Yao Shanglong

Protective effect of curcumin on endotoxin-induced acute lung injury in rats

To investigate the protective effect of curcumin on endotoxin-induced acute lung injury in rats, and explore the underlying mechanisms, 24 male Wistar rats were randomly divided into 4 experimental groups: sham-vehicle (S), sham-curcumin (C), lipopolysaccharide (LPS)-vehicle (L), and curcumin-lipopolysaccharide (C-L) groups. The wet/dry (W/D) weight ratio of the lung and bronchoalveolar lavage (BAL) fluid protein content were used as measures of lung injury. Neutrophil recruitment and activation were evaluated by BAL fluid cellularity and myeloperoxidase (MPO) activity in cell-free BAL and lung tissue. The levels of cytokine-induced neutrophil chemoattractant-1 (CINC-1) in lung tissues were measured by ELISA. The histopathological changes of lung tissues were observed by using the HE staining. Our results showed that lung injury parameters, including the wet/dry weight ratio and protein content in BALF, were significantly higher in the L group than in the S group (P<0.01). In the L group, higher numbers of neutrophils and greater MPO activity in cell-free BAL and lung homogenates were observed when compared with the S group (P<0.01). There was a marked increase in CINC-1 levels in lung tissues in response to LPS challenge (P<0.01, L group vs S group). Curcumin pretreatment significantly attenuated LPS-induced changes in these indices. LPS caused extensive morphological lung damage, which was also lessened after curcumin pretreatment. All the above-mentioned parameters in the C group were not significantly different from those of the S group. It is concluded that curcumin pretreatment attenuates LPS-induced lung injury in rats. This beneficial effect of curcumin may involves, in part, inhibition of neutrophilic recruitment and activity, possibly through inhibition of lung CINC-1 expression.

Effects of ropivacaine and bupivacaine on rabbit myocardial energetic metabolism and mitochondria oxidation.

SummaryTo compare the cardiotoxicity induced by ropivacaine and bupivacaine and to investigate the mechanism of cardiotoxicity, 24 mature New Zealand rabbits were divided randomly into control group (group C), ropivacaine group (group R) and bupivacaine group (group B). Hearts were drawn out rapidly from the anesthetized animals and cardiac perfusion was performed immediately. Ropivacaine 500 ng/ml (group R) or bupivacaine 500 ng/ml (group B) was added to the perfusion solution. Ventricular myocardial ATP, ADP and AMP were measured with high performance liquid chromatogram. The ability of myocardial mitochondria oxidation to pyruvate or palmitoylcarnitine was detected with Clark electrode. Our results showed that myocardial ATP and ADP decreased significantly (P<0.05) in group R and most significantly (P<0.01) in group B as compared with group C. Myocardial ATP and ADP decreased most significantly (P<0.01) in group B as compared with group R. The changes of myocardial AMP revealed significant difference among three groups. The changes of pyruvate oxidation exibited no significant difference among the three groups. Palmitoylcarnitine oxidation decreased markedly (P<0.05) in group R and most significantly (P<0.01) in group B as compared with group C. The present study indicated that the inhibition of lipid substrate oxidation may be responsible for the cardiotoxicity induced by bupivacaine and ropivacaine. The cardiotoxicity induced by ropivacaine is far more less than bupivacaine.

Effect of thiopental sodium on the release of glutamate and γ-aminobutyric acid from rats prefrontal cortical synaptosomes

SummaryTo investigate the effect of thiopental sodium on the release of glutamate and γ-aminobutyric acid (GABA) from synaptosomes in the prefrontal cortex, synaptosomes were male, the spontaneous release and the evoked release by 30 mmol/L KCl or 20 μmol/L veratridine of glutamate and GABA were performed under various concentrations of thiopental sodium (10–300 μmol/L), glutamate and GABA concentrations were determined by reversed-phase high-performance liquid chromatography. Our results showed that spontancous release and evoked relcase of glutamate were significantly inhibited by 30 μmol/L, 100 μmol/L and 300 μmol/L thiopental sodium, IC50 of thiopental sodium was 25.8±2. 3 μmol/L for the spontaneous release, 23.4±2.4 μmol/L for KCl-evoked release, and 24.3±1.8 μmol/L for veratridine-evoked release. But GABA spontaneous release and evoked release were unaffected. The study showed that thiopental sodium with clinically related concentrations could inhibit the release of glutamate, but had no effect on the release of GABA from rats prefrontal cortical synaptosomes.

Effects of intrathecally administerd NaV1. 8 antisense oligonucleotide on the expression of sodium channel mRNA in dorsal root ganglion.

SummaryNeuropathic pain has been hypothesized to be the result of aberrant expression and function of sodium channels at the site of injury. To investigate the effects of NaV1.8 antisense oligonucleotide on the expression of sodium channel mRNA in dorsal root ganglion (DRG) neurons in chronic neuropathic pain. 24 Sprague-Dawley rats weighing 200–260 g were anesthetized with the intraperitoneal injection of 300 mg·kg−1 choral hydrate. The CCI model was made by loose ligation of sciatic nerve trunk by 4-0 chromic gut. The mechanical and thermal pain threshold were measured before operation and 1, 3, 5, 7, 9, 11, 13 days after operation. A PE-10 catheter was implanted in subarachnoid space at lumbar region. On the 7th postoperative day the animals were randomly divided into 4 groups. The drugs were injected intrathecally twice a day for 5 consecutive days in group 2–4. The animals were decapitated 14 days after the surgery. The L4–L6 DRG of the operated side was removed and crushed, and total RNA was extracted with Trizol reagent. The contralateral side was used as control. The change of NaV1.8 sodium channel transcripts was determined by RT-PCR. Pain threshold was significantly lowered after CCI as compared with that in control group and was elevated 3 days after antisense oligonucleotide injection. Sensory neuron specific TTX-R sodium channel NaV1.8 transcript was down-regulated after antisense oligonucleotide injection at the dosage of 45 μg as compared with that in CCI group (P<0.01), and it was even greater at the dosage of 90 μg. The intrathecally injected NaV1.8 antisense oligonucleotide can reduce the mechanical allodynia and thermal hyeralgesia partially by downregulating the SNS transcript expression.

The effect of nitrous oxide and isoflurane on the total RNA yield from the cochlea of the rats

The possible mechanism of inhalation anesthetics on the internal auditory impairment of the rat was investigated by determining the effect of nitrous oxide (N2O) and isoflurane on the total RNA yield from the cochlea of the rats. Thirty healthy Wistar rats were randomly divided into 3 groups: group C (control group, n=10) with a 3-h unremitting inhalation of 50% O2, group N (experiment group, n=10) with a continuous inhalation of 50% N2O+50% O2 for 3 h, and group I (experiment group, n=10) with a 3-h sustained inhalation of 2.5% isoflurane. The TRIzol in combination with RNeasy was used to respectively extract the total RNA from cochlea of rats in the 3 groups. Spectrophotometry was used to detect total RNA yield and electrophoresis to detect the quality. The total RNA extracted from the cochlea of the rats in the groups C and N was 7.69 and 6.51 μg, respectively. There was a 15% decrease in the N group as compared with group C. The total RNA from the rats in the group I was 7.32 μg, and there was hardly any change in the group as compared with the group C. The value of A 260/A 280 in groups C, N and I was 2.07, 2.04 and 2.04, respectively, showing a very high RNA purity. The result of gel electrophoresis suggested that there was no degradation in the total RNA. It was suggested that the interference of N2O on the cochlear RNA yield might be one of the reasons which cause an injury of the ear. The isoflurane shows no harm on the hearing.

Potent antioxidative potential of propofol during cardiopulmonary bypass in the adult

SummaryThe potent antioxidative potential of propofol during cardiopulmonary bypass (CPB) in adults was investigated. The selected 30 patients receiving open heart surgery under CPB were randomly divided into group A and group B. The patients in the group A and group B were given propofol (0. 1 mg. kg−1, min−1 and fentanyl (5 μg. kg−1, min−1) respectively to maintain anesthesia after aorta was cross-clamped. Blood samples were drawn pre-anesthesia, pre-CPB, at 30 min of CPB, at the end of CPB, at 1 h after CPB, at the end of operation, at 12 and 24 h postoperatively. RBC suspension was prepared and erythrocyte glucose-6-phosphate dehydrogenase (G-6-PD) and phosphofructokinase (PFK) activities, total erythrocyte reduced glutathione (GSH) and oxidized GSH (GSSG) were assayed and GSH/GSSG ratio was calculated. In the group A, G-6-PD and PFK activities and GSH/GSSG ratio were almost uneventfully during CPB and postoperatively. In the group B, G-6-PD activity was increased and PFK activity and GSH/GSSG ratio decreased significantly from 30 min of CPB until 12 h postoperatively. It was demonstrated that propofol could obviously attenuate free radical activity during CPB, while fentanyl has no effect on free radical reduction. Propofol could be beneficial as an anesthetic in patients presenting pathologies associated with free radical reactions during CPB.

Expression changes of early response genes in lung due to high volume ventilation

SummaryThe expression changes of early response genes due to ventilation with high volume in adult rats in vivo were observed. Forty SD male rats were randomly divided into control and 30, 60, 90 and 120 min ventilation groups, respectively (n=8 in each group). The animals were ventilated with tidal volume of 42 ml/kg and a PEEP level of 0 cmH2O at a rate of 40 breaths per minute in room air with a ventilator was given to the small animals. The expression of Egr-1, C-jun and IL-1β mRNA and proteins was detected by RT-PCR and immunohistochemical technique, respectively. The pathological changes in lung tissues were examined by HE staining. The results indicated that the expression of Egr-1, C-jun and IL-1β mRNA was detectable at 30th min after overventilation, but there was no significant difference in comparison with that in control group until overventilation for 60 min. However, at 90 and 120 min there was a significent increase as compared with 30 min or control group (P<0.05). The expression of Egr-1, C-jun and IL-1β detected by immunohistochemical assay also showed a similar tendency of the gradual increase. In the 120 min ventilation group, the expression intensity of Egr-1, C-jun and IL-1β proteins in lung cells was the strongest and the nuclear translocation was increased markedly in comparison with any other groups (P<0.05). HE staining suggested that the degree of lung injury was aggravated gradually with the ventialtion going on and had a similar tendency to the expression of these early response genes and proteins. The current data suggested that overventilation activated and upregulated the expression of early response genes and the expression of these genes may be taken as the early signal to predict the onset and degree of lung injury. These results may demonstrated partially that the expression of early response genes induced by the mechanical stretch is associated with biochamic lung injury.

Effects of Isoflurane on the Actions of Neuromuscular Blockers on the Muscle Nicotine Acetylcholine Receptors

SummaryIn this study, we tested the hypothesis that volatile anesthetic enhancement of muscle relaxation is the result of combined drug effects on the nicotinic acetylcholine receptors. The poly A m RNA from muscle by isolation were microinjected into Xenopus oocytes for receptor expression. Concentration-effect curves for the inhibition of Ach-induced currents were established for vecuronium, rocuranium, and isoflurane. Subsequently, inhibitory effects of NDMRs were studied in the presence of the isoflurane at a concentration equivalent to half the concentration producing a 50% inhibition alone. All tested drugs produced rapid and readily reversible concentration-dependent inhibition. The 50 inhibitory concentration values were 889 μmol/L (95% CI: 711–1214 μmol). 33.1 μmol (95 C1: 27.1–11.7 nmol) and 9.2 nmol (95% CI: 7.9–12.3 nmol) for isoflurane, rocuranium and vecuronium, respectively. Coapplication of isoflurane significantly enhanced the inhibitory effects of rocuranium and vecuronium, and it was especially so at low concentration of NMDRs. Isoflurane increases the potency of NDMRs, possibly by enhancing antagonist affinity at the receptor site.

The Development and Application of Airway Devices in China

Airway management is one of the most important tasks for anesthesiologists. Anesthesiologists are experts in airway management and have made tremendous contribution to the development of the airway devices. Chinese anesthesiologists have made significant contribution in introducing advanced airway management and developing innovative techniques and devices for airway management in China. This article overviews the development and application of airway devices in China as well as the dedication and contribution of Chinese experts in the development of novel airway devices. With the development of science and technology accompanied by the advanced knowledge in airway management, more effective and safe artificial airways will be developed for clinical practice. The authors believe that Chinese experts will continue their outstanding contribution to the development of innovative airway devices, systems and knowledge.

Effect of propofol on glutamate and γ-aminobutyric acid release from rat hippocampal synaptosomes

SummaryTo investigate the effect of propofol on the release of glutamate and γ-aminobutyric acid (GABA) from rat hippocampal synatosomes, synaptosomes was made from hippocampus and incubated with artificial cerebrospinal fluid (aCSF). With the experiment of Ca2+-dependent release of glutamate and GABA, dihydrokainic acid (DHK) and nipectic acid were added into aCSF. For the observation of Ca2+-independent release of glutamate and GABA, no DHK, nipectic acid and Ca2+ were added from aCSF. The release of glutamate and GABA were evoked by 20 μmol/L veratridine or 30 mmol/L KCl. The concentration of glutamate and GABA in aCSF was measured by using high-performance liquid chromatography (HPLC), 30, 100 and 300 μmol/L propofol significantly inhibited veratridine-evoked Ca2+-dependent release of glutamate and GABA (P<0.01 orP<0.05). However, propofol showed no effect on elevated KCl-evoked Ca2+-dependent release of glutamate and GABA (P>0.05). Veratridine or elevated KCl evoked Ca2+-independent release of glutamate and GABA was not affected significantly by propofol (P>0.05). Propofol could inhibit Ca2+-dependent release of glutamate and GABA. However, it has no effect on the Ca2+-independent release of glutamate and GABA.To investigate the effect of propofol on the release of glutamate and gamma-aminobutyric acid (GABA) from rat hippocampal synatosomes, synaptosomes was made from hippocampus and incubated with artificial cerebrospinal fluid (aCSF). With the experiment of Ca(2+)-dependent release of glutamate and GABA, dihydrokainic acid (DHK) and nipectic acid were added into aCSF. For the observation of Ca(2+)-independent release of glutamate and GABA, no DHK, nipectic acid and Ca2+ were added from aCSF. The release of glutamate and GABA were evoked by 20 micromol/L veratridine or 30 mmol/L KCI. The concentration of glutamate and GABA in aCSF was measured by using high-performance liquid chromatography (HPLC). 30, 100 and 300 micromol/L propofol significantly inhibited veratridine-evoked Ca(2+)-dependent release of glutamate and GABA (P < 0.01 or P < 0. 05). However, propofol showed no effect on elevated KCl-evoked Ca(2+)-dependent release of glutamate and GABA (P > 0.05). Veratridine or elevated KCI evoked Ca(2+)-independent release of glutamate and GABA was not affected significantly by propofol (P > 0.05). Propofol could inhibit Ca(2+)-dependent release of glutamate and GABA. However, it has no effect on the Ca(2+)-independent release of glutamate and GABA.