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O Benjaminov

Publications and source records attributed to O Benjaminov.

6 recordsLinked to original sources

The halo sign and peripancreatic fluid: useful CT signs of hypovolaemic shock complex in adults.

AIM: To report two new, useful computed tomography (CT) signs of the hypovolaemic shock complex (HSC) in adults admitted after blunt abdominal trauma: the halo sign (ring of fluid around a collapsed intra-hepatic inferior vena cava (IVC)), and peripancreatic retroperitoneal fluid. MATERIALS AND METHODS: CT images of 498 consecutive patients admitted after blunt abdominal trauma were reviewed, of which 27 had CT signs of the HSC. The CT images of these 27 patients were analysed. A control group of 101 patients examined using CT for suspected blunt abdominal trauma who did not have the HSC were chosen for comparison. RESULTS: The most common features involved the vascular compartment: diminished IVC diameter n = 27 a positive halo sign n = 21 diminished anteroposterior diameter of the aorta n = 13 and abnormal vascular enhancement n = 10. Peripancreatic retroperitoneal fluid in the absence of pancreatic injury, pancreatitis or pancreatic disease was observed in eight patients. Hollow visceral abnormalities included: diffuse increased mucosal enhancement of both the small and large bowel n = 19 diffuse thickening of the small bowel wall n =11 and small bowel dilatation n = 7. Solid visceral abnormalities included both decreased and or increased enhancement. Several concomitant intra- and extra-abdominal injuries were also identified. CONCLUSION: In the setting of blunt abdominal trauma, early abdominal CT can show diffuse abnormalities due to the HSC, which occasionally may alert clinicians of unsuspected shock. Recognition of these signs as distinguished from injured viscera is important in order to avoid unnecessary laparotomy. Two new signs are described: the halo sign and peripancreatic retroperitoneal fluid.

Abdominal Injuries↗

Pentoxifylline does not protect against hyperoxic lung injury in rats.

Hyperoxia has been used extensively as a model of acute lung injury. The drug pentoxifylline has been shown to have a protective effect in other models of lung injury. We sought to determine whether pentoxifylline protects against hyperoxic lung injury in rats by decreasing the accumulation of neutrophils within the lung. A total of 84 rats were studied. Twenty four rats were randomized into four groups. Two groups of rats were pretreated for 48 h with either pentoxifylline (20 mg.kg-1) or saline, and then exposed to > 95% O2 for 60 h while treatments continued. Two groups of control rats received the same treatment regimens as the O2-exposed animals, but breathed room air. Neutrophil accumulation in the lung was quantified both by histology and myeloperoxidase activity. Lung neutrophil accumulation increased in the oxygen-exposed group receiving pentoxifylline as compared to oxygen- or air-exposed rats receiving saline injections. Total glutathione was higher in lung homogenates from the hyperoxic, pentoxifylline-treated group than in homogenates from the other three groups. To study survival, 60 rats were exposed to > 95% O2 for 120 h, 30 rats were pretreated with pentoxifylline, and 30 received saline. Survival after 120 h of exposure to hyperoxia was not altered by pentoxifylline treatment (pentoxifylline treated: 6 out of 30 survived; saline treated: 2 out of 30 survived). We conclude that pentoxifylline does not reduce mortality or lung injury in rats exposed to hyperoxia and is associated with an increase in lung neutrophil accumulation.

Animals↗

N-acetylcysteine delays the infiltration of inflammatory cells into the lungs of paraquat-intoxicated rats.

We investigated a possible role for N-acetylcysteine (NAC), a well-known antioxidant and free radical scavenger, against oxidative lung damage as observed in the in vivo model of paraquat-intoxicated rats. The administration of two ip doses of 50 mg/kg NAC to paraquat-intoxicated animals did not change the glutathione status of the lungs, as determined by the measurement of nonprotein sulfhydryl (NP-SH) groups. The administration of NAC did however suppress the paraquat-induced release of chemoattractants for neutrophils in the bronchoalveolar fluid when the lavage was carried out 12 hr after the administration of 30 mg/kg paraquat. Also, in the intoxicated NAC-treated animals, the infiltration of inflammatory cells was significantly reduced, as demonstrated by the examination of the cell composition of the bronchoalveolar lavage (BAL), 24 hr after paraquat. Phorbol myristate acetate-stimulated superoxide anion production from the AM isolated from the BAL of paraquat-intoxicated nontreated animals was lower than that of controls, whereas in the NAC-treated animals, it was close to that of the controls. The obtained results indicate that NAC has a protective effect against oxidative lung damage by delaying inflammation. It also prevents the paraquat-induced reduction of superoxide anion production by stimulated AM. In the present model, however, the NAC administration regimen did not affect the survival rate of paraquat-intoxicated rats.

Acetylcysteine↗

Parathion transfer and acetylcholinesterase activity in an in-vitro perfused term human placenta.

Organophosphate transport through the placenta was investigated in an in-vitro placental perfusion system. The system consisted of maternal and fetal reservoirs in which Krebs Ringer bicarbonate buffer with heparin, albumin and glucose was circulated at a constant pH, temperature and pO2. Parathion was analysed by means of gas chromatography with a N-P detector. 14C Antipyrine, a lipid soluble salt, was used as an internal standard, which allowed for the difference in placental size and permeability. A certain amount of parathion passed the placenta and reached the fetal compartment. Glucose consumption was not influenced by the introduction of parathion; neither was the water content of the placental tissue. Acetylcholinesterase activity in placental tissue decreased 50%. The amount of parathion transferred was not negligible and could have caused damage to a fetus.

Acetylcholinesterase↗