可吸收内固定物治疗关节内骨折

我院自1996年～1998年1月,使用可吸收骨折内固定物治疗关节内骨折24例,疗效满意,结果报告如下。 临床资料 1.一般资料24例关节内骨折患者,男18例、女6例,年龄19～55岁,平均34岁。其中髓臼后缘骨折8例、踝关节骨折6例、胫骨髁间嵴骨折3例、股骨外髁骨折1例、股骨头骨折3例、肽骨头骨折2例、巴通骨折1例,均为新鲜骨折。其中2例合并股骨干骨折,1例合并骨盆骨折,2例合并胫腓骨骨折。 2手术方法(1)材料:采用芬兰产高分子聚合物——聚乙交酯(SR-PGA)和聚丙交酯(SR-PLLA)制成的自身增强拉力螺钉和内固定棒。(2)操作步骤:以髓留后缘骨折为例,腰…     

跟骨关节内骨折内固定手术治疗

目的：探讨波及距下关节跟骨骨折的手术方法和疗效。方法：对63例72足波及距下关节的跟骨骨折行切开复位钢板内固定治疗。结果：全部患者均获得7—29个月的随访,平均18个月,按Maryland评分标准进行评价手术效果：优28足,良33足,可8足,差3足,优良率84．7％。结论：切开复位钢板内固定可作为治疗波及距下关节跟骨骨折的主要方法。     

钢板内固定治疗跟骨关节内骨折

目的 评价切开复位内固定治疗跟骨关节内骨折的疗效。方法 用切开复位内固定治疗跟骨关节内骨折22例。结果术后均得到随访．随访时间6～31个月、平均18、4个月。采用Maryland足部评分标准评价手术效果．优15足，良7足．可3足．优良率88．0％。结论 切开复位内固定是治疗跟骨关节内骨折的理想方法。     

关节内松质骨骨折加压内固定治疗

关节内松质骨骨折行加压固定 ,不仅有利于骨折愈合 ,而且有助于维持骨折的稳定性。我科于1986年 6月至 2 0 0 0年 8月分别采用ＡＯ型松质骨加压螺钉和双端螺纹松质骨加压螺钉治疗关节内松质骨骨折共 5 2例 ,取得较满意结果。本文对两种螺钉的特点、优缺点和在使用上存在的问题进行比较分析。1　临床资料5 2例中男 38例 ,女 14例 ;年龄 2 5～ 64岁 ,平均35岁。用ＡＯ螺钉治疗 38例 (4 4处骨折 ) ,骨折部位16个 ,包括上下肢关节。 4 4处骨折中 ,新鲜骨折 4 1处 ,陈旧骨折 3处。术中加用其它内固定有钢板 13例 ,普通螺钉 6例 ,骨栓 3例。术后使…     

中晚期盆腔内恶性肿瘤的血管内介入治疗

盆腔内恶性肿瘤患者早期多无典型的临床体征和症状，当有症状和临床表现时大多属于晚期，由于盆腔内组织器官复杂，大多患者因病变侵犯周围器官或淋巴转移失去手术机会，随着介入放射学的发展，经供血动脉进行灌注化疗和栓塞已成了不能手术切除恶性肿瘤治疗的主要方法，现将我院血管内介入治疗的24例盆腔内恶性肿瘤报道如下。     

医院内感染

医院内感染（Ｎｏｓｏｃｏｍｉａｌ　ｉｎｆｅｃｔｉｏｎ　Ｈｏｓｐｉｔａｌ　ｉｎｆｅｃｔｉｏｎ）也称医院获得性感染（Ｈｏｓｐｉｔａｌ　ａｃｑｕｉｒｅｄ　ｉｎｆｅｃｔｉｏｎ），是指病人在人院时不存在且又不处于潜伏期，而且在住院过程中获得的感染，也包括住院时处于感染潜伏期，出院后才出现症状。简称在医院内发生的感染（也就是住院期间）。潜伏期不明的感染和发生于住院后８—７２ｈ内，应视为医院内感染。医院感染的主要对象应该是住院病人和医院职工。由于医院职工健康状况良好，机体的免疫功能正常，不易受感染；而住院病人都存在一定的基础疾病，免疫功能低下，很易受感染，因此医院感染的最主要对象是住院病人，多系医源性感染（ｉａｔｒｏｇｅｎｉｃ　ｉｎｆｅｃｔｉｏｎ）。与之相对应的概念社区性感染（ｃｏｍｍｕｎｉｔｙ　ｉｎｆｅｃｔｉｏｎ）指发生于院外正常人群的感染。     

The effect of intra-arterial endothelin on resting blood flow and sympathetically mediated vasoconstriction in the forearm of man.

1. The hypothesis that endothelin (ET) influences sympathetically mediated vasoconstriction was investigated in 13 healthy, male subjects. 2. ET (1 pmol min-1) was infused for 60 min into the left brachial arteries of seven healthy male subjects. Resting forearm blood flow, and sympathetic vasoconstriction produced by lower body negative pressure (LBNP; 15 mm Hg), was measured in both arms by strain gauge plethysmography. In a further six subjects, noradrenaline (NA) was infused intra-arterially at doses of 150-600 pmol min-1, with and without co-infusion of ET (1 pmol min-1), with blood flow measured in both forearms. 3. ET produced a small but significant reduction of blood flow in the infused forearm from 3.9 +/- 0.6 ml 100 ml-1 min-1 during infusion of saline, to 3.3 +/- 0.7 ml 100 ml-1 min-1 during infusion of ET at 60 min (P less than 0.05). Blood flow in the non-infused forearm was not altered by ET infusion. 4. NA produced a significant and dose-dependent reduction of blood flow in the infused forearm from 3.13 +/- 0.5 ml 100 ml-1 min-1 during saline infusion, to 1.49 +/- 0.2 ml 100 ml-1 min-1 with NA at 600 pmol min-1 (P less than 0.001). During co-infusion of ET, blood flow was reduced similarly in the infused arm from 3.15 +/- 0.7 ml 100 ml-1 min-1 during saline infusion to 1.55 +/- 0.2 ml 100 ml-1 min-1 with NA at 600 pmol min-1. Blood flow in the non-infused arm was not altered by ET and NA infusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Nonadrenergic sympathetic vascular control of the human forearm in hypertension: possible involvement of neuropeptide Y.

Animal experimental evidence suggests that neuropeptide Y (NPY) is coreleased with norepinephrine (NE) from sympathetic nerve endings and is involved in nonadrenergic neurogenic vascular control of skeletal muscle. We wished to determine whether these findings may be extended to humans. Forearm blood flow (venous occlusion plethysmography) and the regional overflows of NE and NPY-like immunoreactivity (NPY-LI) were studied at rest and during sympathetic nerve activation by lower body negative pressure (LBNP; -10 mm Hg, 10 min) in 10 hypertensive men before and after local alpha-adrenergic blockade by a dose of phenoxybenzamine (60 micrograms x 100 ml-1 x min-1 for 60 min), which most markedly attenuated responses to exogenous NE; propranolol (10 micrograms x 100 ml-1 x min-1) was present throughout. Phenoxybenzamine increased forearm blood flow at rest (11.5 +/- 1.0 vs. 3.9 +/- 0.3 ml x 100 ml-1 x min-1; p less than 0.001). LBNP-evoked reduction of forearm blood flow (37 +/- 2%, p less than 0.001) was attenuated (p less than 0.001) but not abolished (18 +/- 2%, p less than 0.001) by phenoxybenzamine. LBNP increased the overflow of NE from 5.0 +/- 1.7 to 8.2 +/- 3.0 pmol x 100 ml-1 x min-1 (p less than 0.05) and that of NPY-LI from -9.0 +/- 4.4 to 8.0 +/- 4.9 fmol x 100 ml-1 x min-1 (p less than 0.05) after phenoxybenzamine; effects on the evoked overflows of NE and NPY-LI before phenoxybenzamine were slight. Prejunctional inhibitory alpha-adrenoceptors may thus modulate NPY release as well.(ABSTRACT TRUNCATED AT 250 WORDS)     

The potassium channel opening drug cromakalim produces arterioselective vasodilation in the upper limbs of healthy volunteers

1. The effect of the K+ channel opening drug cromakalim on forearm blood flow during direct infusion into the brachial artery, and on the size of noradrenaline preconstricted hand veins during infusion directly into the vein, was studied in eight healthy volunteers. 2. Cromakalim (0.01-10.0 micrograms min-1) produced a dose-dependent increase in blood flow in the infused forearm, from 5.4 +/- 2.5 to 15.1 +/- 7.3 ml 100 ml-1 forearm min-1 at 10 micrograms min-1 (P less than 0.001). The half-time of offset of its action was 30 min. There was no change in blood flow in the non-infused forearm. 3. There was no increase in the size of noradrenaline pre-constricted dorsal veins during local infusion of cromakalim (0.001-1.0 microgram min-1). Glyceryl trinitrate (0.4 microgram min-1) however, completely reversed the constriction to noradrenaline (P less than 0.001). 4. The clear arterioselectivity of cromakalim, as with other members of this new class of drug, accords with the dependency of venoconstriction on receptor-operated, rather than potential-operated mechanisms which are of importance in resistance vessels. With this haemodynamic profile cromakalim may prove of value in the treatment of arterial hypertension.     

Regional involvement of an endothelium-derived contractile factor in the vasoactive actions of neuropeptide Y in bovine isolated retinal arteries.

1. In vitro experiments in a microvascular myograph were designed in order to investigate the effects of human neuropeptide Y (NPY), its receptor subtype and the mechanisms underlying NPY actions in bovine isolated retinal proximal (PRA) and distal (DRA) arteries. 2. A single concentration of NPY (10 nM) induced a prompt and reproducible contraction which reached a plateau within 1-4 min, after which the response returned to baseline over the next 2-10 min. Cumulative addition of NPY induced concentration-dependent contractions of bovine retinal arteries, with an EC50[M] of 1.7 nM and a maximal response equal to 54 +/- 8% of Emax (absolute maximal contractile levels of vessels) and not different from that obtained by a single addition of the peptide. There were no significant differences in either sensitivity or maximal response to NPY between PRA and DRA. 3. Porcine NPY and the selective Y1-receptor agonist, [Pro34]NPY, also induced concentration-dependent contractions of the retinal arteries with a potency and maximal response not significantly different from those of human NPY; in contrast, the selective Y2-receptor agonist, NPY(13-36), caused only a 5% contraction at the highest concentration used. 4. Removal of extracellular Ca2+ or pretreatment with the 1,4-dihydropyridine Ca(2+)-channel blocker, nifedipine (1 microM), reduced the contractile response of 10 nM NPY to 18.4 +/- 3.3% (n = 6) and 18.6 +/- 3.9% (n = 6); respectively, of the controls. 5. Mechanical removal of the endothelium depressed the maximal contraction elicited by NPY in PRA but did not affect either sensitivity or maximal response to the peptide in DRA. In endothelium-intact arteries, blockade of the cyclo-oxygenase pathway with 3 microM indomethacin increased resting tension in both PRA and DRA and significantly inhibited sensitivity and maximal contraction to NPY of PRA and DRA, respectively. The thromboxane A2 (TXA2)/prostaglandin H2 (PGH2) receptor antagonist, SQ30741, reduced both sensitivity and maximal contraction to NPY in PRA but not in DRA. 6. In endothelium-denuded PRA, indomethacin but not SQ30741 significantly reduced NPY maximal response and induced a marked increase in resting tension suggesting a basal release of a vasodilator prostanoid from smooth muscle cells. 7. Superoxide dismutase (SOD) (150 u ml-1) reduced the maximal contraction to NPY in PRA. Inhibition of the nitric oxide (NO) synthase with NG-nitro-L-arginine (L-NOARG) (30 microM), enhanced sensitivity and maximal contraction to NPY in both PRA and DRA. In the presence of L-NOARG, SOD did not further inhibit NPY responses in PRA. 8. NPY (10 nM) induced a 2.9 fold leftwards shift of the noradrenaline concentration-response curves in PRA and increased maximal response by 50 +/- 16%. Neither 1 nor 10 nM NPY affected noradrenaline responses in DRA. [Pro34]NPY (10 nM), but not NPY(13-36), mimicked the potentiating effect of NPY on noradrenaline responses in PRA. 9. TXA2 analogue, U46619, at 10 nM elicited 3.6 fold leftwards shift of the noradrenaline concentration-responses curves in PRA and increased the maximal contraction by 32 +/- 3%, whereas in the presence of 1 microM SQ30741, 10 nM NPY did not potentiate noradrenaline responses. 10. The present results indicate that NPY may play a role in the regulation of retinal blood flow through both a direct contractile action, independent of the vessel size and a potentiation of the responses induced by noradrenaline in the proximal part of the retinal circulation, both effects being mediated by Y1 receptors. NPY promotes Ca2+ influx through voltage-dependent Ca2+ channels and stimulates the synthesis of contractile prostanoids in PRA and DRA, although only in PRA does the peptide trigger the release of an endothelium-derived contractile factor which facilitates the contraction and also seems to account for the potentiating effect of NPY.     

Nifedipine kinetics in the rat and relationship between its serum concentrations and uterine and cardiovascular effects.

1. The kinetics of nifedipine and the relationship between its serum concentration and uterine and cardiovascular effects were investigated in 3 groups of animals. These were ovariectomized (ovx) anaesthetized non-pregnant rats following bolus i.v. injection (400 micrograms kg-1) and during 300 min infusion (10 micrograms kg-1 min-1) and ovx, progesterone-treated late pregnant rats during infusion. Also, the kinetics were determined in ovary-intact late pregnant rats following bolus i.v. injection (400 micrograms kg-1). 2. Measurement of serum nifedipine concentrations after bolus i.v. injection in ovx non-pregnant rats showed a biexponential decay with time from which the following parameters were calculated: V beta = 300 +/- 30 ml kg-1; rate constants k12 = 0.51 +/- 0.18 min-1; k21 = 0.07 +/- 0.02 min-1; ke1 = 0.10 +/- 0.05 min-1; elimination clearance = 2.4 +/- 0.2 (ml min-1) kg-1; t1/2 alpha = 2.5 +/- 1.0 min; t1/2 beta = 102 +/- 15 min. In intact pregnant rats, a biexponential decay of serum nifedipine concentrations with time was also observed after bolus i.v. administration with similar parameters to non-pregnant animals. These kinetic parameters, used to calculate serum nifedipine concentrations obtained during infusion, predicted values similar to experimental values for 180 min, but thereafter slightly underestimated experimental values. 3. Immediate reductions in uterine contractions, mean blood pressure and heart rate were observed following bolus i.v. injection of nifedipine to ovx non-pregnant rats, with returns towards control values as serum nifedipine concentrations declined. IC15 values (15% change from baseline), calculated from log10 serum concentration-response curves, of 0.3 +/- 0.05 micrograms ml-1 for inhibition of uterine contractions, 0.8 +/- 0.3 micrograms ml-1 for depression of blood pressure and 3.8 +/- 1.0 micrograms ml-1 for reduction in heart rate were obtained. 4. In ovx non-pregnant rats, nifedipine infusion produced a maximum reduction in integral of uterine contractions of 70% by 120 min and a maximum reduction of 15% in heart rate. Mean blood pressure was not significantly different from vehicle-treated rats. IC15 values were 0.7 +/- 0.1 micrograms ml-1 and 2.8 +/- 0.6 micrograms ml-1 for inhibition of uterine contractions and heart rate respectively. 5. In ovx, progesterone-treated late pregnant rats, nifedipine infusion produced similar serum concentrations to those of non-pregnant rats but completely abolished uterine contractions by 70 min. Maximum reductions of 30% in heart rate and blood pressure were observed.(ABSTRACT TRUNCATED AT 400 WORDS)     

The α₁-, but not α₂-, adrenoceptor in the nucleus accumbens plays an inhibitory role upon the accumbal noradrenaline and dopamine efflux of freely moving rats

In vivo microdialysis was used to analyse the role of the α(1)- and α(2)-adrenoceptor subtypes in the regulation of noradrenaline and dopamine efflux in the nucleus accumbens of freely moving rats. Intra-accumbal infusion of α(1)-adrenoceptor agonist methoxamine (24pmol) failed to alter the noradrenaline efflux, but decreased the dopamine efflux. The intra-accumbal infusion of α(1)-adrenoceptor antagonist prazosin (6, 600 and 6000pmol) produced a dose-related increase and decrease of the noradrenaline and dopamine efflux, respectively. An ineffective dose of prazosin (6pmol) counteracted the methoxamine (24pmol)-induced decrease of dopamine efflux. The prazosin (6000pmol)-induced increase of noradrenaline efflux, but not the decrease of dopamine efflux, was suppressed by the co-administration of an ineffective dose of methoxamine (0.024pmol). Neither the α(2)-adrenoceptor agonist clonidine (300pmol) and UK 14,304 (300pmol) nor the α(2)-adrenoceptor antagonist RX 821002 (0.6, 3, 600 and 6000pmol) significantly affected the accumbal noradrenaline and dopamine efflux. The doses mentioned are the total amount of drug over the 60-min infusion period. The present results show that (1) accumbal α(1)-adrenoceptors which are presynaptically located on noradrenergic nerve terminals inhibit the accumbal noradrenaline efflux, increasing thereby the accumbal dopamine efflux, (2) accumbal α(1)-adrenoceptors which are postsynaptically located on dopaminergic nerve terminals inhibit the accumbal dopamine efflux, and (3) accumbal α(2)-adrenoceptors play no major role in the regulation of accumbal efflux of noradrenaline and dopamine.     

Dexamethasone attenuates the depressor response induced by neuropeptide Y microinjected into the nucleus tractus solitarius in rats

An investigation was made of the effect of dexamethasone (Dex) injection into the nucleus tractus solitarius (NTS) on the cardiovascular response to neuropeptide Y in rats. Dex (39 pmol) injected into the NTS inhibited the hypotension and bradycardia caused by NPY (5 pmol) with a short latency (10 min) and a long duration of action (up to 4 h). The rapid inhibition by Dex (39 pmol) of the cardiovascular response to NPY was not blocked by pretreatment with the glucocorticoid receptor blocker, RU38486 (47 or 117 pmol respectively), but was reversed by bicuculline (30 pmol). Microiontophoresis of NPY (0.01 mM, pH 6.5) into the NTS increased the spontaneous firing of the majority (68.4%) of baroreflex-excited cells, but decreased the firing of most (73.7%) baroreflex-inhibited cells. In contrast, Dex (0.02 M, pH 6.5) decreased the spontaneous firing of the majority of baroreflex-excited cells (42.1% of normal response) and decreased the inhibition of baroreflex-inhibited cells (47.5% of normal response). The responses of the majority of baroreceptive cells to NPY were blocked by iontophoretic administration of Dex. Dex (200 microM) increased the delayed rectifier outward K+ current by 31.4+/-1.1% (n=5), whereas NPY alone, at a concentration of 1.5 microM, inhibited the current by 28.6+/-0.8% (n=5). In the presence of Dex (200 microM), addition of NPY (1.5 microM) had no effect on the current. In conclusion, NTS-administered-Dex attenuated the cardiovascular response to NPY injected into the same area via a rapid membrane effect, which was mediated by an action on GABA(A) receptors and on the delayed rectifier outward K(+) channel.     

LACK OF EFFECT OF AGE ON THE CARDIOVASCULAR RESPONSE TO NEUROPEPTIDE Y INJECTION IN THE RAT NUCLEUS TRACTUS SOLITARIUS

1. Neuropeptide Y (NPY) is colocalized with catecholamines in central regions involved in blood pressure regulation and exerts depressor responses in the nucleus tractus solitarius (NTS). Ageing is accompanied by a decline in baroreflex function and a reduction in NPY concentrations in some brain areas. The present study investigated whether the cardiovascular response to NPY microinjection into the NTS and medullary NPY concentrations were conserved in aged rats. 2. Neuropeptide Y (6 pmol in 100 nL) unilaterally injected into the NTS of anaesthetized 3- or 17-month-old male Sprague-Dawley rats produced a prompt 9–10% fall in mean arterial pressure (MAP), which tended to last longer in aged rats. Decreases in heart rate (HR) observed following NPY administration into the NTS were modest but more prolonged than the depressor responses, ANOVA with repeated measures demonstrated no significant effect of age on the MAP or HR response to NPY injection into the NTS. Neuropeptide Y concentrations in the dorsomedial and ventrolateral medulla were not different between the two age groups. 3. Thus, the depressor and bradycardic responses to exogenous NPY administration in the NTS were maintained with age, in keeping with the observation of similar medullary NPY concentrations in adult and aged rats.     

Comparison of the acute vascular effects of frusemide and bumetanide.

The acute peripheral vascular and diuretic effects of intravenous frusemide 10 mg and 20 mg were compared with those of bumetanide 250 micrograms and 500 micrograms in a group of 10 salt depleted volunteers. Significant reductions in forearm blood flow (FBF) were observed after frusemide 10 mg (-0.77 ml 100 ml-1 min-1 P less than 0.05) and 20 mg (-0.75 ml 100 ml-1 min-1 P less than 0.01 at 15 min). No changes were observed after bumetanide. The reductions in blood flow produced by frusemide were significantly different from those of bumetanide (P less than 0.05) at 15 min. Increases in venous capacitance (VC) and mean arterial blood pressure (MAP) were observed after frusemide but these differences were not statistically different from placebo or bumetanide. No increases were seen after bumetanide. Plasma aldosterone concentrations were unchanged after either drug but plasma renin activity (PRA) was increased after frusemide 10 mg (4.42 +/- 1.01----8.50 +/- 1.90 ng A I ml-1 h-1 P less than 0.01) and 20 mg (4.01 +/- 0.72----7.81 +/- 2.27 ng A I ml-1 h-1 P less than 0.05). No increases were observed after bumetanide and significant differences between bumetanide and frusemide were observed (P less than 0.01). This study demonstrates that the acute peripheral arterial effects of frusemide are not observed after comparable diuretic doses of bumetanide. The differences appear to be related to the ability of the drugs to stimulate acute renin release from the kidney.