was as little as 10 micrograms per subject (or approximately 140 ng/kg). This compound is the most potent orally active inhibitor of gastric acid secretion in man that is known. It is likely that the antisecretory and cytoprotective properties shared by 15(R)-15-methyl prostaglandin E2 would be beneficial in the treatment of peptic ulcer and in preventing recurrences.

Administration, Oral↗
PubMed1981

Gastric cytoprotection in man by prostaglandin E2.

In healthy volunteers, the effects of topical prostaglandins E2 (PGE2), 1 mg, on transmucosal potential difference (PD), mucus secretion, and epithelial cell turnover were investigated. PGE2 increased gastric PD by 10 mV on an average and stimulated mucus secretion of the stomach by 50%. In contrast, epithelial cell turnover remained unchanged. Gastric output of H+ decreased, whereas the outputs of volume, Na+, and Cl- rose in response to PGE2, which effects would be compatible with increased secretion of bicarbonate. Topical administration of ethanol 40% (vol/vol) reduced PD by 25 mV (delta PDE) and enhanced epithelial cell shedding by 350% with concomitant discharge of mucus from stomach epithelium. Pretreatment of the stomach with 1 mg PGE2 prevented the ethanol-dependent epithelial cell exfoliation, indicating gastric mucosal cytoprotection. Delta PDE and discharge of mucus were not significantly altered by PGE2. We conclude that gastric cytoprotection by PGE2 in man might be mediated by stimulation of mucus and/or bicarbonate production.

Adult↗
PubMed1981

Peptic ulcer: new therapies, new diseases.

Although hospitalizations and deaths attributable to peptic ulcer have decreased notably during the past decade, it is not certain whether this decrease is because of reduced incidence of new cases or changes in other factors, such as the severity of the disease. Several genetic traits associated with peptic ulcer have been recognized. Hyperpepsinogenemia I is the most prevalent. Peptic ulcer is a heterogeneous group of disorders with multiple genetic and environmental causes. One manifestation of the diversity of ulcer disease is the variety of physiologic abnormalities seen in patients. The use of endoscopy has enabled more reliable evaluation of new treatments. Histamine H2-receptor antagonists are the dominant mode of treatment, but increasing attention is being given to agents that enhance the resistance of the mucosa to injury, such as prostaglandins. Because of the lower frequency of side effects, proximal gastric vagotomy is gradually replacing truncal vagotomy with drainage. The possibility that endoscopic treatments, such as laser coagulation, may reduce mortality from bleeding ulcers is being investigated.

Duodenal Ulcer↗