ObjectiveTo evaluate the effects of ovarian cycle on median-effective target plasma concentration (EC50) of propofol administered by target controlled infusion (TCI) caused loss consciousness.MethodsForty ASA I or II patients who had age 20 - 39 (28.5 ± 4.8) years and were scheduled for elective gynecologic laparoscopic surgery were divided into 2 groups (n =20 each group) : The follicular phase group (F group, serum progesterone concentration O.311.52 ng/ml) and luteal phase group (L group, serum progesterone concentration 5.16 ～ 18.56 ng/ral).No premedication was administered.Propofol was administered by TCI.TCI system was incorporated with Marsh pharmacokinetic model.EC50 was determined by up-and-down sequential trial.The target phsma concentration (Cp) was set at 3.5 μg/ml in the fh-st patient in each group.Each time, Cp was increased/decreased by 10％ in the next patient depending on whether or not the loss consciousness occurred.ResultsThe ECho and 95％ confidence interval of propofol TCI caused loss consciousness were 4.76 (4.52 -5.00) μg/ml in group F, 4.18(3.88 ～4.52)μg/ml in group L.EC50in group L was significantly lower than in group F (t =6.23, P ＜0.01).ConclusionsAs loss consciousness occurred, median-effective target plasma concentration of propofol in luteal　phase was lower than that in follicular phase.

The contractions induced by acetylcholine or Ca2 + after high-K+ depolarization in isolated guinea-pig taenia coli were markedly inhibited by rhynchophylline (Rhy). It caused rightward displacement of the dose-response curve for CaCl2 & significantly depressed the maximal response, showing a non-competitive antigonism. The pD'2 value of Rhy was 4.95?0.05. In Ca2+-free solution,Rhy similar to verapamil (Ver), inhibited acetylcholine-induced contraction of guinea-pig taenia coli, which is dependent on Ca2+ released from an intracellular store. After Ca2+ concentration in bath solution was restored, Ver did not influence the contraction of taenia coli depending on extracellular Ca2 + , However 40 ?mol/L Rhy could exhibit marked inhibitory action.

Objective To investigate the effect of ovarian cycle on the sedative effect of propofol in patients. Methods Forty ASA Ⅰ or Ⅱ patients, aged 20-40 yr, with body mass index 20-25 kg/m2 , scheduled for elective gynecologic laparoscopic surgery, were divided into 2 groups according to the progesterone level ( n = 20 each): follicular phase group (group F, serum progesterone concentration 0.31-1.52 ng/ml) and luteal phase group (group L, serum progesterone concentration 5.16-18.56 ng/ml). Anesthesia was induced with target-controlled infusion (TCI) of propofol and iv injection of fentanyl and cisatracurium. The initial target plasma concentration (Cp) of propofol was set at 2 μg/ml, after the Cp reached the predetermined level, the Cp increased by 0.5 μg/ml every 30 s until the patients lost consciousness and BIS value was decreased to 50. The BIS value and Cp of propofol was recorded when the patients lost consciousness. The Cp of propofol was also recorded when BIS value was decreased to 50. The patients were tracheal intubated and mechanically ventilated. Anesthesia was maintained with TCI of propofol combined with remifentanil. BIS value was maintained at 45-55 by adjusting the Cp of propofol. Results The Cps of propofol were significantly higher when the patients lost consciousness and when BIS value was decreased to 50 in group F than in group L ( P ＜ 0.05 or 0.01) . There was no significant difference in BIS value when the patients lost consciousness between the two groups (P ＞ 0.05). Conclusion Ovarian cycle can affect the sedative effect of propofol in patients, which shows that the sedative effect during the follicular phase is lower than that during the luteal phase.

OBJECTIVE: To observe the protective effects of Corydalis ambailis migo total alkaloids (COAMTA) on cerebral ischemia/reperfusion injury in rats and to investigate its mechanism. METHODS: The effects of COAMTA on decapitated gasping mouse model and rat model of middle cerebral artery ischemia (2 h)/reperfusion (22 h) were observed. The neurological scale, cerebral infarcted volume and cerebral water content subjected to cerebral middle artery ischemia/reperfusion in rats were recorded. The activities of nitric oxide synthase (NOS) and superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in the ratso brain were measured. Cell apoptosis in ischemic penumbral area was observed with light microscope in the method of terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling (TUNEL). RESULTS: The average gasping time of the mice (6.0 mg/kg or 9.0 mg/kg COAMTA) was significantly prolonged, the cerebral infarcted volume and cerebral water content of the rats (5.0 mg/kg or 7.5 mg/kg COAMTA) were significantly decreased, as compared with the control groups. The average activity of SOD in cerebral tissue of the rats (5.0 mg/kg or 7.5 mg/kg COAMTA) was significantly higher than that of the control groups, meanwhile, the average activity of NOS and the content of MDA declined significantly. The cell apoptosis in ischemic penumbral area of the rats (5.0 mg/kg COAMTA) was significantly inhibited as compared with the control groups. CONCLUSION: COAMTA can facilitate the protection against cerebral ischemia/reperfusion damage. The mechanism is related to inhibiting the activity of NOS and lipoperoxidation, increasing the activity of SOD and decreasing the neuronal apoptosis.

Objective To evaluate the effect of dexmedetomidine on lung injury induced by extremity ischemia-reperfusion.Methods Forty patients,aged 18-60 yr,with body mass index of 20-25 kg/m2,of ASA physical status Ⅰ or Ⅱ,with 1 h ≤ predicted duration of surgery ≤ 1.5 h,were randomly divided into 2 groups (n =20 each) using a random number table:control group (group C) and dexmedetomidine group (group D).In groupD,dexmedetomidine 1 (g/kg was infused intravenously for 10 min,followed by continuous infusion of dexmedetomidine at 0.5 μg· kg-1 · h-1 until the end of the surgery,while in group C the equal volume of normal saline was given instead.Immediately before induction of anesthesia (T1,baseline),at 60 min after tourniquet was inflated (T2) and at 30 min,2 h and 6 h after tourniquet release (T3-5),blood samples were collected from the radial artery for blood gas analysis and for measurement of the levels of plasma interleukin-6 (IL-6),IL-8,tumor necrosis factor-α (TNF-α),malondialdehyde (MDA) and superoxide dismutase (SOD),and arterial partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) were recorded.Alveolar-arterial oxygen difference (A-aDO2) and respiratory index (RI) were calculated.Results Compared with group C,PaO2 was significantly increased at T5,and A-aDO2 and RI at T5,the levels of plasma IL-6 and IL-8 were decreased at T4,5 and the levels of plasma TNF-α,MDA and SOD were decreased at T3-5 in group D.Conclusion Dexmedetomidine can attenuate lung injury induced by extremity ischemia/reperfusion via inhibiting inflammatory responses and lipid peroxidation.

Objective To study the effect of protopine (Pro) on the intracellular free calcium ions of the smooth muscular cells of the thoracic aorta in rats. Methods The procedure of calcium absence-calcium addition was designed to observe the changes of the level of calcium ions in the strips of the smooth muscle of the thoracic aorta indirectly. The concentration of calcium ions in the smooth muscle of the thoracic aorta was determined with Fura-2/AM loaded SMCs. The elevation of calcium ions was induced with norepinephrine (NE). The concentration of potassium ions was observed in the presence of Pro. Results Pro significantly inhibited the NE-induced transient contract of the smooth muscle of the thoracic aorta in calcium-free medium and long-lasting contraction after the addition of calcium ions in a concentration-dependent manner. In Fura-2/AM loaded SMCs, Pro (50 ?mol/L or 100 ?mol/L) exerted no effect on the resting calcium ions but obvious effect on the NE-induced and high potassium level-induced elevation of calcium ions. In the presence of extracellular calcium ions, Pro (50 ?mol/L) decreased the NE-induced elevation of calcium ions but showed no effect on potassium-induced elevation of calcium. Pro (100 ?mol/L) significantly decreased NE-induced and high potassium level-induced elevation of calcium ions. Conclusion Pro reduces NE-induced or high potassium level-induced elevation of calcium ions in the smooth muscle of the thoracic aorta through its effect on calcium release and/or calcium influx.

Aim To study the protective effects of Rhynchophyll a of total alkaloids ( RTA ) on cerebral ischemia/reperfusion injury and the possi ble mechanism of action. Methods The effects of RTA on decapit ated gasping model and model of middle cerebral artery ischemia 2 h/reperfusion 22 h were observed. The neurological scores, cerebral infarct volume and cerebr al water content after ischemia/reperfusion were observed in rats respectively. The activities of NOS and SOD and the content of MDA in rat's brain tissue were measured. Neuron apoptosis in ischemia penumbral area were detected by terminal depoxynucleotidyl transferase mediated dUTP-biotin nick end labeling ( TUNEL ) . Results The average gasping times in mice treated with RTA 50 , 75 mg?kg -1 was significantly prolonged. The cerebral infarct volume and cerebral water content in rats treated with RTA 40, 60 mg?kg -1 were sign ificantly decreased in ischemic rats. RTA 40, 60 mg?kg -1 increased the ac tivity of SOD ,and decreased the activity of NOS and the content of MDA in the i schemic brains of rats. The number of apoptotic neurons in ischemia penumbral ar ea of cerebral tissue of rats treated with RTA 40, 60 mg?kg -1 was signif icantly lower than that in control rats. Conclusions RTA has pr otective effect on cerebral ischemia/reperfusion injury; this may be related to inhibit the activity of NOS and lipoperoxidation, and increasing the activity of SOD and decreasing neuron apoptosis.

AIM To study the distrubution and excretion of protopine in rats. METHODS Reversed phase high performance liquid chromatographic method (RP HPLC) was developed for determining the level of protopine in rats. The analytical column were packed with 5 ?m C 18 . The mobile phase was a mixture of methanol, water and 10% acetic acid (80∶20∶2), in which the pH was modulated to 5 6 with 15% ammonia. Protopine biological samples were isolated well, in which two extraction with ether under basical condition and an extraction with 0 02 mol?L -1 sulfuric acid were performed, respectively. The content of protopine in the biological sample was measured by an UV detector at 285 nm. The distrubution and excetion of protopine have been investigated in rats after intravenous administration 10 mg?kg -1 . RESULTS Protopine distrubuted in many tissues after iv a dose of 10 mg?kg -1 . The higher level of protopine was found in lung, kidney, spleen and brain, and the highest was observed in lung at 5, 15 minutes after administration. However the top level tissue was testicle at 3 h, which may be due to small blood circulation. The excretion of the parent compound in urine was 36 87% of dose, but the excretion of the parent compound in feces and bile was less than 1% of dose. Plasma protein binding was less than 5%. CONCLUSION The distrubution of protopine is extensive and the parent compoud was mainly excreted by urine and plasma protein binding was low.

Aim To study the effect of naftopidil(Naf) on noradrenalin(NA)-induced proliferation of rats vascular smooth muscle cells (VSMCs),and explore its mechanisms. Methods The cultured VSMCs was induced to proliferate by NA,and effects of Naf on the VSMCs proliferation was tested by MTT assay and cell counting method respectively. The intra-cellular calcium concentration is investigated by fluorimetry,and the expressions of c-myc,c-fos and hypertension related gene-1(HRG-1) mRNA were tested by Real-Time RT-PCR. Results The proliferation of VSMCs induced by NA was inhibited by Naf(10-7~10-6mol?L-1),which diminished clearly VSMCs [Ca2+]i and decreased mRNA expressions of c-myc,c-fos and increased the expression of HRG-1 mRNA. Conclusions Proliferation of VSMCs induced by NA can be inhibited clearly by Naf. The mechanisms may be related to diminishing [Ca2+]i,antagonizing the up-regulation of c-myc and c-fos mRNA expressions by NA and antagonizing the down-regulation of HRG-1 mRNA expression.

From January 2016 to June 2017, 68 patients with thoracic osteoporotic compression fractures were treated with percutaneous kyphoplasty, including 31 cases with ultrasound-guided thoracic paravertebral nerve block (group A) and 37 cases with local anesthesia (group B). The duration of analgesia in group A was longer than that in group B (P<0.05). The satisfaction of anesthesia in group A was higher than that in group B (90% vs. 68%, P<0.05). There was no significant difference in length of hospital stay and cost between the two groups (P>0.05). The post-operative VAS scores was significantly lower than those of pre-operation in both groups (P<0.05). The intraoperative VAS score of group A was lower than that of group B (P<0.05). There was no significant difference between the two groups in mean arterial pressure and heart rate (P>0.05). No cardiovascular and cerebrovascular adverse reactions occurred in both groups. Ultrasound-guided thoracic paravertebral nerve block is a safe and effective method used in percutaneous kyphoplasty.