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As has been generally accepted, the ventricular fibrillation (VF) occasionally occuring during antimonial therapy may arise from the combined effects of antimonials on the heart muscle itself and on the vegetative nerves. Basing upon the experimental data accumulated in years, two hypotheses have been proposed to explain the nervous mechanism of the pathogenesis of this toxic arrhythmia, one emphasizing the vagal role therein and the other the sympathetic. It was reported in our previous paper that after repeated...

As has been generally accepted, the ventricular fibrillation (VF) occasionally occuring during antimonial therapy may arise from the combined effects of antimonials on the heart muscle itself and on the vegetative nerves. Basing upon the experimental data accumulated in years, two hypotheses have been proposed to explain the nervous mechanism of the pathogenesis of this toxic arrhythmia, one emphasizing the vagal role therein and the other the sympathetic. It was reported in our previous paper that after repeated challenges with ascending doses of potassium antimony tartrate (PAT) combined with fibrillating electric shocks, a large dose of PAT per se could usually induce VF, and this PAT-induced VF could be prevented by prior sympathectomy or reserpinization. In the present investigation the catecholamine (CA) content of rabbit ventricles was determined biologically under the same experimental conditions as previously described. The mean CA content of the ventricles of the saline control group was found to be 1.13±0.06μg/g wet tissue, and that of the electric shock control group 1.72±0.45μg/g, which was characterized by very wide fluctuations among different members in the group, the difference between these two control groups being, however, statistically insignificant. In the group of PAT combined with electric shocks, we noticed the same effects of PAT as previously described, namely, the lowering of VF electric threshold, acceleration of heart rate and the occurrence of PAT-induced VF, and in addition, we found that the CA content of this group significantly dropped to 0.65±0.05μg/g. The CA content of another group, in which ascending doses of PAT were similarly administered without accompaniment of electric shocks averaged 0.47±0.08μg/g, a value also significantly lower than that of the saline control. Reserpinization totally abolished the PAT-induced VF and almost completely depleted the heart's CA store. These data give direct support to our previous postulate that cardiac catechol amines play an important role in the development of the PAT-induced VF. Besides CA content, the acetylcholine (ACh) content of the ventricles of groups of rabbits were also assayed biologically. The saline control group gave a mean value of 0.323±0.013 μg/g, which could neither be changed by PAT in a single large dose or in a course of "3 days treatment", nor by prior vagotomy or atropinization in addition to a large dose of PAT. Moreover, reserpine, in doses effectively protecting rabbits against the PAT-induced VF, did not materially change the ACh content of rabbit ventricles, while larger doses of it markedly elevated that of guinea pig ventricles. From these results, another postulate of ours that the vagus does not take an essential part in this experimental arrhythmia seems to be further substantiated.

前文报导,在麻醉兎观察酒石酸銻鉀(簡称銻鉀)对电致心室顫动的影响实驗中,发現在实驗后期,大剂量銻鉀本身也能产生心室顫动,而这种銻致性心室顫动能被預先切断交感神經或利血平化所防止。本文采用与前文相同的实驗模型和条件,对家兎心室內儿茶酚胺含量进行了生物测定。发現盐水对照组心室儿茶酚胺含量平均为1.13±0.06微克/克。电刺激对照組为1.72±0.45,虽与盐水对照组相比在統計学上差別不显著,但波动較大。在电刺激加銻鉀组中,銻鉀能显著降低全部动物的电致顫阈,稍加速心率,并使6/11兎出現銻致性心室顫动,心室儿茶酚胺含显著减少至0.65±0.05。单注射銻钾組心肌儿茶酚胺含量平均为0.47±0.08,較盐水对照組显著减少,但与电刺激加銻鉀组差別不显著。利血平化(0.1毫克/公斤/天,共2次)后,兎心儿茶酚胺充份地被耗竭,含量降至0.032±0.003,耗竭程度达97%。利血平化后电刺激加銻鉀组的心室儿茶酚胺含量为0.041±0.010,銻致性心室顫动并不出現。上述資料对前文的推論提出直接証明,卽儿茶酚胺在該种心律紊乱发病机制中具有重要意义。除儿茶酚胺含量外,我們又进行了心室乙酰胆碱含量的测定,发現正常盐水对照家兎心...

前文报导,在麻醉兎观察酒石酸銻鉀(簡称銻鉀)对电致心室顫动的影响实驗中,发現在实驗后期,大剂量銻鉀本身也能产生心室顫动,而这种銻致性心室顫动能被預先切断交感神經或利血平化所防止。本文采用与前文相同的实驗模型和条件,对家兎心室內儿茶酚胺含量进行了生物测定。发現盐水对照组心室儿茶酚胺含量平均为1.13±0.06微克/克。电刺激对照組为1.72±0.45,虽与盐水对照组相比在統計学上差別不显著,但波动較大。在电刺激加銻鉀组中,銻鉀能显著降低全部动物的电致顫阈,稍加速心率,并使6/11兎出現銻致性心室顫动,心室儿茶酚胺含显著减少至0.65±0.05。单注射銻钾組心肌儿茶酚胺含量平均为0.47±0.08,較盐水对照組显著减少,但与电刺激加銻鉀组差別不显著。利血平化(0.1毫克/公斤/天,共2次)后,兎心儿茶酚胺充份地被耗竭,含量降至0.032±0.003,耗竭程度达97%。利血平化后电刺激加銻鉀组的心室儿茶酚胺含量为0.041±0.010,銻致性心室顫动并不出現。上述資料对前文的推論提出直接証明,卽儿茶酚胺在該种心律紊乱发病机制中具有重要意义。除儿茶酚胺含量外,我們又进行了心室乙酰胆碱含量的测定,发現正常盐水对照家兎心室乙酰胆碱含量平均为0.323±0.013微克/克。銻鉀一次大剂量注射或銻鉀三日給药法均不明显改变其含量。預先切断迷走神經或注射大剂量阿托品后再給大剂量銻鉀,也对心室乙酰胆碱含量无明显影响。因此完全不能証实黄铭新等关于这方面的报导。利血平在对家兎銻致性顫动具有防止作用的剂量下并不影响心室乙酰胆碱含量,較大剂量却能显著提高豚鼠心室乙酰胆碱的含量(P<0.01)。这些資料也完全支持前文所作出的推論,卽迷走神經在这种实驗性心律紊乱发病机制中的意义不大。

The mechanisms of depletion of the tissue noradrenaline (NA) by tyramine, reserpine and guanethidine are not entirely the same. The influences of phenelzine on the depletion of myocardial NA by these drugs were compared in rats. The NA was separated by Al_2O_3 adsorption and assayed on rat's blood pressure. The average content of NA in normal rat heart was found to be 0.93μg/g. A daily intraperitoneal injection of phenelzine 20 mg/kg for 3 days raised the NA content up to 1.26μg/g. The...

The mechanisms of depletion of the tissue noradrenaline (NA) by tyramine, reserpine and guanethidine are not entirely the same. The influences of phenelzine on the depletion of myocardial NA by these drugs were compared in rats. The NA was separated by Al_2O_3 adsorption and assayed on rat's blood pressure. The average content of NA in normal rat heart was found to be 0.93μg/g. A daily intraperitoneal injection of phenelzine 20 mg/kg for 3 days raised the NA content up to 1.26μg/g. The increase was statistically significant. Subcutaneous injection of tyramine hydrochloride 20 mg/kg reduced in 2 hours the NA content to 0.56μg/g. If phenelzine was administered for 3 days prior to the tyramine injection, the NA content was further brought down to 0.39μg/g. Intraperitoneal injection of reserpine 1 mg/kg almost depleted the NA in 5 hours. But if the reserpine was given after pretreatment with phenelzine for 3 days, the myocardial NA was only half depleted. Increasing the dose of reserpine to 2 mg/kg diminished the NA content to one half in 5 hours, and yielded a near depletion in 15 hours. Intraperitoneal injection of guanethidine sulphate 20 mg/kg caused a well-nigh complete depletion in 5 hours. If guanethidine sulphate 20—100 mg/kg was given subsequent to a 3-day administration of phenelzine, the NA did not decrease. Subsequent to a 3-day administration of phenelzine, intraperitoneal injection of guanethidine and then injection of reserpine or tyramine decreased the NA amount to about 50%. If guanethidine or reserpine was given prior to phenelzine, the NA-depleting action of guanethidine was abolished, but that of reserpine persisted. The above results may be summarized by saying that the NA-releasing action of tyramine seemed to be augmented, that of reserpine was partly diminished and that of guanethidine was wholly antagonized by phenelzine. Referring to results reported previously~[7] it is inferred that the sympatholytic action of phenelzine may be related to interference with the release of NA.

酪胺、利血平和胍乙啶减少組織內NA的机制不尽相同。本实驗比較苯乙肼对它們釋放大白鼠心脏NA的作用。心脏的NA用氧化鋁吸附分离后用大鼠血压法檢定。正常大白鼠心脏NA含量为0.93微克/克。每天腹腔注射苯乙肼20毫克/公斤,共3天,NA含量为1.26微克/克,有明显的增加。皮下注射酪胺20毫克/公斤后2小时,心脏NA含量减少为0.56微克/克;給苯乙肼3天后再給酪胺,NA量更减至0.39微克/克。腹腔注射利血平1毫克/公斤后5小时,心脏NA已几乎耗尽;給苯乙肼3天后再給同剂量的利血平,NA含量只减少一半左右;加大利血平剂量为2毫克/公斤,也仅能减低一半的量,至15小时已近耗尽。腹腔注射胍乙啶20毫克/公斤后5小时,NA已近耗尽;給苯乙肼3天后再注射胍乙啶20—100毫克/公斤,心脏NA未見减少。給苯乙肼3天后,腹腔注射胍乙啶,然后再給利血平或酪胺,NA减少一半。預先給利血平或胍乙啶,再給一次苯乙肼,胍乙啶的釋放作用完全被对抗,而利血平仍有耗尽心脏NA的作用。根据以上結果,苯乙肼似能加强酪胺釋放心脏NA的作用,能部分减少利血平对心脏,NA的耗尽作用,但可完全对抗胍乙啶的釋放作用。結合前文結果推論苯乙肼的抗交感作用是...

酪胺、利血平和胍乙啶减少組織內NA的机制不尽相同。本实驗比較苯乙肼对它們釋放大白鼠心脏NA的作用。心脏的NA用氧化鋁吸附分离后用大鼠血压法檢定。正常大白鼠心脏NA含量为0.93微克/克。每天腹腔注射苯乙肼20毫克/公斤,共3天,NA含量为1.26微克/克,有明显的增加。皮下注射酪胺20毫克/公斤后2小时,心脏NA含量减少为0.56微克/克;給苯乙肼3天后再給酪胺,NA量更减至0.39微克/克。腹腔注射利血平1毫克/公斤后5小时,心脏NA已几乎耗尽;給苯乙肼3天后再給同剂量的利血平,NA含量只减少一半左右;加大利血平剂量为2毫克/公斤,也仅能减低一半的量,至15小时已近耗尽。腹腔注射胍乙啶20毫克/公斤后5小时,NA已近耗尽;給苯乙肼3天后再注射胍乙啶20—100毫克/公斤,心脏NA未見减少。給苯乙肼3天后,腹腔注射胍乙啶,然后再給利血平或酪胺,NA减少一半。預先給利血平或胍乙啶,再給一次苯乙肼,胍乙啶的釋放作用完全被对抗,而利血平仍有耗尽心脏NA的作用。根据以上結果,苯乙肼似能加强酪胺釋放心脏NA的作用,能部分减少利血平对心脏,NA的耗尽作用,但可完全对抗胍乙啶的釋放作用。結合前文結果推論苯乙肼的抗交感作用是与影响NA的釋放有关。

The mixed pituitary glands of Cyprinus carpio, Carassius auratus, Hypophthalmichthys molitrix and Aristichthys nobilis were extracted with ethanol. Then the crude gonadotropin was fractionated by chromatography on DEAE-cellulose and gel filtration. Biological activity as assayed by ovulation test of the loach (Misgurnus anguillicaudatus) in vivo was recognized only in the second fraction (Sephadex G-100). Effective dose of induced ovulation was 1μg/g body weight. The gonadotropin (SG-Ⅱ-2) exhibited...

The mixed pituitary glands of Cyprinus carpio, Carassius auratus, Hypophthalmichthys molitrix and Aristichthys nobilis were extracted with ethanol. Then the crude gonadotropin was fractionated by chromatography on DEAE-cellulose and gel filtration. Biological activity as assayed by ovulation test of the loach (Misgurnus anguillicaudatus) in vivo was recognized only in the second fraction (Sephadex G-100). Effective dose of induced ovulation was 1μg/g body weight. The gonadotropin (SG-Ⅱ-2) exhibited a single band on polyacrylamide gel electrophoresis. The determinable range of this gonadotropin radioimmunoassay was 0.1~16ng.Serum gonadotropin levels of carp (Cyprinus carpio) have been determined by means of radioimmunoassay through the whole reproductive process. Particularly the female exhibited a significant and higher peak during the sexual behaviour and spawning. After the spawning, the serum gonadotropin levels have a quick drop down. This investigation provided some new data for reproductive physiology of fish.

本文报道用鲤、鲢等鲤科鱼混合垂体经乙醇抽提、DEAE-纤维素层析及葡聚糖凝胶过滤来纯化促性腺激素(GTH)的方法。所得GTH初步纯化品(SG-Ⅱ-1)的产卵有效剂量为1微克/1克泥鳅体重。其最终纯化品(SG-Ⅱ-2)在聚丙烯酰胺电泳谱中呈示为一条带,可供作放射免疫测定系统中的标记抗原。GTH放射免疫测定法的检测范围为0.1~16毫微克。在鲤鱼产卵季节,用放射免疫测定血清中GTH含量的变化,表明雌雄鱼在配组后血清中GTH含量逐渐上升,特别是雌鱼,在发情产卵时出现显著的高峰,随产卵活动的停止而下降,呈现出明显的产卵前后血清中GTH含量变化规律。这为研究鱼类生殖生理提供一些新的资料。

 
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