肝毒清颗粒对大鼠实验性肝纤维化的防治作用

目的 :观察肝毒清颗粒的抗纤维化作用。方法 :将Wistar雄性大鼠随机分成 6组 ,即正常对照组、模型组、肝毒清大、中、小剂量组和乙肝宁阳性组 ,采用四氯化碳诱导肝纤维化模型。于造模第 2个月始给予治疗药物。实验持续 3月后将大鼠处死取血作肝功检查及取肝组织做病理检查。结果 :肝毒清能降低AST ,升高TP、ALB ,与模型组比较 (P <0 .0 5 ) ;减轻肝脂肪变性、减少纤维组织增生、促进肝细胞再生。结论 :肝毒清对大鼠肝纤维化有明显防治作用     

Effect of generalized seizures on the structure of the sleep-waking cycle and the EEG in rats with an inherited predisposition to audiogenic convulsions

Data are presented on the effects of generalized tonic-clonic seizures on the structure of the one-day sleep-waking cycle in Krushinskii-Molodkina (KM) rats, which have a genetic predisposition to audiogenic convulsions. Spectral and correlation analysis of EEG activity in the hippocampus, caudate nucleus, medial central nucleus of the thalamus, and in the somatosensory, visual, and auditory regions of the cortex of these animals was carried out for time intervals before and after convulsions. After seizures, rats showed a prolonged (up to 3.5 h) reduction in fast-wave sleep (FWS) with no subsequent compensatory increase in this shase in the sleep-waking cycle, while a disturbance in slow-wave sleep (SWS) was minor and short-lived (not more than 2 h). It is suggested that generalized paroxysmal attacks predominantly involve disorganization of the function of the systems regulating FWS, while the synchronizing mechanisms of the brain, responsible for SWS, are affected to a lesser extent. Laboratory of the Evolution of Sleep and Waking (Director G. A. Oganesyan), I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg. Translated from Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 81, No. 10, pp. 1–8, October, 1995.     

Physicochemical properties of membranes and functional status of liver mitochondria in rats with an inherited capacity for increased radical formation

Liver mitochondria of inbred W/SSM rats with inherited increased radical formation reveal the following anomalies: inhibition of oxidative phosphorylation, a lowered transmembrane potential, and alterations in protein-lipid interaction. The membrane viscosity and osmotic stability of mitochondria are unaffected. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 119, N ^o 6, pp. 628–631, June, 1995     

Frequency and luminance sensitivity of visual evoked response in developing rats

Recent advances in the study of evoked responses settled a definition of transient and steady-state visual evoked responses (VER) and discovered the existence of Temporal Frequency Regions in humans. This paper reports data from visual responses evoked by low and high frequency stimuli. White flashes were performed in albino Sprague Dawley rats from 7 to 90 days of age. Frequency analysis technique offered the possibility to evaluate the amplitude parameters and their variations dependent on intensity of luminance and on development. The responses suggested the existence of two temporal frequency regions in the rat: a first one at about 8 Hz, related to high frequencies of EEG, a second one at frequencies ranging from 12 to 24 Hz, related to luminance sensitivity. The development of the second region is correspondent to the complete development of transient VER parameters.     

Feeding suppression induced by intra-ventricle III infusion of 1,5-anhydroglucitol

1,5-Anhydroglucitol (1-DG) has been known as an antimetabolic glucose analogue. Using gas chromatography, 1-DG was found to be physiologically present in rat serum. In order to investigate its direct and long-term effects on feeding, 1-DG was infused during the light period into the rat third ventricle in doses of 3.0, 6.0 and 12.0 mumol/rat. Its effects were then compared to those of similarly applied 2-deoxy-D-glucose (2-DG). Following initial hyperphagia, both of these glucose-analogues produced suppressive effects on feeding during the subsequent day throughout the light and dark periods. On the third day after 2-DG injection reduction of feeding did not recover completely to the pretreatment baseline levels, but it did recover after 1-DG. Both 1-DG and 2-DG caused linear dose-related hypophagia, with the slope for 1-DG being about half of that for 2-DG. It is suggested that the delayed hypophagia which followed the initial hyperphagia produced by deoxyglucose was a result of sustained inactivation of the Na-pump due to intracellular ATP deficiency caused by accumulation of deoxy-glucose-6-phosphate.     

The genetic architecture of hyponeophagia and the action of diazepam in rats

Rats of 18 genotypes derived from the Roman selected strains were tested for inhibition of feeding due to novelty (hyponeophagia) in the absence or presence of 1 mg/kg diazepam. The resulting data from three behavioral indices were subjected to the Hayman [(1954). Biometrics10:235–244], variance/covariance, Mendelian cross, and single-test cross analyses. Additive genetic variation, directional dominance for high neophobia, and some nonallelic interaction were detected. The genetic architecture of the separate behavioral indices, and its modification in the drugged subjects, was discussed in relation to evolutionary adaptation and the anxiolytic and appetite-enhancing actions of the drug.This work was jointly funded by the Science and Engineering Research Council and Imperial Chemical Industries Pharmaceuticals Ltd. through an award to R.A.S.     

Behavioral and neurochemical effects induced by subchronic combined exposure to toluene at 40 ppm and noise at 80 dB-A in rats

We investigated whether exposure to noise, in addition to its well-known potentiating effect on toluene-induced ototoxicity, may also exacerbate behavioral disturbances and brain neurochemical alterations produced by subchronic exposure to low toluene concentration. To test this hypothesis, we evaluated whether subchronic combined exposure (16 weeks, 104 h per week) to noise at 80 dB-A and toluene at 40 ppm potentiates the recently reported neurotoxic effects of subchronic exposure to 40 ppm toluene. Locomotor and rearing activities, sensitization to narcosis induced by acute toluene at high concentration, and tyrosine and tryptophan hydroxylase activities in the caudate-putamen and hippocampus were investigated in both male and female rats. Our results confirm that subchronic exposure to 40 ppm toluene significantly decreases rearing activity and leads to a sensitization to toluene-induced narcosis, as evaluated by loss of righting reflex, but fails to demonstrate any adverse effect of noise, alone or in combination with toluene. Given that toluene has addictive properties, the lack of potentiating behavioral and neurochemical effect of noise is discussed with regards to a recent study that has shown that methamphetamine neurotoxicity is potentiated by exposure to loud noise.     

Cholinergic control of gastric acid secretion

Summary In the perfused stomach preparation of the anaesthetized rat the cholinergic agonists acetylcholine (ACh) and bethanechol stimulated gastric acid secretion. Both agonists produced similar maximal acid output (70 mol/15 min) when infused intravenously. However, bethanechol was more potent, eliciting half maximal stimulation at 1.98 mol/kg/h. Secretory responses to either agonist were antagonized in a dose related fashion by blockade of muscarinic receptors with atropine. In contrast, inhibition of nicotinic receptors with hexamethonium produced a striking potentiation of ACh stimulated secretion whilst the bethanechol elicited secretion remained unaffected. In the presence of full nicotinic receptor blockade the ACh response curve was shifted to the left sixfold, half maximal stimulation being produced at 1.79 mol/kg/h. Cimetidine partially inhibited the secretory responses elicited by either ACh or bethanechol while blockade of adrenoceptors ( and ) did not affect acid output induced by cholinergic agonists. Secretion elicited by ACh is interpreted as being the composite effect of prosecretory action and an inhibitory mechanism due to the activation of nicotinic receptors. Hexamethonium, through nicotinic receptor blockade, inhibits the restricting mechanism and thus reveals the full stimulatory action of ACh.     

Plasma concentration and vascular effect of β-endorphin in spontaneously hypertensive and Wistar Kyoto rats

Summary In order to find out whether -endorphin (-E) is involved in the development of hypertension, we performed two series of experiments. Firstly, spontaneously hypertensive rats (SHR) and their normotensive Wistar Kyoto controls (WKY) were submitted to ether stress. Plasma concentrations of -endorphin-like immunoreactivity (-EI), adrenocorticotropin (ACTH) and -melanotropin (-MSH) were measured by radioimmunoassay. The basal concentration of -EI was similar in WKY and SHR, whereas WKY had higher levels of ACTH and lower levels of -MSH than SHR. In both strains acute stress enhanced the plasma concentration of -EI to the same extent and with a similar time-course. The increase of plasma -El coincided with a rise in ACTH but not -MSH. Gel chromatography of -EI revealed that plasma extracts contain similar amounts of -lipotropin- (-LPH) and -E-sized immunoreactive components, and that acute stress elevated both forms of -El. Secondly, isolated tail arteries of SHR and WKY were perfused and field stimulated with two pulses at 1 Hz. -E depressed stimulation-evoked vasconstriction with the same potency in both strains. Thus, basal and stress-induced levels of -EI did not differ in SHR and WKY. Moreover, in the tail artery of both strains the sensitivity of presynaptic opioid receptors towards -E was almost identical. If the -E sensitivity of these receptors in other arteries of WKY and SHR is also similar, a major role of the circulating peptide in the development of hypertension is rather unlikely.This work was partly supported by the Deutsche Forschungsgemeinschaft (SFB 325) Send offprint requests to B. Bucher at the above address     

Toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in cold-adapted rats

The toxicity of 60g/kg 2,3,7,8-tetrachlorodi-benzo-p-dioxin (TCDD) given IP in corn oil/5% acetone was examined in male Sprague-Dawley rats adapted to 25 °C or 4 °C ambient temperature. Cold exposure significantly reduced mean time to death and tended to increase mortality. Body weight at the time of death was reduced at both ambient temperatures to about the same extent. Thus, the rate of body weight loss was about twice as fast in nonsurvivors at 4°C than at 25 °C. There was a continuous decrease in feed intake of the non-survivors at 25 °C until death. However, no reduction in feed intake occurred in any of the rats at 4 °C ambient temperature. At 14 days after dosing all TCDD-dosed animals were hypothyroid in terms of T₄ but essentially euthyroid in terms of T₃. Oxygen consumption at 10 days after dosing was reduced to the same extent in all TCDD-dosed rats without regard to survival status. By day 20 after TCDD dosage, survivors increased their oxygen consumption at both ambient temperatures to nearly control levels whereas non-survivors were unable to do so. Body temperature of all animals remained within normal range except for the non-survivors, which showed reduced rectal temperature shortly before death. It is concluded (1) that cold adaptation aggravates the toxicity of TCDD, (2) that reduced feed intake alone cannot explain TCDD-induced wasting syndrome, (3) that reduced oxygen consumption in TCDD-treated rats may be due to reduced feed intake and/or altered thyroid hormone status, and (4) that TCDD is likely to activate metabolic pathways which represent a wasteful utilization of ingested and/or stored energy.