Objective:To study the pathogenetic mechanism of intestinal injury in the aged rat with pneumonia and the effect of Dusuqing(毒素清) on it.Methods:The models of rats with Escherihia coli pneumonia were duplicated and divided into aged control group(ACG),aged model group(AMG),high doses group(HDG) and low doses group(LDG) of Dusuqing and norfloxacin group.The pathological changes in lung tissue and intestine,the contents of intestinal 6-keto-prostaglandim F1α(6-keto-PGF1α),thromboxane B2(TXB2),nitride oxide(NO),malondialdehyle(MDA) and the activity of superoxide dismutase(SOD) were observed.Results:The lung and intestinal injury in AMG was more serious.The decrease of SOD activity and 6-keto-PGF1α content,the increase of content of TXB2,NO,MDA in the AMG were more significant than those in the ACG.In comparison with those in the AMG,the level of SOD activity,6-keto-PGF1α content were increased,otherwise the contents of MDA and NO were decreased in the HDG,the LDG and the norfloxacin group.Conclusions:The injury mediated by prostaglands and free radical is related to the occurance and development of damage of intestinal tissue with pneumonia. Dusuqing is able to improve this damage obviously in aged rats with pneumonia and the mechanisms and regulation of prostaglands metabolism.

AIM\ To study the protective mechanism of ligustrazine(LT), shenmai injection(SI), combination of ligustrazine and shenmai injection (LSI) to injury of kidney after brain ischemia reperfusion in aged rats from the free radical change. METHODS Aged rats (more than 20 months) were divided into model group (Aged model), control group(Aged control), nimotop group(NG), ligustrazine group(LG), shenmai injection group(SIG) and LSI group(LSG). The following items was measured in aged rats with 60 min reperfusion after 30 min brain ischemia: the content of creatinine(Cr), urea nitrogen(BUN), MDA and the activitiy of superoxide dismutase(SOD). RESULTS The distinct pathological and functional injury in the kidney was found in the models, and this change was alleviated in each treatment group. The increase of MDA content in the models kidney tissue was obvious than that in the controls. The MDA level in the LG and the SIG was decreased. CONCLUSION The kidney injury after brain ischemia reperfusion in aged rats is correlated with the injury of free radical. LT, SI ,LSI and nimotop alleviate this injury. LT and SI restraine the injury of lipid peroxidation, this may be one of the mechanisms of restraining kidney injury after brain ischemia reperfusion.

AIM: To study the mechanism of brain ischemia-reperfusion injury from ATPase activity and free radical metabolism in aged rats. METHODS: The young rats (5 months) and the aged rats (more than 20 months) were divided into young control group(YCG), young model group(YMG), aged control group(ACG) and aged model group(AMG). The ATPase and SOD activities and the contents of MDA, Ca 2+ , Na + and K + were measured in the rats with 30 min brain ischemia followed by 60 min reperfusion. RESULTS: The Ca 2+ content in the AMG was higher than that in the YMG and the ACG. The Na +-K +-ATPase activity in the ACG was lower than that in the YCG,was lower in the AMG than that in the YMG . The Ca 2+ -ATPase activities in the YCG was higher than that in the ACG, was lower in the AMG than that in the YMG and was higher than the ACG's. The serum and brain tissue SOD activities in the ACG was lower than that in the YCG, was lower in the AMG than YMG 's. The serum and brain tissue MDA/SOD ratio in the AMG was higher than that in the ACG. CONCLUSION: The brain tissue ischemia- reperfusion injury was related with calcium overload and free radical injury. The pathological changes were obvious and had some characteristics in the aged rats compared with the young rats because of the brain tissue aging changes in ATPase,calcium content and free radical metabolism in the aged rats.

AIM: To study the protecitve mechanism of Ligustrazine (LT), Shenmai Parenteral Injection (SPI), combination of Ligustrazine and Shenmai Parenteral Injection (LSP) to myocardial injury after brain ischemia-reperfusion in aged rats from the change in ATPase and free radical in order to provide theoretical basic for prevention and cure of cerebral infarction. METHODS: Aged rats (more than 20 months) were divided into model group, control group, Nimotop group, LT group, SPI group and LSP group. We measured the following items in aged rats with 60 min of reperfusion after 30 min of brain ischemia: the content of MDA, the activities of superoxide dismutase (SOD), lactic dehydrrogenase (LDH), creatine phosphokinase (CPK), ATPase. RESUTLS: The CPK and LDH activities in the model rats increased obviously. The serum CPK activity in the LSP group, the LT group, nimotop group was lower than those in the model group obviously. The serum LDH activities in LT group and SPI group were obviously lower compared with those in the model group. The activity of Na＋-K＋-ATPase and Ca2＋-ATPase in model group was decreased. Contrast to the model group, the activity of Na＋-K＋-ATPase in LSP group, Nimotop group, LT group and the activities of Ca2＋-ATPase in the LSP group were higher. The serum MDA/SOD ratio was larger than that in the control group. The decrease in myocardial SOD activity and the increase in the MDA level, MDA/SOD ratio in the model group showed significant difference compared with that in the control. The MDA level in the LSP group was lower than that in the model group. The increase in myocardial SOD activity and decrease in MDA, MDA/SOD ratio were obvious in the LSP group compared with the model group. CONCLUSION: The myocardial injury after brain ischemia-reperfusion in aged rats was related to the decrease in the activity of Na＋-K+-ATPase and injury of free radical. LT, SPI, LSP and Nimotop could prevent this inury. Nimotop and LT could enhanced the activity of Na+-K+-ATPase obviously. SPI could enhance the activity of Ca2＋-ATPase and restrain the injury of free redical and lipid peroxidation. This may be the mechanism of restraining myocardial injury after brain ischemia-reperfusion.

AIM: To study the mechanism of myocardial injury after brain ischemia-reperfusion in aged rats from the changes in Dopamine (DA), Noradrenalin (NE), Epinephrine(E) and Neuropeptide Y(NPY).METHODS: Young (5 months) and aged (20 months or more) rats were divided into model groups and normal control groups, respectively. We observed the following items in rats with 60 minute reperfusion after 30 minute brain ischemia: the pathological changed of myocardium, the activities of lactic dehydrrogenase(LDH), creatine phosphokinase(CPK), the contents of NE, DA, E, NPY. RESULTS:The CPK and LDH activities in the young model rats were higher than those in the young control rats was higher than that in the young control rats (P＜0.05). The serum CPK activity in the aged control rats was higher than that in the young control rats (P＜0.05). The myocardial CPK activity was higher in the aged model rats compared with the young molel rats (P＜0.05) and was higher in aged control rats compared with the young control rats (P＜0.01). The myocardial LDH activity was lower in the aged control rats than that in the young control rats (P＜0.05) and aged model rats (P＜0.01). The serum NE level, the level of NE and DA in the hypothalamus were higher obviously than those in the young control rats. The serum NE contents in the two model groups (young and aged) were higher respectively than the two control rats (young and aged). The following items’ contents were higher in the aged model rats than in the young model rats: serum NE, serum E, hypothalamus NE. The hypothalamus NE and E content was lower in the aged model rats than in te aged control rats. NPY level in the brain tissue was lower in the aged control rats than that in the young control rats and aged model rats (P＜0.05).CONCLUSION: The myocardial injury after brain ischemia-reperfusion was concerned with the enhanced excitability of sympathetic-adrenal system, espectially in the aged rats. However, the change in myocardial enzyme was not serious in the aged rats compared with young rats.