The efficacy of intravenous captopril on plasma renin activity (PRA ) and angiotensinⅡ (All ) during isoflurane-induced hypotension were investigated. 24 patients (aged 20-50 years,ASA Ⅰ-Ⅱ )scheduled for elective cerebral surgery were randomly divided into two groups: Group I (isoflurane, n = 12 )and Group J (captopril 0. 15mg/kg plus isoflurane n=12 ). MAP was reduced approximately 30% in all of patients. Angiotensin Ⅱ concentration increased 260% during hypotension in group I, but only a slight reduction in Group Ⅱ. The end-expiratory concentration of isoflurane in Group I were higher than Group I during induced and hypotension period. It is concluded that intravenous captopril can inhibit the increase of PRA and All concentration and less isoflurane required for the deliberated hypotension. Induced-hypotension by the combination of isoflurane with captopril may be advantageous.

Objective To investigate the effects of propofol administered before, with or after lipopolysaccharide (LPS) on the acute lung injury (ALI) induced by IPS in rats. Methods Seventy-six male Wistar rats weighing 250-290 g were randomly divided into 5 groups : (A) control group received only normal saline (n = 8); (B) LPS group received LPS 8 mg?kg-1 iv (n = 17); (C, D, E) propofol group-Ⅰ,Ⅱ, Ⅲreceived propofol (a bolus of 5 mg?kg-1 followed by infusion at 10 mg?kg-1?h-1) 1 h before (group C, propofol - Ⅰ , n = 17) , simultaneously with (group D, propofol-Ⅱ, n=17) or 1h after LPS administration (group E, propofol-Ⅲ , n = 17) . The animals were observed for 5h after LPS administration for MAP monitoring and mortality and then killed. The lungs were immediately removed for determination of expressions of nitrotyrosine protein and iNOS mRNA, wet / dry lung weight ratio and pulmonary permeability index (PPI). The lungs were also lavaged. The bronchoalveolar lavage fluid (BALE) was collected for measurement of TNF-?, NO and protein contents. Results In group C and D propofol given before and simultaneously with LPS significantly inhibited the increase in nitrotyrosine protein and iNOS expression induced by LPS, improved MAP, reduced 5h mortality rate, decreased PPI and protein, NO and TNF-?contents in BALF compared with group B (P

Objective To detect the genes differentially expressed in sepsis-injured lungs and discover new genetic targets for management of sepsis-induced acute lung injury (ALI) and evaluate the role of cDNA microarray in the study of molecular pathogenesis of sepsis. Methods In a murine model of polymicrobial sepsis induced by cecal ligation and puncture (CLP), the gene expression patterns of the lungs of the animals in sepsis group and control group (Sham-operation ) were screened at 6 h and 12 h after CLP by using a commercially available cDNA microarray chips containing 2 201 cDNA clones. The cDNA of differentially expressed unique genes were sorted and analyzed. Results Of the 2 201 cDNA clones on the chip, 80 known unique genes had significant differential expression at 6 and/or 12 h after CLP as compared with those of mice in control group. 40 of the 80 genes were up-regulated and 40 down-regulated and they were related with a range of genetic functions, such as cell defence or immune/inflammatory reaction, acute-phase reaction or heat-shock reaction, redox regulation, cytoskeleton, cell apoptosis, cell signaling and cell metabolism etc. By functional analysis of these differentially expressed genes, some unique genes or expression patterns were interpreted in the context of septic ALI process and warrant further investigation. Conclusion cDNA microarray technique provides a powerful new tool for detecting differentially expressed genes and analyzing gene expression patterns in sepsis-injured tissues. Further study using this technique may yield great insight into the molecular pathologic mechanism of sepsis and discern new targets for therapeutic interventions.

To investigate the effects of clonidine on controlled hypotension induced by sodium nitroprusside,twenty-four patients (male 17,femai 7,aged 20 to 58 years,ASA Ⅰ to Ⅱ)scheduled for elective craniotomy,were randomly assigned to two groups:control group (Ⅰ,n=12),clonidine group (Ⅱ,n=12) with premedication of clonidine 5?g/kg P. O.. The MAP of both groups decreased by 40% with the infusion of 0.01% sodium nitroprusside solution (SNP). The results showed that the blood pressure was more easily reduced and maitained in group Ⅱ,and the MAP after discontinuing of SNP in group Ⅱ was lower than in group Ⅰ(P

0.05)in cell volume between the experimental group and control group after exposured in hypertonic NaCl saline for 15 minutes. Compared with the control level,after 60 minutes and 1 day all astrocytes shrunk significantly, (P0.05). Conclusion:Astrocytes can restore their cell volume following exposition in hypertonic saline.

To investigate the effect of premedication with clonidine on the concentrations of plasma catecholamine (CA), renin, angiotension Ⅱ (A Ⅱ ) and carbohydrate metabolism during eardiopulmonary bypass (CPB). Method: Twenty patients scheduled for cardiac surgery were randomly divided into two groups: clonidine group and control group. Oral premedication with clonidine 5?g?kg~(-1) was taken in colndine group 60 rain before anesthesia in duction in addition to common same premedication in both groups. Arterial plasma concentrations of CA,renin, AⅡ, blood suger, pyruvic acid, lactic acid were measured before anesthesia, before CPB, 30,60,90 and 120 min following CPB and 30 rain after CPB. Result: The levels of CA, blood suger, pyruvic acid and lactic acid increased significantly during CPB in both groups, but were higher markedly in control group than those in clonidine group (P

0.05). The cell volume of astrocytes was not significantly changed after exposition to hypertonic-hyperoncotic solution for 15 minutes. After 60 minutes all astrocytes shrunk significantly until 1 day later. 7 days later,their volumes restored to the value in control group. Conclusion: The hippocampal neuroncs have not the autoregulative ability of the cellular volume. but astrocytes have after exposition to hypertonic-hyperoncotic solution for 15 min: the volume of both cells 7 days later can restore to the previous value.

To investigate the effects of cardiopulmonary bypass (CPB)on the aquired platelet damage and the relationship between the aquired platelet damage and non-surgical postoperative bleeding. Method: Platelet counts (BPC), alphagranule membrane protein (GMP-140), ?-thromboglobulin (?-TG), platelet factor 4 (PF_4), and 5-hydrooxytryptamine levels were measured in 20 patients undergoing cardiac surgery before CPB, 30 min during CPB, 10 min after CPB, and 2, 12, and 24 hours postoperatively. The numbers of patients with bleeding volume over 200 ml within 24 hours postoperatively were counted. Result: BPC decreased markedly during CPB, but never decreased to the degree of 50?10~9/L. GMP-140, ?-TG, PF_4 and 5-HT levels were significantly increased during CPB until 12 hours postoperatively. Eight patients(40%) got the bleeding volume over 200 ml within 24 hours postoperatively. Conclusion: Platelet release reaction is violent during cardiac surgery with CPB. A large number of platelets dysfunctioned because of granula releasing or damage may be the main cause of non-surgical postoperative bleeding.

Objective:The somatosensory evoked cerebral potential (SEP)was used to assess the analgesia effect of clonidine. Method: Twenty-three SD rats was randomly divided into two groups, the control group (n=8) and clonidine group (n=15). The control group rats was injected 1 ml normal saline to peritoneal cavity and the clonidine group rats was injected 10mg(1ml) clonidine peritoneally. The SEP waves were recorded in both groups at preinjection and 20,40,60 min after injection. Pain relief ratio was calculated according to the N15-P25 peak-peak amplitude of SEP wave. Result:SEP amplitude and latency were markedly reduced in clonidine group and remained unchanged in control group. The peak Pain relief ratio was 80. 6％at 20-40 min after clonidine administration. Conclusion:Clonidine does have a effect of pain relief

Objective: To evaluate the safety of controlled hypotension produced by human ?-calcitonin gene-related peptide(?-hCGRP)and sodium nitroprusside. Method: Twenty SD rats were randomly divided into ?-hCGRP(C) and sodium nitroprusside(S) groups. Animals in group C were infused intravenously with 0.001％ ?-hCGRP and those in group S with 0.01％ sodium nitroprusside. The mean blood pressure of rat was reduced to 6.7kPa and maintained for 30 min. Cerebral glucose,lactate,ATP, and phosphocreatine levels were measured at 0 and 30th min of hypotension. Result: Cerebral glucose level increased slightly,lactate level decreased significantly,ATP and phosphocreatine contents did not change in group C at 30th min of hypotension compared with those at 0 min of hypotension,respectively.Cerebral glucose level increased slightly,lactate concentration increased significantly,ATP and phosphocreatine contents decreased significantly in group S at 30th min of hypotension in comparison with those at 0 min of hypotension, respectively. Conclusion: Hypotension induced with alpha-hCGRP can maintain adequate cerebral oxygen supply,but with sodium nitroprusside may cause cerebral hypoxia.