Objective To investigate the effects of different temperature seawater immersion on the hemodynamic of traumato-hemorrhagic shock rats. Methods 40 male traumato-hemorrhagic shock rats were utilized in this experiment. The hemodynamic parameters were determined in rats at preshock, shock, 10min, 30min, 1h, 3h, 5h after immersion in 15℃, 21℃ and 31℃ seawater respectively. Results The hemodynamic parameters of rats immersed in 21℃ seawater were markedly decreased compared with those of land control group. The hemodynamic parameters of rats immersed in 15℃ seawater rapidly decreased as compared with other groups. After 1 hour immersed in 15℃ seawater, the MAP, HR, ?dpdtmax of traumato-hemorrhagic shock rats were significantly decreased (P

Objective To study the protective effect of the hypothermic brain-protection apparatus on hemorrhagic shock rabbits. Methods Applying the modified Wigger's shock animal model, we observed the effects of a self-developed brain-protecting apparatus on the survival time and vital signs of rabbits. Results Hypothermic brain protection could considerably reduce 60% lipid hyperoxide in brain tissues as compared with that in the control group. It could also decrease heart rate and respiration and hence reduce tissue oxygen consumption. Conclusion Hypothermic brain protection can attenuate the brain lesion and obviously prolong the survival time of hemorrhagic shock animals.

The changes of hepatocyte and skeletal muscle membrane potential.the membrane fluidity of microsomes,microviscosity.and the order coefficient of the arrangement of membrane lipid molecules were determined in rats after their cecum was ligated and punctured to induce septic shock.Lipid peroxides of plasma and the liver,phospholipase A2 and salivary acid were determined as well.It was found that both in the first 10 hours and the next 20 hours of septic shock,the resting membrane potential of hepatocytes and skeletal muscles was significantly suppressed as compared with that of the sham-operated rats.The membrane potential of hepatocytes was suppressed prior to the decrease of blood pressure and much earlier and much more severe than that of skelatal muscles.Lipid peroxides of the liver were increased by 1.6 fold(P

Objective To investigate the effect of cellular membrane phospholipids on CD14 protein expression of macrophage stimulated by LPS. Methods Changes of CD14 protein expression and CD14 mRNA of macrophages stimulated by LPS in vitro were determined by Western blotting and RT PCR. Effects of membrane phospholipids on CD14 protein expression were also detected. Results After stimulation by LPS, CD14 expression increased at 1 h, reached the peak value at 5 h and decreased to the normal level at 8 h but CD14 mRNA reached the peak value at 3 h and decreased at 5 h. The levels of phospholipids and membrane fluidity decreased at 5 h but CD14 protein expression increased after LPS stimulation. After pretreatment with liposomes, membrane phospholipid microenvironment improved and CD14 protein expression decreased. Conclusion LPS can up regulate CD14 protein expression, which might be regulated at least at the transcriptional level of the CD14 gene. Changes of membrane phospholipid microenvironment may be an important reason for the up regulation of CD14 induced by LPS.

This paper is to report the determination of the skeletal muscle cellular membrane potential (SMCMP) in vivo with the technique of "Semi-floating"glass microelectrode. The changes of SMCMP and the distribution of extra- and intracellular electrolytes and water in different phases of irreversible hemo-rrhagic shock in rabbits were studied systematically.It was found that SMCMP decreased significantly and immediately as soon as hypotension occurred, which means that the functions of the cellular membrane begin to deteriorate in the early stage of shock; SMCMP continued to decrease when the shock was progressing, which reflects that besides the failure of the cellular membrane function, there is also the degradation of the functions of the cell proper; the leakage of the intracellular potassium across the cellular membrane and the retention of the intracellular sodium and water occurred three hours after the onset of the shock, which indicates that the inability of cells to regulate their volume.

AIM: To appropriately modify the defects of active tourniquets in order to act as various tourniquet attachments in Chinese Army.METHODS: This attachment is classified into individual-solider end and searching-rescue end, and data at both ends are collected and transmitted by using wireless data transmission module. Individual-solider end is composed of timing alarm circuit, bit display tube and GPS module, etc. and the data are processed by using single chip of wireless data transmission module. Searching-rescue end adopts the same data transmission module as individual-solider end, and port connects to computer in order to realize two-dimensional data delivery and communication to individual-solider end by using computer-controlled software, i.e. battleground immediate pursuit rescue system.RESULTS: As various tourniquet attachments, individual-solider end is characterized by timing alarm function in the phase of installing tourniquet. Necessarily, we may start searching-rescue function, and the matching with searching-rescue end may realize personal identification and localization of wounded soldiers.CONCLUSION: As a common tourniquet attachment, it is provided with installing alarm, personal identification and localization of wounded soldiers; however, its function is still thin. It brings a lot of evidences for further improvement through installing a physiological probe at individual-solider end to collect physiological data and distantly monitor real-time vital signs of wounded soldiers.

The multifunctional member for improvement of the active tourniquet adopts data transmission module and GPS receiver, which can be a accessory of the tourniquet. The member has such functions as time alarm, identification and locating of the casualty.

OBJECTIVE: To elucidate the effects of lipopolysaccharide (LPS), phospholipase A(2) (PLA(2)) and oxygen free radical (OFR) on proton transmembrane translocation and H(+)-ATPase. METHODS: The normal rats were sacrificed for preparetion liver mitochondria and submitochondrial particles for experiments in vitro. Submitochondrial particles were incubated with LPS (100 &mgr;g/mL), PLA(2) (10 u/mL) and FeSO(4)/Vit C (30/90 &mgr;mol/L) at 30 degrees C for 30 min. The proton translocation of submitochondrial particles (SMPs) were assayed with the fluorescent probe ACMA (9-amino-6-chloro-2 methoxya cridine). The mitochondria were incubated with different concentration of LPS, PLA(2) and FeSO(4)/Vit C. The H(+)-ATPase, PLA(2) and malondialdehyde (MDA) were assayed. RESULTS: The fluorescent quenching of ACMA and H(+)-ATPase activity in high dose was significantly decreased after treatment with LPS, PLA(2), FeSO(4)/Vit C (P<0.05). The mitochondrial PLA(2) activity and MDA content were significantly increased after treatment with LPS (P<0.01). CONCLUSIONS: FeSO(4)/Vit C in low dose causes increases H(+)-ATPase activity. LPS, PLA(2), FeSO(4)/Vit C might be the important factors changing H(+)-ATPase and proton translocation across the membrane.