ABSTRACT
At present, the research of Moutan cortex carbonisata (MCC) mainly focuses on the changes of chemical composition before and after charcoal production, and there is a lack of material basic research directly related to the efficacy at home and abroad. In this study, Moutan cortex, as a precursor, and was calcined to MCC at high temperature. The Moutan cortex carbonisata nano-components (MCC-NCs) were extracted and separated from MCC to explore its cooling-blood and hemostatic effects. In the experiment, the MCC was calcined at a high temperature in a muffle furnace (350 ℃, 1 h), and then MCC-NCs were extracted for MCC, and characterized by transmission electron microscopy and UV-vis absorption spectroscopy, fluorescence spectroscopy, Fourier transform infrared spectroscopy and X-ray photoelectron spectroscopy. In addition, the study evaluated the blood-cooling and hemostatic effects of MCC-NCs. The results showed that MCC-NCs have a size distribution of 0.80-2.8 nm, a lattice spacing of 0.26 nm. MCC-NCs are mainly composed of C, O and N elements and have abundant surface functional groups such as OH, C=O, C-N and C=C. The fluorescence yield of MCC-NCs was 7.18%. The experiments complied with the Animal Ethics Committee of Beijing University of Chinese Medicine. The result indicated that pretreatment MCC-NCs can significantly (P < 0.05) reduce the high, medium, and low viscosity of whole blood and plasma viscosity, and reduce hematocrit, red blood cell distribution width, hemoglobin and red blood cell level. In addition, MCC-NCs significantly reduced the levels of activated partial thromboplastin time, thrombin time and fibrinogen (P < 0.05). The pathological examination results showed that MCC-NCs can significantly reduce lung tissue damage, reduce bleeding and inflammatory cell infiltration. At the same time, it can also significantly reduce the symptoms of gastric mucosal bleeding. In conclusion, the results indicated that MCC-NCs has significantly the effect of blood cooling and hemostasis, and its hemostatic effect is mainly related to the activation of endogenous coagulation pathway or fibrinogen system, which provided a novel strategy for exploring the material basis of traditional Chinese medicine for hemostasis.
ABSTRACT
Background: Perinatal Asphyxia refers to a condition during the first and second stage of labour in which impaired gas exchange leads to fetal acidosis, hypoxemia and hypercarbia. It accounts for about 23 per cent of the four million newborn deaths worldwide.Methods: To estimate the magnitude of coagulation derangement in babies who suffered birth asphyxia and compare it with non-asphyxiated controls.Results: There were 61.9% and 64 % males in both the groups outnumbering females suggesting that the health care seeking behavior for male children is more than for their female counterparts. Birth weight and mode of delivery are comparable in both the groups. PT and APTT were significantly higher in the asphyxiated babies than in their respective control group. It may be noted , however, that PT and APTT values were higher in the control group also, when compared with the reference values. This may indicate that the hemostatic mechanisms are already compromised in the newborns and perinatal asphyxia further augment the situation tilting it in favour of bleeding. Thrombocytopenia is observed in the asphyxiated group which may be due to placental insufficiency. Severe bleeding is significant in asphyxiated group as compared to the control.Conclusion: Dyscoagulation should be considered in all asphyxiated babies, and they may present with clinically significant bleeding, which may require fresh frozen plasma to restore and maintain their coagulation status.
ABSTRACT
BACKGROUND: In the acute phase of myocardial infarction, the hemostatic mechanism is known to be activated. However, it remains unclear whether increased activity of the hemostatic mechanism is only a marker of the acute thrombotic episode or precedes its appearance. It is also inapparent whether a hypercoagulable state persist for a prolonged period after the apparent resolution of these disorders. METHODS: In a group of 23 patients with acute myocardial infarction who received fibrinolytic therapy with urokinase(group A) or tPA(group B), the plasma level of fibrinogen, antithrombin compared to those of the 10 normal controls. RESULTS: The plasme level of fibrinogen was significantly decreased in both group A and B before and 4 to 24 hours after thrombolytic therapy compared to that of normal controls. But it was increased 7 to 14 days after thrombolytic therapy. In a few of the patients, the plasma level of FDP and D-dimer were positive before thrombolytic therapy and in the most patients they were positive 4 hours after thrombolytic therapy. The plasma level of AT-III was significantly increased in both group A and B before thrombolytic therapy compared with that of normal controls, but, after thrombolytic therapy, there was no significant change in its level. CONCLUSIONS: In the patients with acute myocardial infarction, the thrombolysis occurred before thrombolytic therapy and it lasted for 24 hours after thrombolytic therapy.