Objective To evaluate the effects of low tidal-volume ventilation on blood gases and respiratory mechanics during open heart surgery in children with acyanotic congenital heart disease. Methods Forty NYHA class Ⅰ-Ⅱ patients with atrial or ventricular septal defect aged 3-6 yrs weighing 12-18 kg undergoing open heart surgery were randomly divided into 2 groups according to the tidal volume of mechanical ventilation: group A low tidal volume(V_r=7ml?kg~(-1),n=20) and group B conventional tidal volume(V_T=9 ml?kg~(-1), n=20). The respiratory rate(RR) was 21-23 bpm, I: E ratio 1:2 and FiO_2 100% in both groups. The patients were premedicated with intramuscular morphine 0.1 mg?kg~(-1) and scopolamine 0.01 mg?kg~(-1). Anesthesia was induced with midazolam 0.1 mg?kg~(-1), fentanyl 10 ?g?kg~(-1) and vecuronium 0.1 mg?kg~(-1) and maintained with infusion of fentanyl 4 ?g?kg~(-1)?h~(-1) and vecuronium 80 ?g?kg?h~(-1) supplemented with isoflurane inhalation(

ObjectiveTo investigate the gene expression of Chk1 gene in cerebrum after brain ischemia-reperfusion,trying to provide evidence to elucidatethe molecular mechanism of brain injury. MethodsEighty-five male Wistar rats were divided into 3 groups. Group Ⅰ served as normal control. In group Ⅱ (non-ischemia group) animals underwent the whole experimental procedures except the occlusion of the bilateral vertebro-arteries and common carotid arteries. In group Ⅲ(ischemiareperfusion group) animals were further divided into 3 subgroups according to the duration of ischemia: 10min, 30min and 60min. Each subgroup was again further divided based on the duration of reperfusion: 30min, 2h and 6h. The cerebrum was immediately removed from rats after complete brain ischemiareperfusion. The RNA was isolated and the reverse-transcription-polymerase chain reaction (RT-PCR) was carried out . The cDNA was analyzed by automatic system and the parameters were assessed to define the status of Chk1 mRNA expression in different ischemia and reperfusion groups. ResultsThe quantity of Chk1 mRNA expression in the cerebral cortex of normal adult rat was about half of the glyceraldehyde-3-phosphatedehydrogenase. When reperfused for 30min, 2h or 6h following 10min, 30 min cerebral ischemia and reperfused for 30min or 2h following 60 min cerebral ischemia, the expression of Chk1 mRNA was not significantly different from that in non-ischemia group. Only reperfused for 6h following 60 min cerebral ischemia, Chk1 mRNA expression decreased significantly. ConclusionsThe results indicate that Chk1 gene might be involved in molecular mechanism of cerebrum damage during complete global brain ischemia- reperfusion.

Objective To explore the effect of hemorrhage on cell apoptosis in the hippocampal CA1 region of rats under controlled hypotension (CH).Methods A total of 36 Sprague Dawley rats were randomly divided into 2 groups: Group C (with no CH) and Group H (with CH).According to different ratios of blood loss to total blood volume, Group C and Group H were redivided into 6 subgroups (6 in each group):C_1,H_1(10%);C_2,H_2(20%);C_3,H_3 (30%). Induced by so-dium nitroprusside and esmolol, the mean aterial pressure in Group H was decreased to 50～55 mmHg and kept for 10 minutes, and then blood loss was started, keeping the pump speed. Without CH, the same style of hemorrhage was performed in Group C. The aterial pressure was increased 60 minutes later after the hemorrhage.Expression of bcl-2 and caspase-3 protein was detected by immunohistochemical method, and apoptosis cells were detected by TUNEL staining. Results The average optical density of bcl-2 and caspase-3 was higher in Group H_3 than that in Group C_3(P＜0.05). There were more apoptosis cells examined by TUNEL in Group H_3 than in Group C_3(P＜0.05).Conclusion Thirty percent blood loss under controlled hypotension can induce cell apoptosis in hippocampal CA1 region in rats.

Objective　To introduce the research trence of the medchnisims of ischemia/reperfusion(I/R) injury in transplanted liver(TL). Methods　Making a literature summarization based on papers review.Results　The main mechnisms of I/R injury in TL as the followings: (1) Production of various cytokines resulted from endothelial cell injury with activation of kupffer cells, which can result in TL injury and induce systemic inflammation syndrom. (2) White blood cells and platelets adhere to the liver sinusoid (LS), which can cause TL injury and obstruct the LS causing “no reperfusion" of TL. (3) Alteration of pH in the cells of TL. After recovery of normal metabolism of the reperfused TL, alteration of pH in the TL can cause damage to TL cells, and cause edema of mitochrondria resulting in decresing of TL function. (4) Reoxygenation injury mainly caused by activated oxygen relsased by white blood cell. Conclusions　I/R injury of TL is caused by combination of muttiple foctors. Improving the activity of hepatocytes and endothelial cells, imhibiting the activation of kupffer cells, decreasing the production of activated oxygen and TNF are the key points in preventing I/R injury of TL.

Objective:To observe the protective effects of sodium ferulate (SF) on rabbit myocardial ischemia reperfusion injury. Method: Sixteen rabbits were divided randomly into three groups: group A undergoing all procedures except for ischemia-reperfusion and treatment, group B given the routine treatment after ischemia-reperfusion, and group C receiving the routine treatment combined with the intravenous infusion of SF 40mg?kg~(-1) after ischemiareperfusion. Result: Group C showed a significant reduction in myocardial MDA content and plasma ET level (P

Objective To investigate the effects of low tidal volume ventilation on pulmonary and cardiac function before and after mitral valve replacement. Methods Thirty patients with mitral valve diseases were randomly divided into traditional tidal volume ventilation (groupⅠ), low tidal volume ventilation with conventional respiratory rate (group Ⅱ), and low tidal volume ventilation with high respiratory rate (group Ⅲ). Mean arterial pressure (MAP), cardiac output(CO), cardiac index(CI), mean pulmonary arterial pressure (MPAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), systemic vascular resistance index (SVRI), and pulmonary vascular resistance index (PVRI) were monitored. Arterial oxygen tension (PaO_2), carbon dioxide tension (PaCO_2), oxygen saturation index(PaO_2/FiO_2), alveolar-arterial PO_2 gradient (PA-aO_2), and Q_S/Q_T were measured. Results Before CPB, CO in group Ⅰ was significantly lower than that in group Ⅲ (P

Objective To investigate the gene expression of Chk1 gene in cerebrum after brain ischemia-reperfusion, trying to provide evidence to elucidate the molecular mechanism of brain injury.Methods Eighty-five male Wistar rats were divided into 3 groups.Group Ⅰ served as normal control.In group Ⅱ (non-ischemia group) animals underwent the whole experimental procedures except the occlusion of the bilateral vertebro-arteries and common carotid arteries.In group Ⅲ (ischemia-reperfusion group) animals were further divided into 3 subgroups according to the duration of ischemia: 10min, 30min and 60min.Each subgroup was again further divided based on the duration of reperfusion: 30min,2h and 6h.The cerebrum was immediately removed from rats after complete brain ischemia-reperfusion. The RNA was isolated and the reverse-transcription-polymerase chain reaction (RT-PCR) was carried out .The cDNA was analyzed by automatic system and the parameters were assessed to define the status of Chk1 mRNA expression in different ischemia and reperfusion groups.Results The quantity of Chk1 mRNA expression in the cerebral cortex of normal adult rat was about half of the glyceraldehyde-3-phosphate-dehydrogenase. When reperfused for 30min, 2h or 6h following 10min, 30 min cerebral ischemia and reperfused for 30min or 2h following 60 min cerebral ischemia, the expression of Chk1 mRNA was not significantly different from that in non-ischemia group.Only reperfused for 6h following 60 min cerebral ischemia, Chk1 mRNA expression decreased significantly.Conclusions The results indicate that Chk1 gene might be involved in molecular mechanism of cerebrum damage during complete global brain ischemia-reperfusion.

Objective To design a model of the content structure of websites of large scale modern hospitals which is in keeping with Chinas realities. Methods The First Hospital affiliated to the Fourth Military Medical University was selected as a representative of large scale modern Chinese hospitals and on the spot investigations were carried out. Investigations were also made via the Internet on ten famous domestic websites of hospitals affiliated to medical universities and the first ten American hospital websites as chosen by the American News Website in 2000. The opinions of 20 experts were collected and analyzed by means of expert consultation. Results The basic features of the websites of large scale modern hospitals were summed up and a content structure of websites of large scale modern hospitals, both advanced and in keeping with Chinas realities, was designed. Conclusion There is some regularity to follow in the website contents of large scale modern hospitals and the website contents of hospitals in China are turning from the stage of information to the stage of interaction.

Objective To study the effects of selective mild cerebral hypothermia on endogenous anti-injury mechanism in brain tissue after cardiac arrest and resuscitation. Methods Fifteen healthy mongrel dogs of both sexes were anesthetized and intubated. Cardiac arrest was induced by potassium cardioplegia and cross-clamping of aorta, vena cava superior and inferior and azygos vein and maintained for 18min. The animals were randomly divided into 3 groups: group A, in which no cardiac arrest was induced, served as control ( n = 4) ; in group B animals received routine cerebral resuscitation ( n = 5) ; in group C animals received selective mild cerebral hypothermia (34℃?0.5℃) and routine cerebral resuscitation ( n = 6) . After successful resuscitation, the animals were observed for 8 hours. At the end of the experiment the parietal cerebral cortex was removed for determination of MDA, GSH, LA, FFA content and activities of SOD(T-SOD, Mn-SOD, Cu-ZnSOD) and GSH-Px. Results FFA and LA content of brain tissue in group B was significantly higher than those in group A (P

Objective To investigate the therapeutic effects of rhein on experimental diabetic nephropathy in rats. Methods Rat model of diabetic mellitus was established by interperitoneal injection of streptozotocin (50 mg/kg) . Renal damages and changes of endothelin (ET) in urine and renal tissues were observed at 12 weeks after the induction of diabetic mellitus and after treatment with rhein (70 mg/kg). Results Compared with the normal rats, at 12 weeks after hyperglycemia, diabetic rats had decreased renal weight/body weight(RW/BW), significantly increased mean glomerular plane area (MGPA), mean glomerular volume (MGV), creatinine clearance rate (Ccr), blood urea nitrogen (BUN), and 24 hour urinary protein excretion (UPE) ( P