To observe the time-dependent course of potentiation of vecuronium produced by 1MAC of end-tidal sevoflurane and isoflurane. Method: At the beginning, a steady infusion rate of vecuronium to maintain 90 of neuromuscular block was established in 40 patient undergoing neurosurgical procedures under propofol fentanyl nitrous oxide oxygen anesthesia. The patients were randomly assigned to receiving IMAC end-tidal concentration of either sevoflurane (Group Sev) or isoflurane(Group Iso). Vecuronium infusion rate was adjusted to maintain 90%, neuromuscular block. The change of infusion rate of vecuronium with time was observed after inhalation of Sev or Iso. Result: Sev and Iso decreased the infusion dosage of vecuronium in an exponential manner, maximal potentiation occurred 90 min after inhalation. Maximal reduction in infusion rate was 67.87% in group Sev and 69.87% in group Iso without the significant difference between them. Conclusion: Sev and Iso can potentate the muscular relaxation of vecuronium at similar degree in strong time-dependent way.

Objective: To investigate the effects of AG, an iNOS inhibitor on microcirculation of the septic shock rabbits. Method: The white rabbits were infused endotoxin(LPS, 300?g. kg~(-1)in lh. Two hours after the MAP de creased to 60% of the baseline, the rabbits were grouped randomly as L-NAME(n=6.30 mg. kg~(-1))I. V. group and AG(n=6,20 mg. kg~(-1)) I. V. group. Result: Two hours after MAP decreased, the blood velocity decreased, the arterio lar of mesenterium dilated by 18%(P

Objective: To investigate the effects of selective NOS inhibitor aminoguanidine (AG) on endotoxintreated rat aorta (AO) and pulmonary artery (PA) in vitro. Method: The reaction to noradrenaline (NE) (10~(-9)-10~(-4)mmol/L) was measured in the vessels with complete endothelium, then the vessels were divided into 8 groups after incubated in LPS(300ng/ml)for 4 hours. Each group was incubated with AG(100?mol/L)or L-NAME (300?mol/L)for 20, or 60min, respectively. Result: Both AO and PA showed hyporeaetivity to NE after incubated in LPS. and the reactivity of AO and PA to L-NAME and AG increased significantly after incubated in them for 60min or 20min. The sen sitivities of AO to AG,AO and PA to L-NAME increased greatly. AO had a higher reactivity to AG in 60min than in 20min. L-NAME caused earlier and greater contraction than AG in both 60 min and 20 min groups. Conclusion: LNAME and AG can both increase the decreased reactivities of AO and PA to NE. AG only increases the AO sensitivity.

Objective: To investigate the effects of divided-doses mivacurium on histamine releasing and hemodynamics. Method: Forty-two patients were randomly divided into seven groups (n=6, each group). The total dose of 3?ED_(95)(0.25mg/kg)mivacurium for intubation was injected intravenously in single-dose in group I, or in divided-doses of 0.05+0.2mg/kg, 0.10+0.15mg/kg, 0.125+0.125mg/kg, 0.15+0.1mg/kg, and 0.2+0.05mg/kg in group Ⅱ, Ⅲ,Ⅳ, Ⅴ and Ⅵ respectively, and 0.6mg/kg of atracurium bolus in group Ⅶ, The plasma histamine concentration and systolic blood pressure(SP), diastolic blood pressure(DP) and heart rate(HR) were determined before and 3, 5, 10, and 15 min after injection of mivacurium or atracurium. Result: The plasma histamine concentration and changes of SP, DP, HR were decreased in group Ⅳ compared with those in other groups. Conclusion: The divided dose of 3?ED_(95) mivacurium for intubation may reduce histamine release and changes in hemodynamics.

Objective To understand the effects of NO signal system on the ciliary beating frequency (CBF) of airway epithelial cellMethods Nine normal male Sprague-Dawley rats were anesthetized with isoflurane Their tracheas were rapidly removed using aseptic technique The mucosa of trachea were cut into 1mm2 explants and cultured in DMEM The explants were divided into 5 groups as bellow: L-Arg group, 1-Hydroxy-2-oxo-3-(N-ethyl-2-aminoethyl)-3-ethyl-1-triazene (NOC-12) group, D-Arg group, 8-Br-cGMP group, and phosphate buffered saline (PBS)group Actively beating ciliated cells were observed, and their motion was quantified by measuring CBF using phase-contrast microscopy and videotape analysis Results L-Arg increased CBF from (7 43?0 75)Hz to(8 59?0 93)Hz (P

Objective:To compare etomidate in propylene glycol(Eto-PG) with a new galenic preparation of etomidate solved in a lipid emulsion of soya-bean oil(Eto-Lip).Method:Sixty patients were randomly divided into 2 groups:Eto-PG group and Eto-Lip group.The dosage of etomidate was 0.3mg/kg.Hemodynamic change and side effects(pain on iv-injection,involuntary movement, phlebitis, thrombophlebitis etc.) were observed.Result:There were no difference between the two groups in the incidence of involuntary movement.Side effects at the site of injection,both immediate and after operation,were encountered with Eto-PG but were not encountered in the lipid emulsion. Conclusion:Eto-Lip can reduce some undesired side effects without changing its pharmacodynamics.

Objective:To test the effects of propofol on intracellular calcium free concentration ([Ca~(2+)]i) and inositol 1,4,5-triphosphate (IP_3) biological synthesis induced by norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in aortic smooth muscle cells (ASMC)of rats for the mechanism of relaxtion of propofol on vascular smooth muscle.Method: Using the flurospectrophotometry and Fura-2/AM loading method,the changes of [Ca~(2+)]i levels in primary culture ASMC were measured,and using the specific, IP_3 assay system and isotope radioactive protein binding experiment IP_3 production levels in aortic smooth muscle were measured. Result:The baselines of [Ca~(2+)]i was decreased when primary culture ASMC was pretreated with propofol in 72 hours. Propofol inhibited [Ca~(2+)]i increase induced by NE and 5-HT in dose-dependent way. With extracellular calcium free or calcium channel blocker(Verapamil),inhibition of propofol on NE and 5-HT increasing [Ca~(2+)]i levels were decreased,but could not be cancelled. Propofol depressed IP_3 biological synthesis induced by NE and 5-HT in dose-dependent way. Conclusion:Relaxation of propofol on aortic smooth muscle is closely related to inhibiting IP_3- induced calcium release to decrease intracellular calcium concentration.

Objective: Our purpose was to study the effect of anisodamine on the injury of myocardium after myocardial ischemia reperfusion. Methods: Eighteen patients (ASA grade Ⅱto Ⅲ) scheduled for valve replacement, were randomly divided into 2 groups during extracorporeal circulation. Anisodamine (0.25 mg/kg) was given intravenously in the anisodamine group before reperfusion. Equivalent volumes of normal saline were administered in the control group. The central venous blood samples were collected at different time after ischemia and reperfusion. We then measured the concentrations of lactic dehydrogenase (LDH), creatine kinase (CK), and malondiadehyde (MDA) with biochemical methods. Results: The levels of serum LDH, CK, and plasma MDA increased significantly in the control group during ischemia and reperfusion. In the anisodamine group, the levels of serum LDH and CK increased. But the values were lower at corresponding time than those in the control group (P<0.05) during reperfusion. The plasma level of MDA unchanged in the anisodamine group during ischemia and reperfusion. The postoperative cardiac function recovered much more better in the anisodamine group. Conclusion: Anisodamine can reduce the degree of reperfusion injury. A certain protective effect on myocardial ischemia reperfusion injury exsists during valve replacement.

Objective: To compare hemodynamic effects of infusion of diethylamine/nitric oxide (DEA/NO)and sodium nitroprusside(SNP)during controlled hypotension. Method: General anesthesia was induced in dogs. The twelve healthy adult dogs were randomly assigned into one of two groups. 0.00l％ DEA/NO or 0.01％ SNP was infused to induce mean arterial pressure(MAP) to decrease to 60％ of baseline and be maintained for 30 min. During hypotension, MAP,central venous pressure (CVP), mean pulmonary artery pressure (MPAP)and cardiac output (CO) were measured and recorded. Arterial blood gas, blood lactate and urine output were also measured. Result: HR,CVP and CO were unchanged during hypotension period in both groups, MPAP decreased correspondently with MAP. There were no significantly changes in arterial blood gas,blood lactate and urine output in both groups during hypotension. Conclusion: Controlled hypotension achieved with infusion of DEA/NO has a rapid onset and short duration of action.The hemodynamics were similar to those of SNP.

OBJECTIVETo investigate the role of endogenous carbon monoxide (CO) in hypoxia.

METHODSAfter rats were inhaled with hypoxic gases and the heme oxygenase inhibitor ZnPPIX was administered, we measured the CO levels in plasma, liver, lung and kidney. Meanwhile plasma cGMP levels were observed. Furthermore, we recorded the change of hemodynamic and blood gases.

RESULTSAcute mild hypoxia (10% O2) significantly increaed CO levels in plasma as well as liver, kidney and lung, while acute severe hypoxia (5% O2) significantly decreased CO levels in plasma as well as liver, kidney and lung. In addition, the former significantly elevated cGMP levels in plasma while the latter markedly reduced cGMP levels in plasma. The hemodynamic change occurred in accordance with the changes carbon monoxide.

CONCLUSIONOur results indicate, for the first time, that the endogenous carbon monoxide plays an important role in regulating the vessel tone during hypoxia.

Acute Disease ; Animals ; Blood Gas Analysis ; Carbon Monoxide ; blood ; metabolism ; Cyclic GMP ; blood ; Heme Oxygenase (Decyclizing) ; antagonists & inhibitors ; Hemodynamics ; Hypoxia ; metabolism ; physiopathology ; Kidney ; metabolism ; Liver ; metabolism ; Lung ; metabolism ; Rats ; Rats, Wistar