Effect of acute hypervolemic hemodilution on myocardial damage in severely burned rabbits / 中华麻醉学杂志

Objective To evaluate the effect of acute hypervolemic hemodilution (AHH) on myocardial damage in severely burned rabbits.Methods Eighteen healthy adult rabbits,weighing 2.0-2.5 kg,were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C),burn group (B group) and AHH group.Rabbits were subjected to 3rd degree burn covering 40％ of the total body surface area.After the model was established,6％ hydroxyethyl starch 130/0.4 was infused intravenously,and the target Hct was 25％ in AHH group.Before AHH (To) and at 2,4 and 8 h after AHH (T1-3),left ventricular systolic pressure (LVSP),left ventricular end-diastolic pressure (LVEDP),+dp/dtmax and-dp/dtmax were recorded,and blood samples from femoral veins were taken to determine the concentration of serum cardiac troponin I (cTnI) by ELISA.The rabbits were sacrificed at T3,and myocardial specimens were removed for microscopic examination of pathological changes with light microscope.Results Compared with group C,the serum cTnI concentration and LVEDP were significantly increased,LVSP and +dp/dtmaxwere decreased at T1-3 in B and AHH groups,and-dp/dtmax at T1-3 in group B and-dp/dtmax at T3 in group AHH were decreased.Compared with group B,LVSP,+dp/dtmax and-dp/dtm,x were significantly increased at T1-3,and no significant change was found in serum cTnI concentration and LVEDP in group AHH.There was no significant difference in the pathological changes between group B and group AHH.Conclusion AHH can not aggravate the early myocardial damage in severely burned rabbits.

Effects of sevoflurane preconditioning on cardiomyocyte apoptosis and myocardial inflammation in rats with sepsis / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effects of preconditioning with different concentrations of sevoflurane on cariomyocyte apoptosis and myocardial inflammation in rats with sepsis and explore the possible mechanism of sevoflurane for myocardial protection.</p><p><b>METHODS</b>Forty adult male Sprague-Dawley rats were randomly divided into 4 groups (n=10), namely the control group, LPS group, low-concentration sevoflurane group and high-concentration sevoflurane group. Following sevoflurane pretreatment for 30 min and a washout period for 10 min, all the rats received intraperitoneal injection of LPS or normal saline (NS) and were sacrificed 12 h later to observe the myocardial histopathology. Apoptosis of the ardiomyocytes was detected with TUNEL assay, and enzyme-linked immunosorbent assay was used to detect serum cTnI level and myocardial TNF-α level.</p><p><b>RESULTS</b>Compared with the control group, the rats in the other 3 groups showed significantly increased serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes (P<0.05). Compared with those in LPS group, serum cTnI level, myocardial TNF-α content, and apoptotic index of the cardiomyocytes were significantly decreased in the two sevoflurane preconditioning groups (P<0.05), and the effect was more obvious with a high dose of sevoflurane (P<0.05 CONCLUSION: Sevoflurane preconditioning can concentration-dependently reduce LPS-induced myocardial injury in rats possibly by decreasing cardiomyocyte apoptosis and alleviating myocardial inflammations.</p>

Effects of sevoflurane anesthesia on aquaporin-9 expression in brain tissue after focal cerebral ischemiareperfusion in rats / 中华麻醉学杂志

ObjectiveTo investigate the effects of sevoflurane anesthesia on aquaporin-9 (AQP-9) expression in brain tissue after focal cerebral ischemia-reperfusion (I/R) in rats.MethodsSeventy-five male SD rats weighing 230-270 g were randomly divided into 3 groups ( n =25 each):group sham operation (group S) ; group I/R and group sevoflurane anesthesia (group SE).All the animals were tracheally intubated under 2.0％ sevoflurane and mechanically ventilated.Anesthesia was maintained with fentanyl infusion at 25 μg· kg-1 · h-1 after a bolus of fentanyl 10 μg/kg and inhalation of 65％ N2O in O2 in groups S and I/R and with inhalation of 2％ sevoflurane in 35％ O2 in group SE.Focal cerebral ischemin was induced by occlusion of middle cerebral artery for 2 h using a nylon thread with rounded tip which was inserted into the right internal carotid artery and advanced cranially until resistance was met.The neurologic function was assessed and scored (0=no deficit,4 =unable to move,unconscious) and brain edema rate (volume of ischemic hemisphere-volume of contralateral hemisphere ÷volume of contralateral hemisphere × 100％ ) and expression of AQP-9 were determined at 6 h,1,2,3 and 5 d of reperfusion.ResultsFocal cerebral I/R significantly increased neurologic deficit scores,brain edema rate and AQP-9 expression in brain tissue in group I/R as compared with group S.Sevoflurane anesthesia significantly attenuated the I/R-induced increase in neurologic deficit scores and brain edema rate and further increased I/R-induced increase in AQP-9 expression in brain tissue.ConclusionSevoflurane anesthesia can reduce focal cerebral I/R injury by up-regulating the expression of AQP-9 in brain tissue.