This paper shows the influence of naloxone injected into the lateral ventricle of brain on the SMAO (superior mesenteric artery occlusion) shock in rabbits as well as the electric activity of sympathetic nerve in the course of shock.This experiment in 40 rabbits proved that the electric activity of the sympathetic nerve in the naloxone group was more enhanced and the duration was much longer than the control group after loosing the occuiation. From these it is clear that the central activity of the sympathetic nerve is related to the reversal effect of naloxone on shock. However the blood pressure in the group of naloxone could be maintained at a higher level and much longer after the electric activity of the sympathetic nerve had decreased. As a result, it may be inferred that there are still other factors contributing to the blood pressure, beside the regulation by the tonicity of sympathetic nerve. The significant extension of survival time in the naloxone group fully explained that naloxone played an important role in revering SMAO shock. Therefore naloxone is valuable in clinical treatment.

Using the average technique of the electronic computer, we recorded the somatosensory evoked Potentials (SEPs) by electrical stimulation of median nerve (MN) and posterior tibial nerve (PTN) in twenty-three normal subjects and twenty-five diabetic patients. The peak latencies of SEPs components were prolonged, and the afferent conduction velocities of MN and PTN were reduced in most patients. In some patients, the central conduction time (N13-N20 and P40-N80 conduction time) was prolonged. Besides, there was a significant change in the shape of triphasal potentials recorded from Erb's point.and popliteal fossa. These results suggest: there not only was abnormality of conductive function of peripheralnerves, but also, the conductive function of central nervous system might be involved in diabetes mellitus.

The effect of droxicainide was investigated in a rabbit model of myocardial ischemia and reperfusion. The rabbits were randomized to either a saline-treated control group (n=18) or a droxieainide-treated group (n=11). In the control group, the incidence of ventricular fibrillation after coronary ligation was 14/18 (77.7%) and nine died (64.3%). Ventricular fibrillation occurred in eight (72.7%) droxieainide treated rabbits, but all reverted spontaneously (P

24hr after partial hepatectomy, the isolated remnant liver of rat was perfused to study the effects of several factors on the ability of amino acid intake. The results were as follows: (1). Twenty-four hours after operation the hepatic uptakes of amino acid increased in the hepatectomized groups. The ability of enhanced amino acid uptake by remnant liver depended on hepatic protein synthesis. In a certain range of hepatectomy there was a positive correlation between the amounts of liver which had been cut off and the amounts of amino acid uptake by remnant liver. (2). The addition of insulin alone to the perfusate could stimulate amino acid uptakes by remnant liver and the addition of glucagon alone had no effect. But, when insulin was added to the perfusate in combination with glucagon the hepatic uptake of amino acid was much higher. (3). The extract from regenerating rat liver rather than that from normal adult rat liver may contain certain factor(s) which can stimulate amino acid uptakes by remnant liver.

Fever model induced by endogenous pyrogen was used to study the effect of needling "Bai hui" point on fever. 126 rabbits served as experimental animal. The present experiment was divided into three parts: Ⅰ. Ⅱ. (injection of pyrogen)and Ⅲ. (no injection), and each part was redivided into experimental (needling "Bai hui" point or "non-channel point) and control (no needling) groups.The findings were: (1) In febrile rabbits induced by endogenous pyrogen, needling "Bai hui" points had significant febrifugal effect, i.e, inhibiting the rise of body temperature, increasing the amplitude of defervescence and accelerating the febrifugal rate. (2) In febrile rabbits, needling "non-channel points" had no marked febrifugal effect, i. e. showing the rise of body temperature, after that, accelerating the febrifugal rate. (3) On body temperature of healthy rabbits, needling "Bai hui" points hnd no hignificant effect.

Xinmailong injection solution was invented at 1988 by prof. Li Shunan in Dali medical college. It was made from the material which has high biological activeness to the cardiac and vascular system. During the experimental shock caused by excessive loss of blood in monkey and dog, it was found by ECG that the T-wave of anterion lead on left chest elevated and became high and sharp after acute blood loss. Arterial blood pressure dropped to 8-5.3 kPa for dog and 8-5.3-2.7 kPa for monkey, changes of T-wave all recovered to near normal level after xinmailong solution was injected intravenously (0.05-0.2 mL/kg). These Results implied that xinmailong might improve the ischemia of myocardium induced by hemorrhagic shock.

To study the underlying mechanism of vasovasotomy infertility, we set up the rabbit model and observed the levels of testosterone, IL-1 activity and TNFα, which represent the functions of monocytes and macrophages on the animal model of vasovasostomy, and probed into the in vitro effect of IL-1β on the production of testosterone by Leydig cells. Rabbit model was set up and divided into vasovasostomy fertility group (VFG) and vasovasostomy infertility group (VIG), and set up peer group of Vasectomy group (VG) and sham operation group (SOG) as controls. The results were as follows: The sperm density and total number is highest in SOG, with that in VFG markedly lower than that in SOG, but significantly higher than that in VIG. 　　1. VFG showed significant higher level of testosterone (Ts) than SOG, VG and VIG; Ts of VIG was significantly lower than SOG or VFG. In the vasovasostomy groups, sperm density is positively correlated to the level of testosterone. 　　2. The level of serum cortisol in VIG significantly higher than that in VFG, SOG, and VG. The level of serum cortisol negatively correlated to serum testosterone. 3. Serum estradiol(E2) was similar among all the groups (P＞0.05). E2/T ratio is significantly different among the groups, with that in VIG highest and that in VFG lowest. 4. Serum IL-1 activity in VIG was significantly higher than that in SOG and VFG(P＜0.05). 　　5. Serum TNFα and serum IL-1 activity share similar change, with TNFα in VG significantly higher than that in SOG(P＜0.01), VIG was the highest among the four groups(P＜0.01). Correlation test showed that serum IL-1 activity and TNFα level was negatively correlated to testosterone level; positively correlated to cortisol level and E2/T ratio. 6. Immuno-histo-chemistry of CD68 and TNFα in rabbits with vasovasostomy showed that in the testis tissue of SOG, interstitial tissue was normal with no filtration of inflammation cells including CD68 cells. In VFG and VIG, the tubules with resumed sperm production showed negative staining, and atrophic tubules and their surroundings were expression positive of CD68, with that markedly deeper in VIG than that in VFG. TNFα positive expressed granules was found only in atrophic convolted seminiferous tubules and their surroundings, with that deeper in VIG than that in VFG. 7. Culture Leydig cells were put in the following holes:(1) Control; (2) hCG; (3) IL-1; (4)IL-1 β+hCG; (5) IL-1 β+IL-1Ra; and (6) hCG+IL-1β+IL-1Ra. Determined the levels of testosterone by immuno-radiation technique. (1) IL-1 β showed no obvious effect on the Leydig cultured in vitro, but depressed the induction of Leydig cells by hCG to synthesize testosterone; (2) IL-1Ra blocked the depression of IL-1β Leydig cells' bio-synthesis of testosterone induced by hCG. In summary, one of the obvious changes in animals with vasovasotomy is low density of sperms, which is related to the lowering of testosterone. Low level of testosterone is related to the activation of monocytes and macrophages to produce IL-1 and TNFα, which negatively regulate the production of testosterone.

AIM:To investigate effect of recombinant human thrombopoietin on exsanguine thrombocytopenia mice. METHODS:Normal peripheral platelet counts were performed on sample obtained from the tail vein of purebred Babl/c mice including experimental and control groups before experimentation. rhTPO was injected into the mice by intraperitoneal injection once a day for 7 days. On the seventh and the fourteenth day, the mice were phlebotomized from the supra-obitalis vein in order to make exsanguine thrombocytopenia animal model. At the same time, we observed the biological activity of recombinant human thrombopoietin in vivo and the mice's death rate. RESULTS: On the seventh day and the fourteenth day, platelet counts of mice treated by rhTPO were higher than those by PBS (P＜0.05). Moreover the platelet counts of mice in experimental group of rhTPO showed increasing tendency following experimental days. In addition, death happened in two groups after those mice were phlebotomized from the supra-obitalis vein, but the death rate in negative control group was evidently higher than that in experimental group (P＜0.05). CONCLUSION:rhTPO had obvious biological activity in increasing platelet production, which resulted in the drop in thrombocytopenia mice's death rate.

The primary action of corticotropin releasing hormone (CRH) is stimulation of the synthesis and release of adrenocorticotropic hormone and β-endorphin from the pituitary in response to stress. In addition, a number of studies indicate that CRH exerts other physiological actions within the central nervous system which are independent of the pituitary. These include increased body temperature and thermogenesis. However, the intracellular mechanism responsible for pyrogenic action of CRH is still unclear. The purpose of these studies was to determine whether or not cAMP was involved in the pyrogenic action of CRH in the rat. Intracerebroventricular (icv) microinjection of CRH (2.5 μg, 5.0 μg, 10 μg) caused increases in colonic temperature and hypothalamus cAMP level in conscious rats. The pyrogenic effects of CRH were abolished or markedly inhibited by prior injection (icv) of an adenylate cyclase inhibitor, 2，，3，-dideoxyadenosine (DDA, 30 μg) or an inhibitor of cAMP-dependent protein kinase, adenosine-3，，5，-(cyclic) monophosphorothionate (Rp-cAMPs, 15 μg). This is the first report demonstrating the pyrogenic effcet of centrally administration of CRH on the rat via the cAMP-mediated protein kinase signal transduction pathway.

The present study was undertaken to investigate the effect of human PMNs on the production of TNF-α by the human peripheral blood mononuclear cells (PBMCs) and to elucidate its tentative mechanism. Human PMNs and PBMCs were isolated from the venous blood of healthy donors by dextran sedimentation and density gradient centrifugation. In the presence of lipopolysaccharide (LPS), PMNs and PBMCs were cocultured at the ratio of 2:1 for 20 h and the concentration of TNF-α in the supernatant was measured by enzyme-linked immunosorbent assay. The binding rate of monocytes with the fluorescein isothiocyanate-labeled LPS (FITC-LPS) and the mean surface fluorescence intensity of monocytes were analyzed by flow cytometry. Results showed that PMNs were capable of inhibiting the TNF-α release from PBMCs (P＜0.05). PMNs suppressed the TNF-α release from PBMCs by 45% on average when PMNs and PBMCs cocultured at the ratio of 2:1. Paraformaldehyde-fixed PMNs still demonstrated the same inhibition (P＜0.05)，which proved that the inhibition was dependent on cell-to-cell contact and suggested that effector molecules responsible for this effect existed on the cell surface of PMNs. In the presence of PMNs, the binding rate of monocytes with the FITC-LPS and the mean surface fluorescence intensity of monocytes were not affected compared with PBMCs alone (P＞0.05). As incubation time was prolonged, the binding of FITC-LPS to monocytes increased (P＜0.05). Thus PMNs did not block the binding of LPS with monocytes. It was concluded that PMNs suppressed the TNF-α release from PBMCs via cell-to-cell interaction. In a cell-contact dependent manner, PMNs might interfere with the signal transduction pathway through which LPS activated PBMCs, thus attenuating the response of PBMCs to LPS and downregulating the TNF-α release.