ObjectiveTo explore the influence of norepinephrine on the prediction of fluid responsiveness by passive leg raising (PLR) during septic shock. MethodsForty-six septic shock patients in intensive care unit of Nanjing Drum Tower Hospital were prospectively observed from September to November 2012. Among which 36 septic shock patients were enrolled with a positive PLR test (defined by an increase in stroke volume index ≥10%). A PLR test was performed at baseline (PLR1). A second PLR test (PLR2) was performed at returning to supine position for 10 min and the dose of norepinephrine was increased to maintain MAP ≥65 mmHg for 20 min. The changes of heart rate(HR),mean arterial pressure(MAP),central venous pressure(CVP),cardiac index(CI),stroke volume index(SVI),index of systemic vascular resistance(SVRI),global end-diastolic volume index(GEDVI),and cardiac function index(CFI) were monitored by transpulmonary thermodilution technique (PiCCO). ResultsPLR1 significantly increased SVI by (20.54±9.63)%,CI by (20.57±9.89)%,MAP by (7.64±5.77)%,and CVP by (25.83±23.39)%. As the dose of norepinephrine increased,SVI was increased by (16.97±9.06)%,CI by (16.78±8.39)%,GEDVI by (9.08±4.47)%,MAP by (28.07±12.48)%,and CVP by (7.86±8.52)%. PLR2 increased SVI by (13.74±8.79)%,CI by (13.79±9.08)%,MAP by (2.93±5.06)%,and CVP by (13.36±14.74)%. The PLR2 and the dose increase of norepinephrine augmented SVI to a significantly lesser extent than the PLR1 performed at baseline (both P<0.05). However,SVI increased by <10% in 6 patients while the baseline PLR was positive in these patients. ConclusionIn septic patients with a positive PLR at baseline,norepinephrine increases cardiac preload and cardiac output and influences the fluid responsiveness.
Objective To review the advancement of heat shock protein 70 (HSP70) vaccine in alimentary canal cancer. Methods Related articles were reviewed. Results HSP70 can integrate with tumor special antigen to form HSP70 polypeptide compound. To activate the special and nonspecial immune response of body, HSP70 can participate in the process of tumor immunity as a “molecular partner”. Conclusion HSP70 has shown alluring perspective in the precaution and treatment of alimentary canal cancer.
Objective To investigate the effects of hypertonic saline (HTS) treatment on the function and susceptibility to sepsis of reticuloendothelial system (RES) in mice with hemorrhagic shock. Methods Forty percent of total blood volume of male Balb/c mice was withdrawn by cardiac puncture. Two hours later, the mice were treated with blood infusion and normal saline (10 ml/kg) or 7.5% NaCl (10 ml/kg).The survival rate of the mice was observed after cecal ligation and puncture (CLP). The phagocytosis function of the RES was measured by carbon clearance rate(α) and carbon amount ingested by the macrophages of liver and spleen. In vitro, the peritoneal phagocyte function in solutions of different osmotic pressor was measured by assaying neutral red amount taken in. Results The survival rate after CLP in HTS treated group was 70%, whereas all the mice in the normal saline group died. At the third hour after hemorrhagic shock, the RES carbon clearance rate(α) and carbon amount ingested by the macrophages of liver in the HTS treated mice were 5.61±0.42 and 0.59±0.19 respectively, significantly higher than those in the normal saline treated mice (4.15±0.62， 0.42±0.16). In vitro, hyperosmolarity below 40 mmol/L had no significant effects on the phagocytosis activity of peritoneal macrophages in mice. Conclusion Treating hemorrhagic shock with HTS can decrease the susceptibility to sepsis and improve the RES phagocytosis function indirectly.
ObjectiveTo investigate the expression of heat shock proteins 90α(HSP90α) in human hepatocellular carcinoma and the relationship between its expression and biologic behavior of tumor and prognosis. MethodsUsing the immunohistochemical SP method, HSP90α expression was detected in liver tissue from 10 normal individuals, 40 patients with hepatocellular carcinoma(HCC) and adjacent noncancerous liver tissues. ResultsThe positive expression rate of HSP90α was 10.0%,52.5%,72.5% in normal liver tissues,adjacent noncancerous liver tissues,hepatocellular carcinous tissues respectively. A significantly higher distribution of HSP90α positive expression in HCC tissues compared with adjacent noncancerous liver tissues and normal liver tissues was obtained （P＜0.05）. The positive expression of HSP90α in HCC was correlated with clinical stage, tumor differentiation, serosal condition and lymph node metastasis （P＜0.05）, but not to tumor number （P＞0.05）. It was also correlated with prognosis of HCC. The mean tumorfree survival of patients with HSP90α negative expression was 38.6 months while that of HSP90α positive expression was 25.5 months （P＜0.05）. ConclusionHSP90α is overexpressed in human hepatocellular carcinoma. HSP90α could be used as an indicator to judge the clinical stage, tumor differentiation, serosal condition, lymph node metastasis and prognosis of HCC.
ObjectiveTo study the effects of aminoguanidine (AG), a selective inhibitor of inducible nitric oxide synthase (iNOS) on the pathological changes of liver tissues and ultrastructural changes of liver cells in rodent model of endotoxic shock. MethodsTwentyfour male Wistar rats were randomly divided into normal control group，lipopolysaccharide (LPS) control group and AG treatment group, each group had 8 rats. Rats were challenged by E.coli LPS to set up the model of endotoxic shock, AG group were treated by aminoguanidine. The pathological and ultrastructural changes of liver tissues and plasma NO contents of three groups were observed and compared. ResultsLight microscopy revealed that many tiny abscesses scattered in liver tissue in LPS group, accompanied by necrosis of liver cells and neutrophils infiltration, while liver injuries of AG group were much slighter than that in LPS group. Electron microscopy revealed that there were dissolved plaques in hepatocyte nuclears, swelling of mitochondria, decreasing in number of mitochondrial ridges, while AG play a protective role to nuclears and mitochondria of hepatocytes. The plasma NO levels of LPS control group were higher than that of normal control group, and plasma NO levels decreased significantly after AG treatment, but still higher than that of normal control group. Conclusion Aminoguanidine selectively inhibits iNOS activity and prevents the overproduction of NO induced by iNOS, thus attenuates the damages of liver structure induced by NO. This method has potential value in clinical application, which deserves more deep research.
In this study, hypertonic saline infusion (experimental group ) and blood transfusion plus normal saline infusion (control group) were used for the treatment of uncontrolled hemorrhagic shock in dogs. The amount of blood loss from injured vessels are compared between two groups. Results: the amount of blood loss from injured vessels in shock stage were 35.2ml in the experimental group and 34.6ml in the control group, which showed no marked difference between two groups(Ｐ＞0.05).The amount of blood loss in resuscitation stage for experimental group was 15.10±1.52ml(early stage) and 14.00±1.37ml(late stage) and for control group was 14.20±1.52ml and 12.90±1.71ml respectively(Ｐ＞0.05).The amount of blood loss in resuscitation stage for both groups is much less than that in shock stage (Ｐlt;0.05).The results showed that infusion of hypertonic saline 30 min after uncontrolled shock is a safe and effective treatment which dose not cause further bleeding from the injured vessels. Clinical observation also confirmed the result.
Electron spin resonance (ESR) spectroscopy and spin trapping agent PBN were applied to measure directly the changes of oxygen free redicals (OFR) in gastric mucosa of rats with portal hypertension (PHT) injured by shockreperfusion, and treated with superoxide dismutase (SOD), radix salviae miltiorrhizae (RSM), with concomitant monitoring activity of SOD and pathology of gastric mucosa. Results showed that the amount of OFR increased markedly in gastric mucosa of PHT rats during the shock-reperfusion. The pathological changes were in accordance with alteration of the amount of OFR and the activity of SOD. Gastric mucosa in PHT was more susceptible to shock-reperfusion insult than normal controls. The anti-oxidant SOD, RSM used at early stage exerted mild gastric mucosal insult through different mechanisms.