[Study on the mechanism of how curcumin improves pulmonary vascular remodeling associated with chronic pulmonary arterial hypertension].

OBJECTIVE: To investigate the mechanism of how curcumin improves pulmonary vascular remodeling associated with chronic pulmonary arterial hypertension. METHODS: The model of chromic hypoxia hypercapniapulmoary remodeling was made. Twenty-four male rats were randomly divided into 4 groups (n = 6): group I (normoxia control group), group II (hypxia and hypercapnia model group), group II (disodium cromoglycate control group), group IV (curcumin treated group). The last 3 group rats were put in a hypoxia cabin where the concentrate of O2 was 8% - 11% and the concentrate of CO2 was 3% - 5%, for 8 h a day and lasting 4 w in total. Group III rats were intraperitoneally injected with disodium cromoglycate (20 mg/kg) and group IV rats were administrated with curcumin by gavage (150 mg/kg). The morphological changes of pulmonary vessel walls and the ultrastructure of mast cells were observed by the optics microscope and the transmission electron microscope. Mast cells and its degranulation state were measured by toluidine blue staining and immunohistochemistry. Data were expressed as means ± SD (standard deviation) and analyzed with SPSS17.0 software. RESULTS: (1) By optics microscopy observation, the value of WA/TA was significantly higher in II group than other groups (P < 0.05). (2) Electron microscope showed that the endothelial cells of pulmonary arterioles in III and IV group were near to I group and the proliferation of pulmonary arterial media smooth cell layer and collagen fibers in adventitia was much lighter than those in II group. The membrane of mast cells was more intact in I, III, IV group than II group. (3) The number of mast cells, the degranulation rate of master cells and the number of positive tryptase stained cells in II group were significantly more than those in other groups. (P < 0.05). CONCLUSION: Curcumin may inhibit the remodeling of pulmonary vessel induced by chronic hypoxia hypercapnia by mast cell regulation.

[Relationship between P-selectin and cardiac function in hemorrhagic shock resuscitation: experiment with rats].

OBJECTIVE: To investigate the relationship between the left ventricular function and the expression of P-selectin in the serum and cardiac muscle in hemorrhagic shock resuscitation, and to evaluate the effects of L-arginine (L-Arg) against the harmful effect of P-selectin. METHODS: Thirty SD rats were randomly divided into 3 equal groups: hemorrhagic shock resuscitation (HS) group (undergoing bloodletting until the mean arterial pressure of 40 mm Hg and then re-infusion of the lost blood), L-Arg treatment group (undergoing bloodletting and then re-infusion with L-Arg simultaneously), and normal control (NC) group (undergoing infusion of normal saline). Cannulation was conducted via left carotid artery into the left ventricular to record left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), and left ventricular +/- dp/dtmax. Serum creatine kinase (CK) was detected by colorimetry. Three hours after the HS the rats were killed with samples of blood and apex of heart collected to detect the P-selectin expression by ELISA and immunohistochemistry. Microscopy was used to observe the expression of P-selectin in the vascular endothelial cells and cardiac muscle cells. RESULTS: The LVSP, maximal rate of LV pressure elevation (+ dp/dtmax), and maximal rate of LV pressure depression (- dp/dtmax) of the HS and L-Arg groups were all significantly lower than those of the NC group (all P < 0.01). The LVEDP of the HS and L-Arg groups were all higher than that of the NC group (both P < 0.01). Three hours after resuscitation, the CK levels of the HS and L-Arg groups were significantly higher than that of the NC group (both P < 0.01), and that of the L-Arg groups was significantly lower than that of the HS group (P < 0.05), the P-selectin levels of the serum and cardiac muscle cells of the HS and L-Arg groups were all significantly higher than those of the NC group (both P < 0.01), and those of the L-Arg group were significantly lower than those of the HS group (both P < 0.05). CONCLUSION: After hemorrhagic shock and resuscitation P-selectin may play an important role in cardiac injury, L-Arg can inhibit the expression of P-selectin, thus protecting the cardiac function against the harmful effect of P-selectin.