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Vascular dementia (VD) is a type of memory, cognition, and behavior disorder caused by ischemic stroke or hemorrhagic stroke. It is a common pathogenesis of dementia that is only second to Alzheimer's disease. Inflammation plays a key role in VD. Interleukin-1β (IL-1β) is a kind of pro-inflammatory cytokine, while its mechanism in VD occurrence and development is still unclear.The healthy male rats were randomly divided into three groups, including sham group, VD model group (established by bilateral common carotid artery ligation), and IL-1β group (treated by IL-1β monoclonal antibody intracerebroventricular injection on based on model group). Rat learning ability was evaluated by Morris water maze assay. IL-1β expression in brain tissue and peripheral blood was examined by using Real Time-PCR and enzyme-linked immunosorbent assay (ELISA), respectively. Hippocampus apoptosis was detected by caspase 3 activity detection kit. B-cell lymphoma-2 (Bcl-2) and p38 mitogen-activated protein kinase (MAPK) protein levels were assessed by Western blot assay.IL-1β expression was increased, caspase 3 activity was enhanced, Bcl-2 level was declined, and p-P38 phosphorylation was elevated in brain tissue and peripheral blood from VD model group compared to sham group (p0.05). IL-1β monoclonal antibody significantly reduced IL-1β expression, improved learning ability, attenuated caspase 3 activity, increased Bcl-2 level, and declined p-P38 expression in VD rats compared to model group (p0.05).IL-1β can delay VD occurrence and development through the P38-MAPK signaling pathway to regulate cell apoptosis and improve learning ability.

A special local burn wound treatment, using a healing promotion factor, attempted to achieve earlier wound closure. Clinically it is not difficult to harvest autologous human platelet-derived wound healing factor (HPDWHF) from burn patients. Another study has proved that porcine pituitary extract (PPE) could be one of the supplements for growing human keratinocytes in vitro (Wang HJ, Chen TM, Tung YM et al. Burns 1995). Initially, using the ELISA immunoassay, we detected titres of platelet-derived growth factor heterodimer AB (PDGF-AB) and epidermal growth factor (EGF) in HPDWHF and PPE. After elevating a 6 X 9 cm2 flap on the backs of Sprague-Dawley (SD) rats 1 ml of heterologous HPDWHF and PPE were sprayed topically on the wound and followed by grafting six pieces of 1 cm2 autologous full-thickness skin. The flap wound was then closed with a piece of large-pore Biobrane interposed between the skin graft wound and the flap. On postgraft day 7, the wound was reopened to measure the area of the full-thickness skin graft (FTSG) using micrographic paper; the results are reported as the percentage of graft expansion beyond the original size. In the cytokine study, we found that the concentrations of PDGF-AB dimer in HPDWHF and PPE were 5222 +/- 102 and 375 +/- 12 pg/ml (both values are reported after a 1:10 dilution) (n = 3), whereas the EGF concentration was 245 +/- 9 pg/ml, and undetectable in undiluted PPE (n = 3), thereby proving that the PDGF-AB and EGF fibres in the HPDWHF were significantly higher than in the PPE Both the HPDWHF (n = 6, with each animal grafted with six skin graft samples) and PPE (n = 7) demonstrated significant accelerations of FTSG growth, with 14.41 +/- 1.08 per cent and 13.16 +/- 3.25 per cent increases in the FTSG size when compared to the sham control group 1.39 +/- 3.26 per cent (n = 5) (P0.05). Comparisons between the treatment groups showed no evidence to indicate that the HPDWHF is superior to the PPE in accelerating FTSG growth (P0.05). This supports the hypothesis that PDGF appears to transduce its signal through wound macrophages and may trigger the induction of positive autocrine feedback loops and synthesis of endogenous wound PDGF and other growth factors, thereby enhancing the cascade of tissue repair (Pierce GF, Mustoe TA, Altrock B et al. 1991; J Cell Biochem 1991; 45: 319-326), and the effect that PDGF-AB on wound healing is not dose dependent (Mustoe TA, Cutler NR, Allman RM et al. Arch Surg 1994; 129: 213-219). In future studies we expect to show that autologous HPDWHF and heterologous PPE will promote skin graft wound healing in burn patients since they contain a high concentration of PDGF-AB.

Objective. Through the observations of dynamic changes of eNOSmRNA and iNOSmRNA in arterial endothelial cells of systematic circulation and pulmonary circulation under simulated weightlessness, to collect some data for studies of the adaptive mechanisms of local regulation in arterial systems. Method. Wistar rats were -30 degrees tail suspended to simulate the effects of weightlessness. The rats were randomly divided into three groups: control group (CON), 7-day tail suspension group (TS7) and 14-day tail suspension group (TS14). Changes of NOSmRNA expresses in endothelial cells of the thoracic aortae and pulmonary arteries were observed with in situ hybridization technique. Result. The eNOSmRNA and iNOSmRNA of thoracic aortic and pulmonary arterial endothelial cells in TS7 rats increased very significantly. The eNOSmRNA of thoracic aortic endothelial cells from TS14 rats returned to control level, but remained very significantly increased in pulmonary arteries. The iNOSmRNA in pulmonary arterial endothelial cells from TS14 rats decreased very significantly, but that in thoracic aortae returned to the control level. Conclusion. The responses of eNOSmRNA and iNOSmRNA in arterial endothelial cells of systematic circulation to tail suspension were similar, but they were different in pulmonary arterial endothelial cells, which might be due to the difference in the peak course of the shift of fluid from lower body entering the pulmonary or systematic circulation during initial period of simulated weightlessness. It could be a kind of important sign of depressed local regulative function under simulated weightlessness and might contribute to orthostatic intolerance after simulated weightlessness.

To clarify the effects of simulated microgravity on the local regulating function of the pulmonary circulation.Rat tail-suspension (TS) was used as the animal model to simulate the effects of microgravity. The changes in responses of pulmonary artery to several vasoactive agents were determined by using in vitro vessel rings perfusion technique.As for the endothelium-intact vessel rings from TS group compared with those from the control (C) group, the contractile responses of pulmonary artery to potassium chloride (KCl, 10 ~ 70 mmol/L) did not change obviously after 7 d tail-suspension, which were markedly diminished as to phenylephrine (PE, 10(-9) ~ 10(-5) mol/L). The vasodilatory responses to acetylcholine (ACh, 10(-9) ~ 10(-5) mol/L) were markedly enhanced, which did not change obviously as to captopril (Cap, 10(-5) ~ 3 x 10(-3) mol/L). The vasoreactivity of endothelium-removed pulmonary artery rings to all vasoactive agents did not change after 7 d tail-suspension as compared with those from control rats.The release of nitric oxide (NO) by rat pulmonary arterial endothelium was enhanced after 7 d tail-suspension. The vasodilatory function of pulmonary artery was enhanced.

The effects of Zn2+ on GABAA-receptor mediated responses in acutely isolated rat sacral dorsal commissural nucleus (SDCN) were studied using nystatin-perforated whole cell recording techniques. The results demonstrated that (1) GABA induced inward currents through activation of GABAA-receptor at a holding potential of -40 mV; (2) GABAA-receptor mediated responses were suppressed by Zn2+ in a reversible and voltage-independent manner; and (3) in the presence of Zn2+, the concentration-response curve of GABA-induced responses was shifted to the right in a parallel manner. The results suggest that Zn2+ allosterically depresses GABAA-receptor mediated currents.

Using nystatin-perforated whole-cell recording configuration, the modulatory effect of serotonin (5-hydroxytryptamine, 5-HT) on taurine (Tau)-activated current (ITau) was investigated in neurons dissociated from the rat sacral dorsal commissural nucleus (SDCN). The results are as follows: (1) Tau acted on strychnine-sensitive glycine (Gly) receptors and elicited inward currents at a holding potential (VH) of -40 mV in SDCN neurons; (2)in a range of 0.01 to 100 mumol/L, 5-HT enhanced ITau in a concentration-dependent manner; (3) both the reversal potential of Tau and the binding affinity of Tau to Gly receptor were not affected by 5-HT; (4) when the neurons were loaded with 3 mumol/L chelerythrine, application of 1 mumol/L 5-HT failed to enhance ITau. The above results thus indicate that intracellular PKC pathway is at least partially involved in the enhancement of ITau by 5-HT. In accordance with our previous study, it is suggested that 5-HT may play an important antinociceptive function in SDCN through enhanced Gly and Tau inhibitory effects.

The electrophysiological and pharmacological properties of GABA- and glycine (Gly)-induced responses were investigated in neurons acutely dissociated from the rat sacral dorsal commissural nucleus (SDCN) using the nystatin perforated patch recording configuration under voltage-clamp conditions. At a holding potential of -40 mV, the currents evoked by GABA and Gly increased in a sigmoidal fashion with increasing agonist concentration. The reversal potentials of I(GABA)and I(Gly) were close to the Cl- equilibrium potential. Bicuculline (BIC) and strychnine (STR) suppressed I(GABA) and I(Gly) in a concentration-dependent manner, although they have different affinities for GABA and Gly. 5-HT potentiated both I(GABA) and I(Gly) via intracellular protein kinase C on the same neurons. The results indicated that the acutely dissociated SDCN neurons responded to both exogenous GABA and Gly, which activated GABA(A) and STR-sensitive Gly receptors, respectively, and 5-HT may produce spinal antinociception through postsynaptic potentiation of I(GABA) and I(Gly) when they are coreleased; GABA and Gly may act as cotransmitters implicated in the control of spinal nociceptive signal processing in the mammalian spinal cord.

The effect of N-methyl-D-aspartate (NMDA) on the glycine (Gly) response was examined in neurons acutely dissociated from the rat sacral dorsal commissural nucleus (SDCN) using the nystatin-perforated patch-recording configuration under voltage-clamp conditions. The application of 100 microM NMDA to SDCN neurons reversibly potentiated Gly-activated Cl- currents (IGly) without affecting the Gly binding affinity and the reversal potential of IGly. A selective NMDA receptor antagonist, APV (100 microM), blocked the NMDA-induced potentiation of IGly, whereas 50 microM CNQX, a non-NMDA receptor antagonist, did not. The potentiation effect was reduced when NMDA was applied in a Ca2+-free extracellular solution or in the presence of BAPTA AM, and was independent of the activation of voltage-dependent Ca2+ channels. Pretreatment with KN-62, a selective Ca2+-calmodulin-dependent protein kinase II (CaMKII) inhibitor, abolished the NMDA action. Inhibition of calcineurin (CaN) further enhanced the NMDA-induced potentiation of IGly. In addition, the GABAA receptor-mediated currents were suppressed by NMDA receptor activation in the SDCN neurons. The present results show that Ca2+ entry through NMDA receptors modulates the Gly receptor function via coactivation of CaMKII and CaN in the rat SDCN neurons. This interaction may represent one of the important regulatory mechanisms of spinal nociception. The results also suggest that GABAA and Gly receptors may be subject to different intracellular modulatory pathways.

The localization of Barrington's nucleus in the dorsolateral pons of the rabbit and its projections to the sacral spinal cord were examined by using retrograde and anterograde labeling methods combined with immunohistochemistry. After injection of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) or a fluorescence tracer, tetramethylrhodamine-dextran amine (TMR), into the sacral spinal cord segments, a cluster of neurons labeled with WGA-HRP or TMR were seen in the pontine dorsolateral tegmentum. To identify whether the retrogradely labeled neurons were situated within the locus coeruleus, the sections containing TMR-labeled neurons through the pons were incubated with anti-tyrosine hydroxylase (TH) antibody and observed under epifluorescence microscope. It was shown that the cluster of TMR-labeled neurons in the dorsolateral tegmentum were surrounded by TH-positive neurons, but they were negatively immunostained with TH-like immunoreactivity. In anterograde experiment, injection of WGA-HRP into the dorsolateral tegmentum resulted in many anterogradely labeled nerve fibers and terminals in the sacral spinal cord, including the sacral parasympathetic nucleus. The present results suggest that the cluster of neurons in the dorsolateral tegmentum of the rabbit may correspond to Barrington's nucleus revealed in the rat and cat, and thus may be involved in micturtion reflex of the rabbit.

Sixty cases with hyperlipoproteinemia (30 cases each group) were observed. The total effective rate of the treated group with Yinchen Wuling Powder was 93.3%. And that of the control group with Gynostemma pentophyllum capsule was 86.7%. The result revealed that significant difference existed between the above-mentioned two groups (P0.01). According to the animal experiment, on both prevention and treatment, this recipe could inhibit the increase of the hyperlipemia model rat's serum TCh, TG, LDL-C and the ratio of LDL-C/HDL-C (P0.01). Besides, this recipe had the effect of marked antioxidation. It could reduce the level of peroxidative lipids, and strengthen the glutathion peroxidase activities.

To observe the effect of diacetylamethystoidin A (6 alpha, 13 beta-diacetyl-11, 15-dioxo-19-hydroxyl-kaurene, DAA-A) on myocardial ischemia reperfusion injury.Working heart mode was induced in isolated rat heart subjected to a 40-min ceasing perfusion followed by a 25-min reperfusion.DAA-A 0.13, 0.25, 0.50 mmol.L-1 reduced the incidence of ventricular fibrillation (1, 1, 0 vs 4 in Vehicle and 5 in Control, respectively), increased the coronary flow (mL.min-1, 1.8 +/- 0.9, 1.9 +/- 0.8, 1.7 +/- 0.6 vs 1.0 +/- 0.3 in Vehicle and 0.9 +/- 0.5 in Control as reperfusion time 5 min, respectively), improved the contractile function of heart, decreased the release of lactic dehydrogenase (LDH) and malondialdehyde (MDA). DAA-A 0.25 mmol.L-1 reduced the injury of myocardial cell ultrastructure.DAA-A has cardioprotective effect through diminishing cellular lipid peroxidation induced by oxygen free radicals.

Local skin blood flow (LSBF) using the Walker's deep burn rat model was studied on the first three postburn days using the carbon-14 iodoantipyrine ([ 14 C]IAP) perfusion method. The radioactive [ I4 C]IAP (12.5 μCi) was infused through the femoral vein over a period of 30 seconds and the blood samples were collected by a free flow from the femoral artery at 5-s intervals to evaluate the concentration of the isotope, in the blood. At the conclusion of the infusion, the rats were guillotined and biopsies were obtained from the burned skin, unburned skin from burned rats and skin from sham control rats to assay the isotope in the skin. The LSBF was calculated from the skin tissue and plasma radioactivity data using Jay's equation. The results showed significant decreases of the skin blood flow in the deep burn wound with 4.05 ± 1.16, 5.31 ± 1.32 and 4.77 ± 2.48 ml/100 g/min as compared to the LSBF of unburned skin 10.27 ± 1.49, 12.39 ± 2.05, 14.79 ± 1.85 ml/100 g/min on postburn days 1, 2 and 3 (P < 0.05). The blood flow of the control group skin was 11.5 ± 1.97 ml/100 g/min (P < 0.05). There were also significant differences of LSBF among burn wounds on postburn days 1, 2 and 3 (P < 0.05). Pathological study of the deep burn wound showed that more of the blood flow was in the subcutaneous adjacent areolar tissue, than in the deep reticular dermis, and only a little occurred in the upper reticular dermis occasionally. These results provide a reproducible model to study burn depth by determining LSBF in a deep burn wound.

We have studied the ultrastructure of gap junction of rat atrial myocytes of primary culture in situ embedded by ultramicrotomy. We observed a kind of gap junction-associated vesicles (GJAV), a kind of cluster of particles which are surrounded by plasma membrane, and a concatenate GJAV complexes (CGJAVC) in some big clusters. We found that both of GJAV and CGJAVC are very near the plasma membrane at the intercellular space, and at the same time they are usually adjacent the assembled GJ. So we infered that they are the pre-body or midproduct of the assembled GJ probably. This article analysed these observes and probed into the process about how to assemble the gap junction.

In order to investigate the distribution and excretion of sterigmatocystin, a carcinogenic mycotoxin, radioactively labelled compound was studied in rats. The highest concentration of radioactivity in serum appeared 3 h after administration of 0.5 microCi/g bw. The half-lives of distribution and excretion were 0.51 h and 43.9 h, respectively. The radioactivity was concentrated mainly in liver, stomach, kidney, duodenum and lung and to a lesser extent in fat, muscle, testis, rectum and bone. By 48 h, 56.4% had been excreted in faeces and 20.1% in urine. Biliary excretion may be the major route of excretion of sterigmatocystin.

An isolated working rat heart underwent 40 min of normothermic ceasing perfusion and 25 min of reperfusion. Superoxide dismutase (SOD) or/and mannitol were added to the perfusate 15 min before ceasing perfusion and 15 min after reperfusion. The results indicate that SOD (37,000 IU/L) improved significantly the contractile function of heart and increased the aortic output and coronary flow. Mannitol 0.02 mol/L provided additional benefit. The rat myocardial cells were cultured in the medium for 3 h with hypoxia followed by 2 h of reoxygenation. The content of lactic dehydrogenase (LDH) in the medium was increased and the degree of fluorescence polarization of myocardial cell membrane was raised. SOD was effective in preventing LDH release and decreasing the degree of fluorescence polarization. These results clearly demonstrate that ischemic reperfusion are capable of causing significant myocardial injury, which can be reduced or prevented by administration of oxygen free radical scavenger SOD.