Effect of heat shock precondition on reperfusion arrhythmia in rats

AIM:To investigate the effect of the heat shock response on the reperfusion arrhythmias(RAs) and the possible mechanism involved. METHODS:Fifty-five Sprague Dawley rats were randomly divided into 2 groups: the heat shock group (group H,n=29) and the control group (group C,n=26). The rats in group H were preconditioned with heat shock 24 hours before, and that in group C were not. The hearts of 16 rats in group H and 16 in group C were exercised and mounted on a non-circulating Langendorff perfusion apparatus and perfused retrogradely with modified K-H buffer and mimic ischemia/reperfusion was applied. Additionally, conventional intracellular microelectrode techniques were used for recording such electrophysiological parameters as resting potential(RP), action potential amplitude(APA), over shot(OS), maximum depolarization velocity(Vmax) of the hearts of other 13 rats in group H and 10 in group C. RESULTS:①Prior heat stress significantly decreased reperfusion arrhythmia. ②The amount of CK release in the effluent in group H was much less than that in group C. ③Myocardial HSP70 content was elevated significantly in group H. ④Heat stress significantly increased myocardial anti-oxydases activity and decreased lipid peroxydative products. Additionally, heat stress significantly reduced the Vmax of action potential. It indicated that rapid Na⁺ channel of papillary muscles may be inhibited by heat shock. The degree of change of Vmax after ischemia in H group was significantly less than that in group C. And the time of reperfusoin with Tyrode's solution till the action potential appeared as large as that before perfusion with mimic ischemic solution is shorter in group H than in group C. CONCLUSION:Heat shock pretreatment markedly reduces ischemia/reperfusion-induced injury of heart and ventricular arrhythmias in rats and this effect may be associated with the inhibition of rapid Na⁺ channel of papillary muscles by heat shock and the increase in myocardial HSP70 and anti-oxydase activity.     

Effect of mesenteric lymph reperfusion on multiple organs injury in superior mesenteric artery occlusion shock rats

AIM: To explore the effect of mesenteric lymph reperfusion (MLR) on blood pressure, survival rate and organ injury in superior mesenteric artery occlusion (SMAO) shock rats.METHODS: Male Wistar rats were randomly divided into 4 groups: in sham group, only anesthetized and operation; in MLR group, performed 1 h occlusion of mesenteric lymphatics (ML) followed by 2 h of reperfusion; in SMAO group, performed 1 h occlusion of superior mesenteric artery (SMA) followed by 2 h of reperfusion; in MLR+SMAO group, performed 1 h occlusion of SMA and ML followed by 2 h of reperfusion. Histopathological and function changes of the lung, liver, kidney and myocardium in rats were assessed after 3 h of mean arterial pressure (MAP) was observed continuously in rats. The survival rate of 24 h was recorded.RESULTS: ① The 24 h survival rates of rats in sham, MLR, SMAO group (100%, 83.3%, 66.7%, respectively) were significant higher than those in MLR+SMAO group (0%). ② The changes of MAP in 4 groups were not statistically different before occlusion. The MAP in SMAO group was higher than that in MLR+SMAO and sham groups at multi-time points after clamping. After reperfusion, the change of MAP in MLR and sham groups was not obvious, and the MAP in SMAO group at multi-time points was decreased than that in MLR and sham groups. MAP in MLR+SMAO group was decreased compared with SMAO, MLR, sham group at all time points after reperfusion. ③ The levels of AST, ALT, BUN, Cre, LDH-1 and CK-MB in MLR+SMAO group in serum were higher than those in sham, MLR and SMAO groups, and these indexes in SMAO group were higher than those in sham and MLR groups. The morphologic observation showed that the structures in kidney, lung, liver and myocardium were normal in sham and MLR groups, however, inflammation, hemorrhage, congestion and necrosis were found in MLR+SMAO group, but only mild histopathological injury was found in SMAO group.CONCLUSION: Our data suggest that the MLR aggravates the multiple organs injury in SMAO shock, therefore, intestinal lymph pathway may play an important role in the pathogenesis of SMAO shock.     

Effect of heat shock protein 70 expression induced by glutamine on vascular hyporeactivity in rats caused by LPS

AIM: To observe the effect of heat shock protein 70(HSP70) expression induced by glutamine on Escherichia coli lipopolysaccharides(LPS)-induced vascular hyporeactivity in rats.METHODS: Twenty four healthy male Sprague-Dawley rats were randomly divided into: the control group (n=8);LPS shock group (n=8);glutamine(Gln) treated group (Gln 0.75 g·kg-1 iv,n=8).6 h after LPS shock,phenylephrine (PE,0.5-2.5 μg·kg-1 ) was applied intravenously to all groups and the percentage increase in mean arterial pressure(MAP) was detected,respectively.The concentration-response curves of aorta rings were obtained by cumulative addition of phenylephrine (PE),and PE Emax,EC50 were calculated.The blood concentration of malondialdehyde (MDA),TNF-α and IL-6 were assayed in all groups 30 min and 360 min after LPS shock,respectively.The expressions of HSP70 from heart and aorta were also assayed after 6 h LPS shock.RESULTS: The MAP level induced by PE significantly decreased by 51.4% in LPS shock group compared with the control (P<0.05).However,PE induced MAP level increased by 17.5% in Gln group compared with LPS shock group (P<0.05).Emax and EC50 to PE were significant reduced in LPS shock group compared with control group (P<0.05),but significantly improved in Gln group (P<0.05).The expressions of HSP70 from heart and aorta were much higher in Gln group than those in LPS shock group (P<0.05).The blood concentrations of TNF-α,IL-6 and MDA were much lower in Gln group than those in LPS shock group.CONCLUSION: Glutamine effectively improves α-adrenergic receptor-mediated vascular reactivity through inducing the expression of HSP 70,reducing inflammatory cytokine release and peroxide biosynthesis in LPS shock.These results suggest that glutamine have potential beneficial therapeutic effect for septic shock patients.     

Blockage of mesenteric lymph return promotes the vascular reactivity and calcium sensitivity in hemorrhagic shock rats

AIM: To observe the effects of mesenteric lymph duct ligation and mesenteric lymph drainage on the vascular reactivity and calcium sensitivity in hemorrhagic shock (HS) rats, and to investigate the role of mesenteric lymph on the vascular hyporeactivity during shock. METHODS: Seventy-two male Wistar rats were randomly divided into sham group (only operation), shock (duplicating HS model) group, shock+ligation group (duplicating HS model and mesenteric lymph duct ligation) and shock+drainage group (duplicating HS model and mesenteric lymph drainage). The changes of mean artery pressure (MAP) after injection of norepinephrine (NE, 3 μg/kg) at different time points were recorded. After hypotension (40 mmHg) for 3 h, the vascular ring of superior mesenteric artery (SMA) was made for determining the vascular reactivity and sensitivity to calcium by observing the contraction initiated by NE and Ca²⁺ under depolarizing conditions (120 mmol/L K⁺) in the isolated organ perfusion system. Meanwhile, the effects of angiotensin Ⅱ (AngⅡ) and insulin (Ins) on the vascular reactivity were also observed. RESULTS: Compared to sham group, the △MAP in shock group was increased significantly at 0 h and 0.5 h after shock, and that was decreased markedly at 1.5 h, 2 h, 2.5 h and 3 h after shock, respectively, and that in shock+ligation group and shock+drainage group was increased at 0 h, 0.5 h and 1 h after shock, decreased at 2.5 h and 3 h after shock, respectively. The △MAP in shock+ligation group and shock+drainage group was higher than that in shock group at 0.5 h after shock and all the time points followed. The SMA reactivity to NE and sensibility to Ca²⁺ in shock group, shock+ligation group and shock+drainage group were lower markedly than those in sham group. The vascular reactivity and calcium sensitivity in shock+ligation and shock+drainage groups were higher than those in shock group. The vascular reactivity and calcium sensitivity in shock group, shock+ligation group and shock+drainage group were lower than those in sham group, and those in shock+ligation and shock+drainage groups were increased as compared to shock group, respectively. CONCLUSION: Blockage of mesenteric lymphatic return with the methods of mesenteric lymph duct ligation and mesenteric lymph drainage promotes the vascular reactivity of HS rats. The mechanism may be related to improving the calcium sensitivity in the vasculature.     

CO2 与养分交互作用对番茄幼苗养分利用的影响

以番茄(Lycopersicon esculentumMill.)‘合作906’为材料进行溶液培养试验,设2个因子:CO2和营养液浓度;CO2浓度设正常(360μL/L)和倍增(720μL/L)2个水平;营养液浓度设基本营养液(日本山崎番茄营养液),微量元素采用阿农营养液配方的1/2、1/4、1/8、1/164个水平,完全试验方案8个处理,3次重复。pH为6·0±0·2,3d更换1次营养液。移植到1·2L盆(2株/盒)中,植株在CO2生长箱(VS-3DMC)中培养,全天施放CO2,白天25℃,晚上15℃,光照为14h/d,光照强度11000lx,相对湿度60%。46d时收获,根、茎、叶经蒸馏水冲洗吸干水分后,放入纸袋105℃杀青,75…     

Protective effect of pyrrolidine dithiocarbamate on cardiac muscles in diabetic rats

AIM: To investigate the effect of pyrrolidine dithiocarbamate (PDTC) on reducing blood glucose level and its protective effect on cardiac muscles in diabetic rats.METHODS: Thirty-seven male Wistar rats were randomly divided into normal control (NC) group and the high-fat diet (HFD) group. After 8 weeks of feeding, the rats in high-fat diet group were given a single dose of streptozotocin (STZ, 27 mg/kg) by intraperitoneal injection to induce type 2 diabetes. The diabetic rats were randomly divided into diabetes mellitus (DM) group and PDTC treatment(PDTC) group. The rats in PDTC group were intraperitoneally injected with PDTC (50 mg/kg) once daily. The rats in NC group and DM group were injected with equivalent volume of saline in the same way. After 1-week treatment, the level of blood glucose was measured, and all animals were killed. The concentration of malondialdehyde (MDA) and the activity of superoxide dismutases (SOD) and glutathione peroxidase (GSH-Px) were determined using commercial kits. The ultrastructural changes of the cardiac tissues were observed under transmission electron microscope. The expression of inducible nitric oxide synthase(iNOS) and content of nitrotyrosine was examined by the method of immunohistochemistry.RESULTS: The levels of blood glucose and MDA were significantly higher, while the activity of SOD and GSH-Px was lower in DM group than those in NC group (P<0.01). Treatment with PDTC markedly decreased the blood glucose and MDA content, and increased the activity of SOD and GSH-Px. Severe degeneration, necrosis, mitochondrial damage and inflammatory cell infiltration were found in the cardiac tissues in DM group. Treatment with PDTC markedly attenuated mitochondrial damage. The expression of iNOS and content of nitrotyrosine in cardiac tissues were significantly higher in DM group than those in NC group, and those were reduced after administration of PDTC.CONCLUSION: High glucose induces oxidative stress, increases the expression of iNOS and content of nitrotyrosine, and impairs the structure and function of myocardium. PDTC reduces blood glucose level, decreases the expression of iNOS and content of nitrotyrosine, and delays or attenuates the development of diabetic cardiomyopathy in diabetic rats.     

中甘21号

AIM: To observe the pathological role of 3-nitrotynosine (3-NT) on Escherichia coli LPS-induced vascular hyporeactivity in rats and the therapeutic effect of antioxidants. METHODS: Forty male SD rats weighting from 200 g to 250 g were randomly divided into four groups: the control group (n=10); LPS shock group (n=10); uric acid-treated group (n=10); melatonin-treated group (n=10). 6 h after LPS shock, phenylephrine (0.5-2.5 μg·kg-1) was applied intravenously to all groups and the percentage increase in MAP was detected, respectively. The concentration-response curve of aorta rings from all groups rats were obtained by cumulative addition of phenylephrine (PE), and PE Emax, EC50 were calculated. The concentrations of plasma malondialdehyde (MDA), nitrate/nitrite and 3-NT were assayed in all groups 6 h after LPS shock. RESULTS: The MAP level induced by PE significantly decreased to 54.60% in LPS shock rats compared with the control (P<0.05). However, PE induced MAP level increased 37.70% and 43.05% in uric acid and melatonin treated rats, respectively, compared with the LPS shock rats (P<0.05). The maximum response and EC50 to PE were significant reduced in LPS shock rats ［Emax, 35.30%±9.80%; EC50, (15.70±4.50)nmol/L］ compared with control group ［Emax, 100%; EC50, (4.71±2.04)nmol/L, P<0.05］; but the reactivity of aorta to PE was improved obviously in uric acid and melatonin treated groups (P<0.05). The plasma concentration of MDA, nitrate/nitrite and 3-NT were much lower in uric acid and melatonin groups than those in LPS shock group (P<0.05). CONCLUSIONS: 3-NT is an important pathological factor on vascular hyporeactivity in LPS shock. Antioxidants effectively improve α-adrenergic receptor-mediated vascular reactivity in LPS shock rats partially by removing lipid peroxidative production, reducing nitric oxide and 3-NT biosynthesis in LPS shock. These results suggest that antioxidants have potential beneficial therapeutic effect for septic shock patients.     

Effects of electrical stimulation of vagus nerve on gut injury following intestinal ischemia-reperfusion in rats

AIM:To investigate the effects of electrical stimulation of vagus nerve on gut injury following intestinal ischemia-reperfusion in rats. METHODS:30 adult male Wistar rats subjected to bilateral cervical vagotomy were randomly divided into three groups (n=10 per group):(1) Intestinal ischemia-reperfusion group (group I/R):laparotomy and I/R induced by clamping arteria mesenterica superior for 1 h followed by reperfusion for 2 h. (2) Vagus nerve stimulation group (group VNS):laparotomy, I/R and electric stimulation with pulse train of constant amplitude 5V, pulse width 2 ms and frequency 1 Hz at the left caudal vagus ends for 20 minutes before and after occlusion. (3) Sham control group (group SC):sham operation and sham stimulation. Carotid artery was cannulated for mean arterial pressure (MAP) monitoring. A strip of small intestine was taken from distal end of ileum for light microscopic (LM) and transient electron microscopic (TEM) examination at the time of 2 h after reperfusion. Improved Chiu’s scale was used to quantitatively assay the damage degree. The levels of malondialdehyde (MDA) and TNF-α in plasma were detected. RESULTS:MAP in every group kept steady during ischemia, but decreased gradually with the prolongation in the time of reperfusion. MAP decreased more dramaticly in group I/R than that in group VNS (P<0.05). Histological changes by LM and TEM were more significant in group I/R than those in group VNS and SC. The improved Chiu’s scale in group VNS was obviously slighter than that in group I/R (P<0.05). In group I/R, the levels of MDA and TNF-α in plasma were significantly increased compared with group VNS and SC (P<0.01, P<0.05). MDA level in group VNS was significantly higher than that in group SC, but there was no significant difference in TNF-α between the two groups. CONCLUSION:Electrical stimulation of vagus nerves can lessen pathological changes of intestinal mucosa induced by I/R and improve BP during reperfusion, which may be related to reducing lipid peroxidation, and down-regulating TNF-α synthesis.     

Dexmedetomidine attenuates acute kidney injury induced by hemorrhagic shock/resuscitation in rats

AIM: To investigate the effects of dexmedetomidine on hemorrhagic shock/resuscitation (HS/R)-induced acute kidney injury (AKI) in rats, and to explore the possible mechanisms. METHODS: Wistar rats (n=32) were randomly divided into 4 groups (n=8):normal saline control group (NS group), dexmedetomidine group (D group), HS/R group and HS/R+D group. The animals were sacrificed at 6 h after resuscitation. The levels of serum creatinine (Cr) and blood urine nitrogen (BUN) were examined. The kidneys of all rats were removed for evaluation of histological characteristics, and the levels of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and superoxide dismutase (SOD) were measured. The expression of nuclear factor-κB (NF-κB) and hemeoxygenase-1 (HO-1) was determined by Western blot. RESULTS: Compared with NS group, the levels of Cr, BUN, MDA, TNF-α and IL-1β were obviously increased in HS/R group, which were obviously decreased in HS/R+D group (P<0.05). Compared with NS group, the SOD activity was obviously decreased in HS/R group, which was obviously increased in HS/R+D group (P<0.05). Compared with NS group, the protein expression of NF-κB was obviously increased in HS/R group, which was obviously decreased in HS/R+D group (P<0.05). Compared with NS group, the protein expression of HO-1 was increased in HS/R group. Compared with HS/R group, the protein expression of HO-1 was obviously increased in HS/R+D group. Compared with NS group, HS/R induced marked kidney histological injury, which was less pronounced in HS/R+D group.CONCLUSION: Dexmedetomidine effectively protects rats against AKI caused by HS/R, and its mechanism may be associated with the increase in HO-1 expression and the inhibition of NF-κB expression.     

Role of β-endorphin in the suppression of cellular immunity of rats following trauma-hemorrhagic shock()

AIM: To explore the role of plasma β-endorphin(β-EP) in the suppression of cellular immunity following trauma-hemorrhagic shock(T-HS). METHODS: ① Wistar rats with T-HS were sacrificed at 0 h, 1 h, 3 h, 6 h, 12 h, 24 h after T-HS. Plasma sample was collected and β-EP levels in plasma was measured. Rats with sham-operated were served as the controls. ②In in vitro experiment, splenic cells were isolated and mixed from four normal rats and cocultured with shock plasma (SP) or SP +β-EP antiserum. ConA-induced splenic cell proliferation, IL-2 production, IL-2R expression were examined. RESULTS: ① Levels of plasma β-EP elevated remarkably after T-HS immediately, peaked at 1h , showed decreasing tendency and restored normal 24 h after T-HS. ② Shock plasma significantly suppressed ConA-induced splenic cell function. Levels of plasma β-EP were negatively correlated with spenic cell proliferation and IL-2 production and IL-2R expression. Compared with SP group, splenic cell function elevated markedly in SP + β-EP antiserum group, but still lower than that in controls. CONCLUSION: The elevated plasma β-EP following T-HS was involved in the suppression of cellular immunity.     

Effect of hypertonic saline solution on the geometry of erythrocyte in rats subjected to hemorrhagic shock

AIM:To study the effect of hypertonic saline solution on the geometry of erythrocyte in hemorrhage-shocked rats,using micropippette aspiration technique. METHODS:Wistar rats were randomized into three groups of 0.9% NaCl(NS),7.5% NaCl(HS) and 5% NaCl-3.5% NaAc(HSA). The animals were bled to reach a mean arterial pressure of 5.3 kPa in 10 minutes and maintained in shock for 90 minutes. 4 mL/kg NS,HS or HSA was given intravenously and respectively in 5 minutes following hemorrhagic shock. The blood was collected to determine the geometry of erythrocyte at baseline,after shock and treatment. RESULTS:There were no significant difference in surface area/volume ratio and spherical index between baseline and shock.The diameter of erythrocyte were decreased obviously following hemorrhagic shock. The surface area/volume ratio was significantly lower in HS group than that in NS and HSA group after treatment. HS and HSA raised spherical index of erythrocyte remarkbly compared with NS.Otherwise,the spherical index of erythrocyte was reduced significantly in HSA group compared to HS group. Both HS and HSA decreased diameter of erythrocyte notably compared with NS. CONCLUSION:Both HS and HSA have deleterious effects on the geometry of erythrocyte in rats subjected to hemorrhagic shock.Whereas, HSA could decrease the side effect compared with HS.     

Reversion of the decline of cardiac function in endotoxin shock rats by cholecystokinin octapeptide

AIM: To verify the effect of cholecystokinin octapeptide(CCK-8) on cardiac function in endotoxin shock (ES) rats. METHODS: The rats were divided into four groups:control,lipopolysaccharide(LPS),CCK-8 and CCK-8+LPS. The left ventricle pressure(LVP),the maximal/minimum rate of LVP,heart rate (HR) and mean arterial pressure (MAP) were measured. The activity of superoxide dismutase (SOD),the contents of malondialdehyde (MDA) and nitric oxide (NO) in both serum and myocardium were also measured,respectively. RESULTS: CCK-8 (40 μg·kg^-1, iv) elicited bradycardia in short time and gently increase MAP,LVP and ±LVdp/dt_max. Lipopolysaccharide(LPS, 8 mg·kg^-1, iv) caused a variation in heart rate (HR)(a bradycardia following a tachycardia) and rapid decreases in MAP,LVP and ±LVdp/dt_max. The rapid variation of HR and the decline of MAP,LVP and ±LVdp/dt_max were reversed by pretreatment with CCK-8 in ES rats, but didn't restore to normal. The activity of SOD was increased and the contents of MDA and NO were decreased by pretreatment with CCK-8 in ES rats. CONCLUSION: The decline of cardiac function in ES rats could be reversed by pre-administration of CCK-8 and the decrease in NO production may be one of the mechanisms.     

Effect of puerarin on pulmonary arterioles wall collagen metabolism of chronic hypoxia hypercapnia rats

AIM:To investigate the effect of puerarin on pulmonary vessel collagen metabolism in pulmonary hypertension rats induced by chronic hypoxia and hypercapnia.METHODS:Collagen Ⅰ, Ⅲ and their mRNA were observed in pulmonary arterioles by the technique of immunohistochemistry and in situ hybridization.RESULTS:① Light microscopy showed media thickness of pulmonary arterioles was much higher in HH(hypoxic-hypercapnia) group than that of NC(normal control) group, and, vessel cavity turned more straiter in HH group than that of NC group.However, the damage of pulmonary arterioles in HP(hypoxic-pueratin) group was much slighter than that of HH group. ② The levels of plasma ET-1 and lung homogenates Hyr were much higher in HH group than those of NC group(P＜0.01), and lower in HP group than HH groups(P＜0.01).Plasma NO content in group HH was lower than that of group NC(P＜0.01), it was higher in group HP than that of group HH(P＜0.01).③Expression of collagen Ⅰ and collagen Ⅰ mRNA in pulmonary arterioles were significantly higher in HH groups than those of NC group (P＜0.01), and they were lower in HP group than those of HH group (P＜0.01).Expression of collagen Ⅲ and collagen Ⅲ mRNA showed no difference among three groups(P＞0.05).CONCLUSION:Puerarin inhibited the deposition of collagen and improved pulmonary vessel remodeling.     

Mechanism of calcium sensitivity in lymphatic hypo-reactivity in hemorrhagic shock rats

AIM: To observe the changes of lymphatic reactivity to norepinephrine (NE) and calcium sensitivity in vitro in hemorrhagic shock (HS) rats. METHODS: Male Wistar rats were randomly divided into sham group (with only operation), HS group (duplicating HS model, and divided into shock 1 h and shock 2 h subgroups). The thoracic duct rings (n=48 in each group) were prepared for assaying the lymphatic reactivity to NE and calcium sensitivity by lymphatic tension measurement technique in vitro with isolated perfusion system. Meanwhile, the effects of angiotensin Ⅱ (Ang Ⅱ) and insulin (Ins) on lymphatic reactivity were also observed. RESULTS: Compared with sham group, the NE concentration-response curves in HS 1 h and HS 2 h groups, and calcium concentration-response curves in HS 2 h group were obviously shifted to right. The lymphatic reactivity to NE, contraction to calcium, maximum effect(E_max)and avidity index (pD₂) were markedly reduced. In HS group, after incubating with calcium sensitizer Ang Ⅱ, the lymphatic reactivity to NE and calcium sensitivity were significantly increased but reduced in sham group. However, calcium sensitivity inhibitor Ins decreased the lymphatic contractile response to NE and Ca²⁺. CONCLUSION: The lymphatic hypo-reactivity in hemorrhagic shock rats is related to calcium desensitization, indicating a mechanism of lymphatic hypo-contraction.     

LBP regulates PI3K/Akt/eNOS signaling pathways in ovariectomized rat myocardium to exert antioxidative effect

AIM: To observe the influence of Lycium barbarum polysaccharide (LBP) on the PI3K/Akt/eNOS signaling pathways in ovariectomized rat myocardium. METHODS: Female SD rats (n=30) were divided into sham operation group, ovariectomized group, progynova group, high-dose LBP group and low-dose LBP group. The serum levels of estradiol, lactate dehydrogenase (LDH) and creatine kinase (CK) were measured by ELISA. The myocardial contents of H₂S and oxidative stress injury-related indicators were also detected. The morphological changes of the myocardium were observed with HE staining. The expression of eNOS and PI3K/Akt pathway-related proteins in the myocardium was determined by Western blot. RESULTS: Compared with sham operation group, the serum level of estradiol, the content of H₂S, the activity of GSH-Px, and the expression of eNOS and PI3K/Akt pathway-related proteins in the myocardium in ovariectomized group were all decreased, and the levels of ROS and MDA in the myocardium were increased (P<0.05). The serum levels of LDH and CK were also increased. The arrangement of the myocardial cells was disordered, and the intercellular space was also increased in the ovariectomized group. Compared with ovariectomized group, the serum level of estradiol, the myocardial levels of H₂S and GSH-Px, and the protein levels of eNOS and phosphorylated Akt were all increased in high dose group, while the levels of ROS and MDA in the myocardium were decreased (P<0.05). The serum levels of LDH and CK were also decreased. The morphological changes of the rat myocardium were improved in high dose group. CONCLUSION: LBP prevents and treats postmenopausal cardiovascular lesions through regulating PI3K/Akt/eNOS signaling pathways in ovariectomized rats.     

Intervention of hydrogen on memory damage induced by chronic hypoxia-hypercapnia in rats

AIM: To investigate the effects of hydrogen on the memory damage caused by chronic hypoxia-hypercapnia in rats. METHODS: Twenty-four SD rats trained by eight-arm radial maze test were randomly divided into 3 groups:normal control group (NC), hypoxia-hypercapnia+saline group (MS) and hypoxia-hypercapnia+ hydrogen group (MH). The rats in the latter 2 groups were placed in a closed cabin for 8 h/day,6 days/week and lasted for 4 weeks, in which O₂ was 9％-11％ and CO₂ was 5％-6％. In every time after the animals were out of the cabin, the MS rats were intraperitoneally injected with saline (5 mL/kg) and the MH rats were intraperitoneally injected with hydrogen solution at the same dose. The learning and memory function, the activity of superoxide dismutase (SOD), the content of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) were examined after the cabin training. The ultramicrostructures of hippocampus were also observed. RESULTS: (1) Compared with NC group, the number of working memory errors, the total errors, the content of hippocampus 8-OHdG and serum MDA in MS and MH groups were higher and the activity of serum SOD was lower (P<0.05). The hippocampus structure was destroyed and some degree of edema and more apoptosis in the neurons were obserued in MS group and MH group. (2) Compared with MS group, the number of working memory errors(WME), the total errors, the content of hippocampus 8-OHdG and serum MDA were lower and the activity of serum SOD was higher in MH group (P<0.05). In MH group, the morphology of hippocampus structures kept nearly normal arrangement and the only mild edema and fewer apoptosis in the neurons were found. CONCLUSION: Hydrogen may attenuate chronic hypoxia-hypercapnia-induced memory damage in rats by inhibiting apoptosis of the neurons and decreasing detrimental free radicals reaction.     

Changes of lymphatic vessel response to norepinephrine in hemorrhagic shock rats

AIM: To observe the changes of lymphatic vessel response to norepinephrine (NE) in hemorrhagic shock (HS) rats, and to explore the role of lymphatic reactivity in the pathogenesis of shock. METHODS: The lymphatic vessel pressure was observed through intubating into abdomen thoracic duct in 8 rats in sham group and HS group (which was bled from femoral artery until the mean arterial pressure to 40 mmHg). The changes of lymphatic vessel pressure response to NE at different time points were observed by injection of NE (5 μg/kg) through femoral vein. The spontaneous contraction frequency (F), maximal contraction diameter (a), maximal diastolic diameter (b) and static diameter (c) of mesenteric lymphatic (ML) living samples in 8 rats of each group were recorded through microcirculation video systems continuously. The changes of lymphatic fractional contraction index (index I), total contractile activity index (index II) and lymphatic dynamic index (LD-index) (to show the value using △F, △index I, △indexⅡ, △LD-index) were calculated after injection of NE at different time points. RESULTS: The changes of lymphatic boosting pressure response to NE in HS group was started to diminish 30 min after shock, and showed a progressive decreasing trend which significantly reduced than that in sham group at all time points of shock 1 h-3 h. In HS group, the △F, △indexⅡ, △LD-index at shock 1 h, the △F, △index I, △indexⅡ, △LD-index at shock 1.5 h and 2 h were significantly lower than those in sham group, and the △F, △index I, △indexⅡ, △LD-index at all time points were significantly decreased as compared to the values of pre-shock. CONCLUSION: Lymphatic vessel reactivity in shock rats is progressive declined in the process of hemorrhagic shock. The lymphatic vessel hypo-reactivity might play an important role in the pathogenesis of shock.     

热激锻炼诱导猕猴桃耐热性研究

以美味猕猴桃(Actinidia deliciosa)品种秦美组培苗为试材,研究了热激锻炼对猕猴桃耐热性的诱导。试验结果表明,热激锻炼抑制了高温胁迫下猕猴桃叶片叶绿素的分解、细胞膜透性的增大和MDA含量的增加,使H2O2含量维持在较低的水平,增强了高温胁迫下抗氧化酶(SOD、CAY、POD、APX)活性和抗氧化剂(ASA、Pro)含量。说明热激锻炼诱导猕猴桃获得了耐热性。     

Oxidative stress promotes KCa3.1 expression in myocardium of AGT-REN double transgenic hypertension mice

AIM: To study the relationship between oxidative stress reaction and K_Ca3.1 protein expression in the process of myocardial remodeling.METHODS: The male AGT-REN double transgenic hypertension (dTH) mice (2, 4, 8 and 12 months old, each n=6) were used to detect the changes of the corresponding indexes. The male dTH mice (6 months old) were randomly divided into 2 groups: dTH group and N-acetylcysteine (NAC) group, and 6 wild-type(WT) C57B6 mice served as controls. The mice in NAC group were treated with NAC at dose of 400 mg·kg^-1·d^-1, and the WT and model mice were treated with normal saline. After 4 weeks, the concentrations of Ang Ⅱ and Ang (1-7) in the plasma were measured by ELISA. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected using SOD and MDA kits. The protein levels of collagen I, collagen III and K_Ca3.1 were determined by Western blot. RESULTS: Compared with the WT mice, mean arterial blood pressure (MAP), concentration of Ang Ⅱ in the plasma, the content of MDA, and the protein expression of collagens and K_Ca3.1 in the myocardium of 4-, 8- and 12-month-old dTH mice were increased, and gradually raised along with the age from 2 to 12 months (P<0.05), but the SOD activity in myocardium and Ang (1-7) content in plasma were decreased (P<0.01). NAC reduced the MAP, the content of MDA, and the protein expression of collagens and K_Ca3.1 in the myocardium of 6-month-old dTH mice (P<0.05 or P<0.01), and increased SOD activity compared with dTH group (P<0.01).CONCLUSION: Increased protein expression of myocardial K_Ca3.1 during myocardial remodeling induced by hypertension may be associated with enhancement of myocardial oxidative stress level.     

Hyperhomocysteinemia induces endothelial dysfunction and aggravates microcirculation dysfunction and microthrombosis

AIM: To establish a microthrombus model by carrageenan (Ca)/ lipopolysaccharides (LPS) intraperitoneal injection in rats with hyperhomocysteinemia (HHcy) and endothelial dysfunction induced by L-methionine intake.METHODS: ① Male Sprague Dawley rats were randomly divided into 2 groups: control and endothelial dysfunction (HHcy) groups. L-methionine was administered by gavage in HHcy group for total 4 weeks.Purified water was administered by gavage in control rats.Plasma Hcy,NO and vWF were examined and the thoracic aorta were excised after 4 weeks of L-methionine treatment to evaluate endothelial function.② Male Sprague Dawley rats were randomly divided into 3 groups to establish a microthrombus formation model with Ca/ LPS: control,microthrombus formation (Ca/LPS) and endothelial dysfunction plus mitoarothrombus formation (HHcy＋Ca/LPS) groups.Control rats were injected with normal saline (NS).Ca/LPS rats were intraperitoneally injected with carrageenan (Ca) and followed by lipopolysaccharides (LPS) 16 h later.HHcy＋Ca/LPS rats were intragastric gavaged by L-methionine for total 4 weeks,and then were injected with Ca/LPS in the same way as Ca/LPS group.Cruor parameters and platelet count were detected at 20 h after LPS or NS injection and the mesentery microcirculation was monitored.Plasma NO and vWF were also detected at 24 h after LPS or NS injection.RESULTS: ① Plasma Hcy concentrations and vWF level were significantly increased in HHcy group,while plasma NO content was significantly decreased compared with that in control group.Endothelial dependent relaxation (EDR) of aortic rings was significantly decreased in HHcy group,suggesting endothelial damage/dysfunction was induced by HHcy.② Mesentery capillary was obviously blocked by microthrombus in Ca/LPS rats and was blocked more seriously in HHcy＋Ca/LPS rats.Cruor parameter results suggested that Ca/LPS rats were in hypercoagulable phase and HHcy＋Ca/LPS rats were in hypocoagulable phase at 20 h after LPS injection.Platelet count and plasma NO content in HHcy＋Ca/LPS group were significantly decreased,while plasma vWF level was significantly increased compared with Ca/LPS group.CONCLUSION: L-methionine intake induces severe HHcy and causes endothelial dysfunction in rats.Microcirculation dysfunction and microthrombosis can be caused by Ca/LPS intraperitoneal injection and may be aggravated by endothelial dysfunction.