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Objective:To explore the protective effect and underlying mechanism of hyperbaric oxygen (HBO) on delayed encephalopathy after carbon monoxide poisoning (DEACMP) in mice.Methods:Totally 225 adult male Kunming mice were selected to establish CO poisoning model via intraperitoneal injection carbon monoxide (CO), and were randomly divided into the air control group, CO poisoning group, and HBO group. Each group was further divided into five time points group, that was 1, 3, 7, 14 and 21 d. The mice in the air control group were injected intraperitoneally with the same amount of air, and the HBO group received HBO treatment at the same time every day. DEACMP mice model was screened by behaviors using the open field test, new object recognition test and nesting test, and the content of myelin basic protein (MBP) were assayed. The mouse brain tissue and mitochondrial were prepared and malonialdehyde (MDA) and adenosine triphosphate (ATP) content were measured with ultraviolet spectrophotometer. MBP content in brain tissue and cytochrome C (CytC) content in the mitochondrial were measured by ELISA. The mitochondria membrane potential (MMP) was measured by flow cytometry.Results:Compared with the air control group, the content of carboxyhemoglobin (COHB) in blood increased significantly and the content of MBP in brain tissue decreased significantly in CO poisoning mice. CO poisoning mice showed motor ability and cognitive dysfunction. Compared with the air control group, the contents of MMP, CytC and ATP were significantly decreased ( P<0.01) in the CO poisoning group; while the MDA content was significantly increased ( P<0.01). Compared with the CO poisoning group, mice behaviors were improved significantly ( P<0.05), the content of MBP, MMP, CytC and ATP were increased ( P<0.05), while the MDA content decreased significantly ( P<0.01) in the HBO group. Conclusions:The abnormal mitochondrial function might be closely related to the occurrence and development of DEACMP, and HBO therapy plays an effective role in preventing and treating the DEACMP mice model via the mitochondrial pathway.
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Objective To investigate the therapeutic effect and side effect of prourokinase (Pro-uk) on the patients with acute myocardial infarction. Method From May 2004 to May 2005, a total of 68 cases of acute myocardial infarction treated by thrombolytic agents within 6 hours after onset were divided randomly into Pro-uk group ( n = 43) and urokinase (UK) group ( re = 25). In the Pro- uk group, there were 22 eases treated with 50 mg Pro-uk and 21 cases prescribed in 60 mg Pro-uk. The patency of involved coronary artery was evaluated by using selective coronary angiography at 90 minutes after thrombolytic therapy. The incidence of early heart events, bleeding and adverse reaction, were alse observed. Results (1) The total rates of resumed patency of obstructed coronary artery (TIMI grade 2 and 3 flow) were 76.7% in Pro-uk treated patients and 52.2% in UK treated patient ( P = 0. 041). (2) The occurrence of hyporrhea was lowered more significantly in Pro-uk treated patients than in UK treated patients (P = 0.029), but there were no intracranial hemorrhage found in both group. (3) Early cardiac events and adverse reactions were similar between two groups. Conclusions Pro-UK is safe and effective for the patients with acute myocardial infarction.