in this paper we report the blood cobalt, methemoglobin and blood cyanide concentration-time equations and related parameters of pharmacokinetics after abministra-tion of sodium cobaltinitrite(18.6mg/kg)or potassium cyanide(3mg/kg)in dogs.It was found that 10% dimethyl sulfoxide used as a solvent, as compared with water, accelerated sodium cobaltinitrite absorption by intramuscular administration.The half absorption time was reduced from 14.5 min to 5.5 min, the time of maximum concentration of blood cobalt reduced from 1.11 h to 0.56 h, and the maximum conce-tration of blood cobalt raised from 2.71?g/ml to 3.35?g/ml.There was a significant difference of blood cobalt concentrasions between 10-60 and 120 min after intramuscular administration.

This paper reports the antagonistic effect of sodium cobaltinitrite by intramus-cular injection on cyanide intoxication. The sodium cobaltinitrite (10%) dime-thylsulfoxide solution was administrated intramuscularly when convulsion appeared in dogs 5-10 min after intramuscular injection of potassium cyanide(1-2.5LD) or 15s after inhalation of hydrocyanic acid (2LD50). The animal survival rate was 20/22 and 8/10, respectively. The cats intoxicated by lethal dose of hydrocyanic acidinhalation were given sodium cobaltinitrite intramuscularly, and a good therapeutic effect was also obtained.This study provides an experiment basis in search of an antagonist of cyanide, which takes effect rapidly, is administrated conveniently and is suitable rescue in the field, with a convenient administrating means.

BACKGROUND:At present, there is no effective treatment strategy for cavernous transformation of portal vein and basic research about its etiology is rarely reported.
OBJECTIVE:To establish the models of cavernous transformation of portal vein, detect the expression of matrix metal oproteinase-2,-9 (MMP-2, MMP-9) and tissue inhibitors 1, 2 of metal oproteinase (TIMP-1, TIMP-2) in rat portal vein and peripheral tissue, and discuss the roles in the process of peripheral angiogenesis.
METHODS:Eighty Sprague-Dawley rats were randomly divided into three groups. The rat models of cavernous transformation of portal vein were established with partial coarctation in portal vein by using 21 G blunt pinhead. Control group was normal rats without operation (samples were harvested after portal vein radiography). Model group and sham operation group were divided into three groups respectively according to different time points, namely 2, 4 and 6 weeks after operation. Rats of each group were randomly chosen at week 2, 4 and 6 after operation to observe the formation of col ateral circulation of portal vein and its peripheral tissues by performing portal vein radiography. CD31 was detected by immunohistochemistry. The expression of MMP-2, MMP-9, TIMP-1, TIMP-2 mRNA and protein in portal vein and peripheral tissue were determined by RT-PCR and immunohistochemistry respectively.
RESULTS AND CONCLUSION:Peripheral angiogenesis of model group was increased obviously by portal vein radiography and immunohistochemistry. RT-PCR and immunohistochemistry results demonstrated that, compared with the control group and sham operation group, the expression of MMP-2 mRNA and protein in model group were significantly increased at weeks 2, 4, and 6 (P<0.01, P<0.05), while expression of MMP-9 mRNA and protein at week 2 in model group were significantly higher than that in the control group and sham operation group. Expression of TIMP-1 and TIMP-2 in model group showed no significant difference compared with control group and sham operation group at weeks 2, 4, and 6 (P>0.05). Ratio of MMP-2/TIMP-2 of model group was significantly higher than that of control group and sham operation group (P<0.05) at week 2. the rat models of cavernous transformation of portal vein have low mortality, high success rate and are stable. Upregulation of the expression of MMP-2, MMP-9 and the disbanlance of the ratio of MMP-2/TIMP-2 might contribute to the peripheral angiogenesis in rats with cavernous transformation of portal vein.

Objective:To observe the regulatory effect of p38 mitogen-activated protein kinase (p38 MAPK) on aquaporin 4 (AQP4) in rats after hydrocephalus, and to explore its significance in hydrocephalus prevention.Methods:Fifty SD rats were randomly divided into sham-operated group ( n=10), hydrocephalus group ( n=20), and hydrocephalus+inhibitor (SB203580) group (SB group, n=20). The rat models of hydrocephalus in the latter two groups were prepared by intracerebroventricular injection of kaolin suspension; rats in the sham-operated group were injected with same amount of normal saline into the lateral ventricle. The p38 MAPK specific inhibitor SB203580 (10 mg/kg) was intraperitoneally injected into the rats of SB group on the 8 th d of modeling for 7 consecutive d; same volume of dimethylsulfoxide was given to the rats of hydrocephalus group on the 8 th d of modeling for 7 consecutive d; rats in the sham-operated group did not give any treatment. The severity of hydrocephalus in these rats was observed by MRI. The inflammatory factor tumor necrosis factor (TNF)-α level in the cerebrospinal fluid was detected by enzyme-linked immunosorbent assay (ELISA). The AQP4 and TNF-α mRNA expressions were detected by real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The phosphorylated p38 MAPK and AQP4 expressions in the periventricular brain tissues were detected by Western blotting and immunohistochemistry. Results:No hydrocephalus developed in sham-operated group and hydrocephalus developed in the latter two groups. As compared with sham-operated group, hydrocephalus group and SB group had significantly increased lateral ventricle volume, significantly aggravated periventricular edema, significantly higher EVAN's index, and statistically increased brain water content ( P<0.05). Two weeks after modeling, the TNF-α expression levels in cerebrospinal fluid of sham-operated group, hydrocephalus group and SB group were (20.49±0.96), (42.04±3.17), and (28.00±3.71) pg/mL, respectively, with significant differences ( F=186.000, P<0.001); the TNF-α expression level in SB group was significantly higher than that in sham-operated group and significantly lower than that in hydrocephalus group ( P<0.05). Two weeks after modeling, the TNF-α and AQP4 mRNA expression levels in brain tissues of the three groups were significantly different ( P<0.05); the TNF-α and AQP4 mRNA expression levels in hydrocephalus group were significantly higher than those in sham-operated group and SB group ( P<0.05). Correlation analysis showed that there was a positive linear correlation between AQP4 mRNA expression and TNF-α mRNA expression in hydrocephalus group ( r=0.511, P=0.026), and there was a positive linear correlation between AQP4 protein expression and phosphorylated p38 MAPK protein expression in hydrocephalus group and SB group ( r=0.560, P=0.013; r=0.463, P=0.030). Immunohistochemical staining results showed that AQP4 expression was abundant in glial cells of the three groups; the p38 MAPK distribution was uniform and non-polar; the phosphorylated p38 MAPK protein expression in the hydrocephalus group was significantly higher than that in the sham-operated group, and that in the SB group returned to the level of the sham-operated group. Conclusion:The p38 MAPK pathway is involved in the positive regulation of AQP4 expression, which could be inhibited by SB203580.