Objective To explore the levels of serum angiotensin Ⅱand their clinical significance on pheochromocytomas. Methods Fifty-eight patients were randomly divided into three groups: Group Ⅰwith normal blood pressure; Group Ⅱ are essential hypertension; Group Ⅲ are pheochromocytomas. The levels of serum angiotensin Ⅱ (ATⅡ) in each group and at eleven time points: were measured. Results The levels of serum ATⅡ of groupⅡand Ⅲ were significantly higher than those of groupⅠ(P

Objective To discuss the influence of intravenous anesthesia with procaine on the release of central nervous Ach. Methods 50 samples of plasma were collected from healthy people, and 30 samples of plasma from cases prior to surgical operation, during anesthesia and after operation respectively. The activity of Ach in the plasma was measured. Then observe the dropping speed and concentration of procaine at different time during anesthesia, and the subsequent changes of the activity of plasma Ach and the slowdown of its activity. Results The data showed that the activity of plasma Ach prior to operation was considerably lower than that of the control group (P

Objective To assess the relationship between auditory evoked potential (AAI) index and plasma concentration of propofol administered by target-controlled infusion (TCI) in Chinese.Methods Ten ASA Ⅰ～Ⅱ tumor patients (5 males,5 females) scheduled for elective abdominal surgery under general anesthesia was enrolled in this study.Age ranged from 34 to 61 years,body weight from 52 to 79 kg and height from 155 to 178 cm.Radial artery was cannulated for blood sampling.The patients were premeditated with intravenous injection Midazolam 0.06 mg/L.Anesthesia was induced by fentanyl 2μg/kg,vecuronium 0.1 mg/kg and TCI of propofol which the target plasm concentration was set at 3 mg/L.After intubation,the target plasma concentration of propofol was adjusted at 1.7～2.5 mg/L.Vecuronium was continuous infusions at 2～3mg/h.Anesthesia was maintained with fentanyl-TCI of propofol-vecuronium and inhalation of 0.5 MAC isoflurane.The TCI system was composed of Base Primea company orchestra infusion pump using,the schnider pharmacokinetics model.ECG,Bp,HR,PETCO2,SpO2 and TETISO were monitored during anesthesia.Danmeter company A-line depth of anesthesia monitor recorded AAI index.Blood samples were taken at induction of anesthesia (To baseline),1,3,5,10,15,30,60 min (T1-7) and after cessation of infusion 10 and 20 min (T9-10).Plasma propofol concentration were determinated by fluorescence photometry.Results Compared with target concentrations,the measured concentrations of propofol were significantly lower during TCI(P＜0.05).There was negative correlation between AAI and plasma propofol concentrations(r=-0.818,P＜0.01).Conclusion On base of the Schnider pharmacokinetics model,the target propofol concentrations are not paralleled to plasma propofol concentrations which is descending with time prolongation.From negative correlation between AAI index and plasma propofol concentrations,AAI index will reflect indirectly plasma propofol concentrations.

Objective To investigate whether naloxone postconditioning could attenuate the focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods Eighty-eight adult male SD nits weighing 270-330 g were randomly divided into 4 groups (n = 22 each) : group I sham operation (S); group Ⅱ I/R; group Ⅲ , Ⅳ I/R + low and high dose naloxone ( N_1, N_2). Focal cerebral I/R was produced by occlusion of right middle cerebral artery for 90 min followed by 24 h reperfusion. In group N_1, and N_2 naloxone 1 and 10 mg/kg were injected intraperitoneally at initiation of reperfusion respectively. In group I/R normal saline was injected instead of naloxone. HR, MAP and EKG were continuously monitored throughout the experiment. He neurological deficits were scored (0 = no deficit, 4 = unable to crawl, mental dysfunction) at 2 h and 24 h of reperfusion. The animals were then decapitated. The brains were immediately removed for determination of infarct size ( n = 10) and the expression of microtubule-associated protein-2 ( MAP-2) in brain tissue ( n = 6) . In the other 6 rats in each group FICT-dextran 1 ml (50 mg/ml) was injected iv at 1 min before decapitation. The cerebral plasma volume and diameter and segment length of cerebral microvessels on the I/R side were measured using laser scanning confocal microscopy (LSCM). Results Focal cerebral I/R significantly increased neurological deficit scores, induced cerebral infarct, and decreased MAP-2 expression in the brain tissue, cerebral plasma volume and the diameter and segment length of cerebral microvessels on the I/R side. Postconditioning with 10 mg/kg naloxone significantly attenuated the above-mentioned focal cerebral I/R-induced changes. Conclusion Postconditioning with naloxone can attenuate focal cerebral I/R injury in a dose-dependent manner.