Background Alcohol intoxication has a detrimental effect on hypovolemic shock. Our aim, was to study its effects on "pure" cardiac tamponade (i.e., without hypovolemia) in patients with penetrating chest injuries. Methods Thirty-five intoxicated and 15 nonintoxicated patients (blood alcohol > and < 17 mmol/L) were studied. Initial vital signs (trauma scores), special investigations (hematologic profiles, blood gases, glucose, lactate, and catecholamines), clinical progress (24- and 72-hour acute physiology and chronic health evaluation II scores) and outcome were compared. Results Intoxicated patients were older (p = 0.02) and more tachypneic on admission (p = 0.006), but no other differences were noted. Mortality was proportional to the degree of shock and was greater in patients who had "front-room" thoracotomies (p < 0.001). Despite the higher percentage of intoxicated patients who were "lifeless" or "in extremis" on admission, they fared no worse than nonintoxicated patients. Conclusion Alcohol intoxication does not have an adverse affect on traumatic cardiac tamponade.
Bile duct ligation in the pig results in ulceration of the pars oesophagea (oesophagogastric junction) within 48 h with 100% reproducibility. This work describes novel observations made during development of such ulcers using an endoscope introduced at intervals postoperatively via a Thomas gastric cannula. Macroscopic and histological changes were recorded and compared with quantitative and qualitative changes in crude mucus scrapings and purified mucins. Crude mucus scrapings of the cardiac gland region had a higher protein content in the ulcerated states than in the normals. After bile duct ligation, the (degraded) mucin glycopeptide/total protein ratio was higher in partially purified mucus from pre-ulcerated and ulcerated stomachs as compared with normal samples. The quantity of purified mucin was less in samples from ulcerated stomachs, and the N-acetylgalactosamine and fucose contents were also decreased. It is possible that these changes resulted in the failure of the mucus barrier and the development of oesophagogastric junction ulceration.
In a previous study, we showed that plasma concentrations of catecholamines were increased during the anhepatic phase in pigs. In this study, we investigated if a constant depth of anaesthesia would prevent these changes and, if not, if the changes were caused by impaired extraction of catecholamines. We measured arterial and venous pressures, heart rate and cardiac output in 10 anaesthetized pigs. Hepatic arterial and portal venous flows were measured. Blood for measurement of catecholamines was sampled from carotid and pulmonary arteries and portal, hepatic and renal veins. After a 2-h observation period, the liver was removed and the circulation reconstituted. Measurements were made and samples obtained for another 2 h. Catecholamine concentrations increased 2-10-fold after hepatectomy. Before hepatectomy, noradrenaline was extracted by the lung (mean extraction ratio 23 (SEM 8)%) and the liver (30 (11)%); after hepatectomy, there was extraction by the kidney (24 (12)%) but extraction by the lung (29 (8)%) was unchanged. Before hepatectomy, adrenaline was extracted predominantly by the kidney (73 (5)%) and the liver (70 (6)%), with minimal extraction by the lung; after hepatectomy, extraction by the lung increased (25 (4)%) and decreased slightly in the kidney (56 (6)%). While mean arterial pressure did not change, heart rate increased by approximately 50% and cardiac index declined (ns) within 2 h after hepatectomy. There was a sharp increase in pulmonary vascular resistance after removal of the liver and changes correlated with increases in arterial plasma concentrations of catecholamines.
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