[The autonomic nervous system involved in regulation of immune function in rats during hypoxia].

AIM: To study of autonomic nervous system modulation of lymphocyte proliferation during hypoxia. METHODS: Rats were exposed to 5 km and 7 km altitude in a hypobaric chamber for 24 h or 48 h, the effect of autonomic nervous system on mitogen-induced spleen lymphocyte response to the acute hypoxia was investigated. RESULTS: When rats were exposed to 5 km altitude for 24 h, which inhibited spleen T lymphocyte proliferation induced by concanavalin (Con A), but the action was abolished through peripheral sympathetic-destroyed. When mouse were exposed anoxia environment at 0.07 MPa for 10 min, the norepinephrine and epinephrine in plasma were increased markedly. T cells of rats were in vitro incubated simultaneously with ACh showing a concentration dependent enhancement of T cell proliferation. The plasma levels of ACh were decreased after rats were exposed to 5 km for 24 h. CONCLUSION: Autonomic nervous system was involved in the regulation of immune function in rats during hypoxia.

[Hippocampal slice - a model in vitro for screening antiepileptic drugs].

AIM: To establish a model in vitro for screening antiepileptic drugs. METHODS: Perfusing guinea pig hippocampal slice with penicillin offers a stable epileptiform discharge which was tested by two commonly clinically used antiepileptic drugs, phenytoin sodium and phenobarbital sodium at different concentration. RESULTS: The experimental result showed that penicillin induced epileptiform discharge in the hippocampal slice and two antiepileptic drugs, phenytoin sodium and phenobarbital sodium inhibition of this discharge induced by penicillin. CONCLUSION: This electrophysiological model has the advantage of simplicity, flexibility and ease of quantitation and has potential value for screen antiepileptic drugs and epilepsy research.

[The enhancing effects of arginine-vasopressin on antibody level and lymphocyte proliferation of rats].

The effects of arginine-vasopressin (AVP) on some immune parameters of rats were studied by using icv of AVP. The hemolysin to sheep red blood cell and IgG production were enhanced by icv of 100, 800 ng AVP. Both the actions were partly blocked by icv preinjection of the V1 receptor antagonist DPAVP. It was also found that the NE and corticosterone levels in the serum of rats were significantly reduced after icv of AVP. The above results suggest that AVP executes immunofunctions through V1 receptors in the paraventricular nucleus of the brain. Considering our previous results, the AVP enhanced immunofunction may be related to its inhibition of corticotropin releasing factor release or the excitatory activity of sympathetic nerves.

[Beta-endorphin involved in the regulation of humoral immune function of rats during acute hypoxia].

In order to investigate the role of beta-endorphin in the regulation of humoral immune function of rats during acute hypoxia, the effects of beta-endorphin on mitogen-induced spleen lymphocyte DNA synthesis and hemolysin formation as well as IgG production to chicken egg albumen were observed. It was found that after rats received icv injection of beta-endorphin (1 ng/rat), the T-lymphocyte DNA content, the hemolysin-forming capacity of SRBC-sensitized rats and the IgG level were reduced significantly compared with the control (icv normal saline). Similar suppressive effects on immune function could be found after rats were exposed to 7 km altitude in a hypobaric chamber for 48 h. Pretreatment with icv injection of naltrexone, the immunosuppressive effects of acute hypoxia were partially blocked. Icv administration of beta-endorphin produced an increase in splenic cathcholamines, similar to those of hypoxia treated group (7 km for 12 h). All the above findings suggest that beta-endorphin may modulate the immune response to hypoxia stress via opioid receptor and its inhibitory action may be mediated by activating sympathetic nervous system.

[Norepinephrine regulation of T-lymphocyte proliferation of rat during acute hypoxia].

Interaction between the immune and neuroendocrine systems has long been noted. In the present study, the role of norepinephrine (NE) in immunoregulation of rats during simulated hypoxia in hypobaric chamber was examined. It was found that 7 km for 24 h of hypoxia inhibited T-lymphocyte proliferation by 41%. 7 d and 20 d of hypoxia, simulating 5 km altitude, reduces T-lymphocyte proliferation respectively 34% and 60%. Intracerebroventricular (i.c.v.) injection of 5 x 10(-6) mol/L NE decreased T-lymphocyte proliferation by 29%. I.c.v. injection of phentolamine 25 micrograms/rat prior to 7 km for 10 h hypoxia attenuated the hypoxia-induced suppression of T-lymphocyte proliferation from 42% to 21%. In additon, 7 km 10 h hypoxia increased CRF levels in blood and catecholamines in hypothalamus. An increased circulation CRF level was also noted after NE injection (i.c.v.) of 5 x 10(-6) mol/L. Hypoxia corresponding 7 km altitude for 10 h stimulates spleen-lymphocytes incubated with CRF, but T-lymphocyte proliferation decreclsed with increasing CRF concentration. These findings suggest that hypoxia inhibits T-lymphocyte proliferation probably through an immune inhibition action by CRF-NE.

[Inhibition effect of hypoxia on humoral immunity of rats].

To study the effect of hypoxia on humoral immunity function of rat and Ochotona curzoniae (pika), the specific antibody production to novel antigen IgG and immunoresponse to sheep red blood cell (hemolysin forming) were measured. The results show that hypoxia at altitude of 5 km and 7 km for 10 d resulted respectively in 10.3% (P < 0.05) and 21.9% (P < 0.05) decrement in hemolysin formation in rats, as compared with the control group kept at 2.3 km. When the rats were secondarily immunized and kept at the same hypoxia for 10 d, the reduction in hemolysin formation was 4.2% (P < 0.05) and 4.6% (P < 0.05) for the two respective altitudes. These changes, however, were not found in pikas. When rats were immunized two days before hypoxia, 5 km hypoxia for 5 d and 8 d failed to suppress hemolysin formation. Intracerebroventricular (i.c.v.) injection of CRF (1.0 microgram/rat), decreased hemolysin formation and production of IgG by 8.6% (P < 0.05) and 14.0% (P < 0.05) respectively, but intraperitoneal (i.p.) injection of CRF (1.0 microgram/rat) had no effect. On the other hand, i.c.v. injection of CRF receptor antagonist (alpha-helical CRF (9-41), 50 micrograms/rat) prior to 7 km hypoxia caused a hypoxia-induced suppression of IgG production from 24.2% to 12.1% (P < 0.05). Adrenalectomy in rats lowered hemolysin formation by 6.6% (P < 0.05). The above results demonstrate that hypoxia suppresses humoral immunity function and alters initial antigen processing probably through an increase of CRF in the central nervous system.