Cysteamine, the most potent ulcerogenic drug known so far, powerfully activates carbonic anhydrase I, II and IV. In vitro and in vivo studies.

Cysteamine is known as the most efficient substance in producing experimental duodenal ulcers reaching 100% after a single dose administration in rats. It is also described the acid hypersecretion and the duodenal mucosa blood flow decrease after cysteamine administration. The mechanism of action is still unknown. Starting from our recent studies which show that carbonic anhydrase (CA) I is involved in vascular changes and CA II and CA IV are involved in the secretory modifications we followed the effect of cysteamine on these CA isozymes. In vitro, we followed the effect of cysteamine on CA I, CA II and CA IV isolated from the gastric mucosa parietal cells and from kidneys using the Maren technique. In vivo, 2 groups of rats Gr.1 (N = 31) received a single s.c. dose of cysteamine, 500 mg/kg b.w. and Gr.2 (N = 32) - s.c. isotonic saline solution. We determined CA I, II and IV activity from parietal cells and renal CA IV activity. CA activity was determined by the stopped-flow method, using a rapid kinetic apparatus HI-TECH SF 51 MX. The results show that in vitro cysteamine activated the purified CA I and CA II, as well as gastric mucosa parietal cell CA IV by a direct mechanism of action. The renal CA IV was not significantly activated by cysteamine. In vivo cysteamine activated gastric mucosa CA I, CA II and CA IV and did not modify the activity of the same isozyme from the kidneys. In vivo and in vitro CA I activation had confirmed our results, and this fact proved the enzyme's involvement in the vasocontrictive process cysteamine-induced. The powerful activation of gastric CA II and CA IV through the H+ source, could explain the HCl excess produced by cysteamine. The absence of cysteamine activating effect on renal CA IV proved organ specificity. The results suggested the involvement of gastric mucosa CA I, II and IV in the experimental cysteamine ulcerogenesis.

Efficacy of antibiotic prophylaxis for preventing intrathoracic infections, after thoracostomy, for traumatic haemo/pneumothorax - experience of Oradea county emergency hospital.

UNLABELLED: The aim of the paper is to observe the effectiveness of prophylactic administration of antibacterials against empyema and pneumonia after tube thoracostomy for traumatic collections. MATERIAL AND METHODS: Observational retrospective study over a ten years period (2002-2011), at the Oradea County Emergency Hospital on 939 patients with chest tube drainage for traumatic haemo/pneumothoraces. The morbidity by intrathoracic infections was 5,5% in the curative antibiotic group. RESULTS: The median number of risk factors for surgical infections and case severity were not statistically different (p=0.9653 and p=0,6601) between cases with antibioprophylaxis and curative treatment, but the incidence of intrathoracic infection in the prophylaxis group (n=86) was half (2,3%). Antibioprophylaxis was effective in over 95% of the cases and it associated in-hospital length of stay, length of stay in the ICU and costs of care significantly (p<0.0001, p<0.0001, p=0.0046) lesser than of those patients treated with curative regimen. The overall mortality was 8.6% within the curative regimen group with an attributable mortality to infections of 17.39%; but it was only 2.3% and respectively 0 within the prophylaxis group. CONCLUSIONS: Antibiotic prophylaxis for intrathoracic infections after tube thoracostomy for traumatic collections was justified by case severity and risk factors and was effective and cost-efficient, but it should be administered selectively.

The effects of electroconvulsant shocks on phagocytic activity and on phagocytic response.

The influence of a single or several subsequent convulsant electroshocks at different time laps (2-4 day), over a month, on the phagocytic activity was studied on seven dogs. The electroconvulsant shock was performed with bitemporal electrodes, at a liminal electric power. Phagocytosis was studied in vitro with amidon particles in whole blood, incubated 1h at 37 degrees C. After 4 hours the phagocytosis increases in all animals and remains higher for 12 days. Later on the repeated shocks produce very different changes of the phagocytic activity, depending, not only on the stressor agent, but also on the animal particular reactivity, conditioned genetically and by its individual history.