首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 0 毫秒
1.
2.
3.
4.
5.
6.
《Insect Biochemistry》1987,17(7):1103-1107
The effects of juvenoids on the autonomic nervous system, which controls certain physiological functions by means of special extracardiac pulsations in hemolymph pressure, have been studied in pupae of the mealworm, Tenebrio molitor. Prolonged tensiometric monitoring of the hemolymph pressure changes revealed that the extra-pupal development that had been caused by juvenoids evoked unusual reappearance of prepupal pattern of extracardiac pulsations. By contrast, the specific pharate adult types of the pulsations completely disappeared. The functioning of the autonomic nervous system was aberrant or incomplete during an unsuccessful extra-pupal ecdysis. It is suggested that malfunction of the autonomic nervous system in the extra-pupal instars may be the reason for the ecdysial failures associated with the use of juvenoids.  相似文献   

7.
8.
1. Adenosine and its analogs depress the firing of neurons in various brain regions. The primary mode of action of adenosine in exerting this effect appears to be the depression of transmitter release from presynaptic nerve terminals. This is a result of reduced calcium mobilization. 2. Adenosine uptake inhibitors and deaminase inhibitors depress the firing of central neurons. Adenosine antagonists, caffeine and theophylline, excite central neurons. Adenosine is therefore likely to be released in sufficient quantities to exert an ongoing modulation of synaptic transmission in the intact brain. 3. A number of groups of centrally active drugs inhibit adenosine uptake by brain synaptosomal preparations. These include the benzodiazepines, phenothiazines, various other sedatives and hypnotics, tricyclic antidepressants, non-steroidal anti-inflammatory analgesics, some steroids, diphenylhydantoin, puromycin and toyocamycin. 4. It is proposed that many agents with anxiolytic, sedative, analgesic or anti-convulsant actions may achieve their effects by inhibiting adenosine uptake and thus potentiating extracellular adenosine levels. 5. Morphine also elevates extracellular adenosine levels but achieves this by enhancing adenosine release.  相似文献   

9.
10.
11.
As compared to the time of median control death (i.e. the time inducing 50% death in untreated birds at 50 degrees C), exogenous noradrenaline afforded 100% survival in the blue rock pigeon, Columba livia. The survival percentages with the other autonomic drugs were: chlorpromazine 70%; reserpine 60%; adrenaline 60%; pentolinium 50% and dihydroergotamine 30%. The time of median control death at 50 degrees C was found to be 3.5 hours in the pigeon. During 10-day exposure at 45 degrees C all the birds pre-treated with noradrenaline survived, and 47% of those treated with adrenaline and 42% of the untreated birds survived the stress. It is concluded that noradrenaline acts definitely as a "heat protective" hormone in the pigeon.  相似文献   

12.
13.
Volunteers with normal hearing were tested for vegetative balance with the aid of vegetative reflexes and with the aid of the atropine test. The effect of white noise stimulated on hearing thresholds was then investigated together with their recovery. The vegetative system was affected experimentally by intravenous administration of atropine, and the beginning and recession of hearing fatigue was observed. Atropine caused a small change only. In a similarly arranged experiment, 1% pilocarpin administered subcutaneously in a dose of 1.4 minus 1.6 ml, resulted in increased hearing fatigue and retarded recovery at higher frequencies. The effect of pilocarpin is explained by the fact that it supports the inhibitory processes checked by the parasympathetic nervous system on the periphery.  相似文献   

14.
《Journal of Physiology》1998,92(3-4):317-323
To evaluate delayed (prolonged) neurobehavioral and neurophysiological effects of acute sarin poisoning, nine male and nine female patients of the Tokyo subway sarin poisoning in Japan were examined by neurobehavioral tests, posttraumatic stress disorder (PTSD) checklist, brain evoked potentials, computerized static posturography, and electrocardiographic R-R interval variability, 6–8 months after the poisoning. Their serum cholinesterase activities on the day of the poisoning (March 20, 1995) were 13–131 (mean 72.1) IU/L. The results suggested delayed effects on psychomotor performance, the higher and visual nervous system and the vestibulo-cerebellar system with psychiatric symptoms resulting from PTSD.  相似文献   

15.
16.
17.
18.
19.
20.
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号