左主干狭窄的外科治疗

目的 探讨左主干狭窄（ＬＭＳ）≥５０％患者的外科治疗效果。方法 ４２例ＬＭＳ的患者接受了冠状动脉旁路移植术（ＣＡＢＧ）。平均年龄６８．７岁。ＬＭＳ介于５０％￣７５％者１６例,大于７５％者２６例,不稳定型心绞痛２９例。按ＣＣＳＳ标准心绞痛分级,Ⅰ级２例,Ⅱ级５例、Ⅲ级１７例,Ⅳ级１８例。左室射血分数小于５０％者２４例。结果 术前平均住院时间２．３ｄ人均移植血管３．３根,无手术死亡。术后所有患者心绞痛     

Rodent model of chronic central pain after spinal cord contusion injury and effects of gabapentin

Spinal cord injury (SCI) often results in abnormal pain syndromes in patients. We present a recently developed SCI mammalian model of chronic central pain in which the spinal cord is contused at T8 using the NYU impactor device (10-g rod, 2.0-mm diameter, 12.5-mm drop height), an injury which is characterized behaviorally as moderate. Recovery of locomotor function was assessed with an open field test and scored using the open field test scale (BBB scale). Somatosensory tests of paw withdrawal responses accompanied by supraspinal responses to both mechanical punctate (von Frey hairs) and nonpunctate (4 mm diameter blunt probe) as well as thermal (radiant heat) peripheral stimuli were performed. Comparisons at the level of the individual animal between precontusion and postcontusion responses indicated significant increases in reactions to low threshold punctate mechanical stimuli, non-punctate stimuli and thermal stimuli (p < 0.05). To demonstrate the validity of this model as a central pain model, gabapentin, an agent used clinically for central pain, was given i.p. at 10 or 30 mg/kg. Gabapentin treatment significantly and reversibly changed the responses, consistent with the attenuation of the abnormal sensory behavior, and the attenuated responses lasted for the duration of the drug effect (up to 6 h). These results support the use of the spinal contusion model in the study of chronic central pain after SCI.     

Repeat Chlamydia trachomatis infection in women: analysis through a surveillance case registry in Washington State, 1993-1998

Repeat infections with Chlamydia trachomatis are associated with increased risk for long-term sequelae. The authors analyzed the frequency and predictors of repeat chlamydial infection by using a population-based chlamydia registry in Washington State and evaluated whether women would seek care at the same clinic for repeat infections. Among 32,698 women with an appropriately treated initial chlamydial infection during 1993-1998, 15% developed one or more repeat infections during a mean follow-up time of 3.4 years. Among women less than age 20 years at the time of initial infection, 6% were reinfected by 6 months, 11% by 1 year, and 17% by 2 years. Young age was the strongest predictor for one and two or more repeat infections after controlling for the length of follow-up and other variables. Only 36% of the repeat infections were diagnosed at the same clinical setting as the initial infection, and 50% were diagnosed at the same type of clinic. Adolescent girls had the least consistency in the source of care for chlamydia. This study suggests that efforts to prevent repeat chlamydial infection in young women remain an urgent public health priority and that the burden of repeat infection may be substantially higher than estimates from clinic-based studies.     

自体心包瓣“内皮化”的实验研究

目的 探讨有利于自体心包瓣内皮化的处理方法。方法 将体外培养小牛主动脉内皮细胞接种于不同方法处理的自体牛心包表面。采用＾３Ｈ－ＴｄＲ摄取量测定、扫描电镜及放射免疫法观察不同处理方法对接种后内皮细胞生长、前列环素（ＰＧＩ２）合成量和细胞内ｃＡＭＰ含量的影响。结果 三种不同浓度戊二醛短时间（１０ｍｉｎ）处理的心包表面内皮细胞均可生长,其中以体积分数为０．２％戊二种不同浓度戊二醛短时间（１０ｍｉｎ）处理     

Foreign metallothionein-I expression by transient transfection in MT-I and MT-II null astrocytes confers increased protection against acute methylmercury cytotoxicity

The mechanisms associated with metallothionein (MT) gene regulation are complex and poorly understood. Only a modest increase in brain MT expression levels is attained by exposure to metals, MT gene transfection, and MT gene knock-in techniques. Accordingly, in the present study, MT null astrocytes isolated from transgenic mice deficient in MT-I and MT-II genes were introduced as a zero background model of MT expression. MT protein levels were determined by western blot analysis. MT proteins in MT-I and MT-II null astrocytes were undetectable. Transient MT-I gene transfection increased the levels of foreign MT expression in MT-I and MT-II null astrocytes by 2.3-fold above basal levels in wild-type astrocytes. Intracellular Na(2)51CrO(4) efflux and D-[2,3-3H]aspartate uptake were studied as indices of acute methylmercury (MeHg) (5 microM) cytotoxicity. In MT-I and MT-II knockout astrocytes MeHg led to significant (p<0.01) increase in Na(2)51CrO(4) efflux and a significant (p<0.05) decrease in the initial rate (1 min) of D-[2, 3-3H]aspartate uptake compared to MT-I and MT-II knockout controls. Transfection of the MT-I gene in MT-I and MT-II null mice significantly (p<0.01) decreased the effect of MeHg on Na(2)51CrO(4) efflux in MT null, as well as wild-type astrocytes. MT-I gene transfection in MT-I and MT-II null astrocytes reversed the inhibitory effect of MeHg on D-[2,3-3H]aspartate uptake, such that initial rates of uptake in MT-I transfected cells in the presence and absence of MeHg (5 microM) were indistinguishable. These results demonstrate that: (1) astrocytes lacking MTs are more sensitive to MeHg than those with basal MT protein levels, (2) the MT-I gene can be overexpressed in MT-I and MT-II null astrocytes by transient MT-I gene transfection, and (3) that foreign MT expression endows astrocytes with increased resistance to MeHg.     

Adenosine release upon spinal cord injury

The hypothesis that release of adenosine following spinal cord injury (SCI) may provide neuroprotective feedback is explored. Consistent with this hypothesis, substantial release of adenosine, estimated to reach 100 microM in the extracellular space, was detected by microdialysis sampling immediately following contusion SCI. There is also considerable release of excitatory amino acids following SCI. The latter was not affected by administration of the general adenosine receptor antagonist theophylline and the A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine, implying that the adenosine released following SCI does not significantly influence the release of neurotoxic amino acids. Administration of the concentration of glutamate released upon SCI into the spinal cord caused only about 1% as much release of adenosine as did injury, evidence that elevated excitatory amino acids do not elicit an appreciable fraction of the release of adenosine that follows SCI. Results obtained suggest that release of endogenous adenosine is not neuroprotective by blocking release of excitatory amino acids following SCI.     

Marked enhancement of anti-allodynic effect by combined intrathecal administration of the adenosine A1-receptor agonist R-phenylisopropyladenosine and morphine in a rat model of central pain

BACKGROUND: There is often no satisfactory treatment for chronic pain after spinal cord injury. We have previously reported that intrathecal (i.t.) administration of the adenosine A1-receptor agonist R-phenylisopropyl-adenosine (R-PIA) or the opioid morphine has anti-allodynic effects in a model of presumed chronic central pain after photochemically induced spinal cord injury in rats. In the present study, we set out to investigate the possible interaction between i.t. R-PIA and morphine in spinally injured rats. METHODS: Sprague-Dawley rats displaying allodynia-like behaviors to mechanical and cold stimuli after photochemically induced spinal cord injury with minor motor deficits were used. R-PIA and morphine, either alone or in combination, were administered i.t. through an implanted catheter to lumbar spinal cord. RESULTS: Cumulative doses of R-PIA or morphine dose-dependently reduced the mechanical allodynia-like behavior, with a threshold of 1 nmol and 1.5 nmol, respectively. When co-administrated, R-PIA and morphine produced marked suppression of mechanical allodynia at doses of 5 pmol and 7.5 pmol, respectively. The effect of i.t. co-administration of R-PIA and morphine on cold allodynia was comparable to i.t. R-PIA alone. The combination of R-PIA and morphine did not increase adverse effects such as motor deficits in comparison to either drug alone. CONCLUSION: These results demonstrate a supra-additive interaction between the adenosine A1-receptor agonist R-PIA and morphine to reduce mechanical allodynia-like behavior in rats with chronic spinal cord injury. The combination of R-PIA and morphine administered spinally may be superior to R-PIA or morphine alone for treating such pain.     

The effects of ropivacaine on sodium currents in dorsal horn neurons of neonatal rats

We used a whole cell patch clamp technique to study the effects of ropivacaine on rat dorsal horn neurons. Under voltage clamp, ropivacaine (10-400 microM) produced a dose-dependent inhibition of sodium current. From a holding potential (V(h)) of -80 mV, sodium currents evoked by test pulses to 0 mV were inhibited by ropivacaine with a mean drug concentration required to produce 50% current inhibition (IC(50)) value of 117.3 microM, which was more than the value of the bupivacaine (IC(50) 53.7 microM). The inhibition effect of ropivacaine was also voltage-dependent. Current evoked from a V(h) of -60 mV was inhibited by ropivacaine with a mean IC(50) value of 74.3 microM, which was less than that obtained at the V(h) of -80 mV. The inhibition effect of ropivacaine on sodium current was use dependent. Repeated activation by a train of depolarizing pulses (5 Hz, 20 ms) increased the inhibitory effects of ropivacaine. The ratio amplitudes of the 20th to the first pulse were 91.2% and 71.1%, respectively, in the absence and presence of ropivacaine (50 microM). Ropivacaine also produced a significant hyperpolarizing shift of 11 mV in the steady-state inactivation curve of sodium current. The inhibition of ropivacaine on the sodium channel may contribute to the mechanism of action of local anesthetics during epidural and spinal anesthesia.