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.

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 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.

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: Effects of human ?-calcitonin gene-related peptide (?-hCGRP) on renal function and renin-angiotensin system were studied during controlled hypotension. Method:Twenty SD rats were divided into ?-hCGRP (C) and sodium nitroprusside (S) groups. The mean blood pressure of rats was reduced to and maintained at 6.7kPa for 1h. The glomerular filtration rate (GFR),effective renal plasma flow (ERPF),plasma renal activity (PRA),angiotensin Ⅱ(AⅡ), urine volume, heart rate (HR)and the excretory rates of sodium,chloride and potassium of rats were measured beforeand 1h following hypotension. Result:GFR and ERPF increased significantly at the end of 1h hypotension when compared to pre-hypotension in the group C. GFR and ERPF decreased mark during hypotension period in group S. In both groups during hypotension,PRA and A Ⅱ increased by eight-folds or so,the excretory rates of sodium and chloride decreased significantly and the excretory rate of potassium increased slightly, urine volume de creased and HR increased markly. Conclusion:The ?-hCGRP,a potent vasodilator,has a protective effect on renal function as a controlled hypotensive agent. Sodium nitroprusside may harm renal function. The increased excitation of renin-angiotensin system may be responsible for the changes of urine volume,heart rate and the excretory rates of sodium ,chloride and potassium during hypotension.

To evaluate the influence of human ?-caleitonin gene related peptide (?-hCGRP) used in the controlled hypotension on hepatic blood flow, oxygen supply and oxygen consumption in rats. Method: Alpha-hCGRP and sodium nitroprusside were administered intravenously to reduce the blood pressure of rats to 6.7 kPa maintained for 1 h. Radiomierospheres were employd to measure hepatic arterial blood flow (HABF), portal venous blood flow (PVBF), and total hepatic blood flow (TABF). The arterial0portal,and hepatic venous blood gases were analyzed. The hepatic oxygen supply and oxygen consumption were calculated according to values of blood flow and gases. Result: HABF, TABF, and hepatic oxygen supply increased significantly, and PVBF decreased slightly during ?-hCGRPinduced hypotension. HABF, TABF and hepatic oxygen consumption increased significantly, and hepatic oxygen supply decreased significantly during sodium nitroprusside hypotension. Rebound hypertension occurred after the discontinua tion of sodium nitroprusside rather than ?-hCGRP. Conclusion: Alpha-hCGRP does not cause hepatic hypoxia during controlled hypotension, while sodium nitroprusside may result in hepatic hypoxia. Alpha hCGRP is more adequate to be used to controlled hypotension than sodium nitroprusside. No rebound hypotension is another advantage of ?-hCGRP.