ABSTRACT
Dexmendetomidine hydrochloride [DEX] is a new common adrenergic receptor agonist, which not only keeps children calm but also has analgesic effect. Dexmedetomidine hydrochloride will enable children to maintain the natural
non-REM sleep, which can be stimulated sedation or language arousal. The aim of this study is to observe the sedative effect and adverse drug reactions of dexmedetomidine hydrochloride injection and propofol injection in MRI
examination. In this study, no children in the experimental group were required to add sedative drugs, and 2 cases in the control group were treated with sedative drugs. In experimental group, it used dexmedetomidine hydrochloride as
[1.64+/-0.91] g/kg; in control group, dosage of narcotic drugs as [5.26+/-1.82] g/kg, and the total complication rate of the children in the experimental group was lower than that of the control group [P<0.05]. After returning to the ward, the doses of phenobarbital sedation were dexmedetomidine group [4.28+/-1.53] mg/kg and propofol group [6.40+/-1.71] mg/kg.There was significant difference between the two groups. The total complication rate in the experimental group was lower than that in the control group [P<0.05]. The quality of MRI in the test group was significantly higher than that in the control group, which showed that dexmedetomidine hydrochloride could provide a satisfactory sedative effect in the MRI examination of children. To sum up, dexmedetomidine hydrochloride is a wide range of clinical applications. It is an effective drug for the maintenance of sedation in clinical disease treatment. It is flexible in the way of administration and with less adverse reactions. It is suitable for popularization and application in clinical practice
ABSTRACT
Objective To evaluate the efficacy of clemastine fumarate in antagonizing atracuriuminduced release of histamine in the patients undergoing surgery under general anesthesia.Methods Eighty American Society of Anesthesiologists physical status Ⅰ or Ⅱ patients,aged 21-59 yr,with body mass index of 17-26 kg/m2,scheduled for elective modified radical mastectomy,were divided into 2 groups (n=40 each) using a random number table:control group (group C) and clemastine fumarat group (group CF).Clemastine fumarate 2 mg was injected intramuscularly at 20 min before induction of anesthesia.Anesthesia was induced with iv midazolam 0.1 mg/kg,etomidate 0.3 mg/kg,fentanyl 4-6 μg/kg and atracurium 0.8 mg/kg.The patients were mechanically ventilated after insertion of the larygeal mask airway.Anesthesia was maintained with inhalation of 2％ sevoflurane.Before administration of clemastine fumarate,at 20 min after administration,immediately before administration of atracurium,and at 2,5,10 and 20 min after administration of atracurium,arterial blood samples were taken for determination of plasma histamine concentrations,and the peak airway pressure and degree of cutaneous color were recorded.The development of histaminemia and adverse cardiovascular events was assessed.Steward recovery scores and Ramsay sedation scores were recorded at 10 min after removal of the laryngeal mask airway.Results The incidence of histaminemia was 60％ and 8％ in C and CF groups,respectively.Compared with group C,the plasma histamine concentrations,incidence of histaminemia,degree of cutaneous color,and incidence of hypotension and tachycardia were significantly decreased (P＜0.05),and no significant change was found in the peak airway pressure,Steward recovery scores and Ramsay sedation scores in group CF (P＞0.05).Conclusion For atracurium-induced release of histamine in the patients undergoing surgery under general anesthesia,clemastine fumarate 2 mg injected intramuscularly before operation can not only antagonize histamine at H1 level,but also reduce histamine release,and exerts no influence on recovery from anesthesia and produces good antihistamine efficacy.
ABSTRACT
Objective To investigate the effects of sevoflurane pretreatment on the myocardial injury in patients undergoing cardiac valve replacement with cardiopulmonary bypass (CPB).Methods Twenty NYHA class Ⅱ or Ⅲ patients,aged ＜ 60 yr,undergoing cardiac valve replacement with CPB,were randomly divided into 2 groups (n =10 each):sevoflurane group (group S) and control group (group C).The patients were premeditated with intramuscular morphine and scopolamine.Anesthesia was induced with iv injection of midazolam 0.05-0.08 mg/kg,fentanyl 10-15 μg/kg and pipecuronium 0.08-0.10 mg/kg.Anesthesia was maintained with intermittent iv boluses of midazolam,fentanyl and pipecuronium and in addition sevoflurane was inhaled before aortic clamping and the end-tidal concentration was rapidly increased to 1.0％ and maintained at the level for 5 min in group S.Blood samples were taken from the central vein before skin incision (T1),immediately after aortic clamping (T2 ),at 0 and 30 min after aortic unclamping (T3-4),and at 2,6,12 and 24 h after operation (T5-8) for determination of the concentration of serum cardiac troponin Ⅰ (cTnI) and activities of creatine kinase (CK) and creatine kinase isoenzyme-MB (CK-MB).Myocardial specimens were taken from right auricle before aortic clamping and at 10 min after aortic unclamping for electron microscopic examination.Results The concentration of serum cTnI and activities of CK and CK-MB were significantly increased at T4-8 in both groups ( P ＜ 0.05).The serum cTnI concentration at T4-8 and the activities of CK and CK-MB at T8 were significantly lower in group S than in group C ( P ＜0.05).Different degrees of mitochondrial swelling were observed after aortic unclamping in both groups,but the changes were milder in group S than in group C.Conclusion Sevoflurane pretreatment can attenuate the myocardial injury in patients undergoing cardiac valve replacement with CPB.
ABSTRACT
Objective The aim of this study was to determine the effects of ulinastatin, a broad spectrum proteinase inhibitor, on fibrinolytic system and platelet function during open heart surgery performed with cardiopulmonary bypass (CPB) .Methods Twenty ASA Ⅰ-Ⅱpatients of both sexes undergoing cardiac surgery under CPB were randomly divided into two groups of ten patients: control group(C) and ulinastatin group (U). In group U patients received ulinastatin 12 000 U?2kg-1 . Half of the dose was given iv 10 min before CPB and the other half was added to the priming solution. In group C patients received normal saline instead of ulinastatin. Blood samples were taken before CPB (T1 ) , 30 min after CPB was started (T2), at the end of CPB (T3), 2 h and 4 h after CPB(T4 , T5) for determination of plasma levels of D-Dimer, ?-granule membrane protein-140 (GMP-140), thromboxane B2 (TXB2) and 6-Keto-prostaglandin F1? (6-Keto-PGF1?) .Results The demographic data, aortic cross-clamping time, CPB time and duration of operation were comparable between the two groups. The plasma levels of D-Dimer, GMP-140, TXB2 and TXB2/6-Keto-PGFl? were significantly increased at T2 , T3 and T4 as compared with the baseline (T1 ) in both groups, but the increase was significantly larger in group C than in group U(P
ABSTRACT
Objective To investigate the protective effect of ulinastatin on myocardium against ischemia-reperfusion injury in open heart surgery with cardiopulmonary bypass (CPB) .Methods Twenty ASA Ⅰ - Ⅱ patients undergoing atrioseptopexy or surgical repair of VSD under CPB were randomly divided into two groups: in ulinastatin group (U n = 10) patients received ulinastatin 12000 unit?kg-1, half of the dose was given iv, 10 min before aorta cannulation and another half was added into the priming fluid; in control group (C n = 10) the patients received same volume of saline instead of ulinastatin. Premedication consisted of intramuscular pethidine 1 mg?kg-1 and scopolamine 0.01 mg?kg-1 .Anesthesia was induced with midazolam 0.1 mg?kg-1, fentanyl 10 ?g?kg-1 and pancuronium 0.1 mg**kg-1 and maintained with fentanyl, enflurane or isoflurane, diazepam and pancuronium. Arterial blood samples were taken before CPB (T1), at release of the aortic cross-clamp (T2), 30 min after aortic release (T3), 4h and 24h after discontinuation of CPB (T4, T5 ) for determination of plasma levels of cardiac troponin I (cTnI), creatine phosphokinase (CK) and creative phosphokinase isoenzyme (CK-MB) .Results The demographic data were comparable between the two groups. The CPB time, aortic cross-clamping time and duration of operation were also comparable. The plasma cTnI level and CK, CK-MB activity were all within normal range before CPB in both groups. In group C the plasma level of cTnI started increasing at T2, peaked at T4 and started decreasing at T5. In group U the plasma level of cTnI at T3 and T4 was significantly higher than the baseline (P
ABSTRACT
Objective To determine the effects of sevoflurane (SEV) on angiotensin Ⅱ(AngⅡ)-induced contraction of isolated rat aorta with or without endothelium. Methods Sixty 4-10 week-old Wistar rats weighing 250-350 g were used. The animals were anesthetized with halothane and killed by exsanguination from carotid artery. The thoracic descending aortas were dissected. The adipose and connective tissue adherent to the aorta were carefully removed. The isolated aortas were cut into segments of 4 mm in length and mounted on isometric force transducer and bathed in Krebs bicarbonate solution (KBS) which was aerated with 95% O2/5% CO2. Aortic rings were stretched to a resting tension of 3.0 g. The viability of vascular smooth muscle cells was tested by contraction of aortic ring in response to KCl (3 ? 10-2 mol ? L-1) and the endothelial function was examined by phenylephedrine-induced vasoconstriction and acetylcholine-induced endothelium-dependent vasodilation. The aortic segments were divided into 2 groups: (1) endothelium-intact group ( + ET) and (2) endothelium-denuded group (- ET). The experiment was performed in 3 parts in both groups:(1) aortic segments were exposed to increasing concentrations of AngⅡ(10-9, 3 ? 10-9, 10-8, 3 ? 10-8, 10-7, 3 ? 10-7, 10-6 mol?L-1) with or without 15 min SEV (5.1%) pretreatment to determine the effect of 5.1 % SEV pretreatment on Ang Ⅱ-induced contraction; (2) aortic rings were bathed in KBS containing 10-4 mol?L-1 L-NAME, a NOS inhibitor, for 15 min then exposed to Ang Ⅱ 10-7 mol?L-1 to determine if NO released from endothelium is involved in Ang Ⅱ-induced contraction; (3) aortic rings were first exposed to 1.7% , 3.4% or 5.1% SEV for 15 min then stimulated with Ang Ⅱ 10-7 mol?L-1 to determine if the inhibitory effect of SEV is dose-dependent.Results Ang Ⅱ elicited transient contraction in + ET aortic rings in a dose-dependent manner, reaching the maximal response at concentration of 10-7mol?L-1. Removal of endothelium significantly augmented Ang Ⅱ-induced contraction. The presence of L-NAME significantly enhanced Ang Ⅱ -yielded contraction in + ET rings comparable to the level of contraction in - ET rings, but did not potentiate the contraction in - ET rings. SEV inhibited Ang Ⅱ-induced contractile response of aortic + ET rings in a concentration-dependent manner. Removal of endothelium enhanced the inhibitory effect of SEV on Ang Ⅱ -induced contraction. Conclusion This study demonstrated that Ang Ⅱ elicites vascular smooth muscle contraction, but on the other hand, it also induces NO release from endothelium and vascular relaxation. Sevoflurane inhibits the dual actions of Ang Ⅱ in a dose-dependent manner.