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Lipińska S., Szkudlarek U., Traczyk W. Z.: Hypophysial portal blood flow during preganglionic stimulation of the superior cervical ganglion under condition of systemic arterial blood pressure stabilization in rat. Acta Physiol. Pol. 1990, 41(1-3): 53-61. The presence of hypothalamic hormones in the pituitary portal blood is regarded as the principal factor by which the hypothalamus controls pituitary secretion. In contrast to numerous investigations on hypothalamic hormone release, the regulation of the hypophysial-portal blood flow (HPBF) has been scarcely studied. Hypophysial-portal vessels were exposed according to the Worthington’s method [1966]. The 10-min blood samples were collected before and during unilateral or alternative bilateral electrical stimulation of the preganglionic fibers of the superior cervical ganglia (SCG). During blood samples collection the stable systemic arterial blood pressure was maintained by a barostat. The HPBF was estimated according to the determination of the hemoglobin in samples of washed and collected blood from the cut pituitary portal vessels. The mean HPBF was 3.5 μ /min. Electrical stimulation of SCG. did not change HPBF. This indicates that sympathetic efferents do not participate in the regulation of HPBF under conditions of stabilization of the systemic arterial blood pressure.
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The post-haemorrhagic vasopressin release into the blood

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The aim of the present study was to compare the influence of the renin-angiotensin and sympathetic system in the process of post-haemorrhagic vasopressin release. A dialysis of the venous blood from the sella turcica region was performed in male rats under anaesthesia. The animals were divided into eight experimental groups: 1) control; 2) bleeding; 3) 20 days after superior cervical ganglionectomy; 4) 20 days after superior cervical ganglionectomy and bleeding; 5) injection of captopril; 6) injection of captopril and bleeding; 7) 20 days after superior cervical ganglionectomy and injection of captopril; 8) 20 days after superior cervical ganglionectomy, injection of captopril and bleeding. The content of vasopressin in dialysates was determined by radioimmunoassay. In control rats the release of vasopressin into dialysates was constant during 180 min of the experiment. Bleeding, as well as, superior cervical ganglionectomy caused an increase in vasopressin release. Captopril did not change vasopressin release in comparison to control group. Furthermore, vasopressin release after both, bleeding and sympathetic denervation performed simultaneously was significantly abolished. We conclude that renin-angiotensin, as well as, sympathetic nervous system are involved in the increased post-haemorrhagic vasopressin release.
In uretane-chloralose anaesthesia the pituitary gland was exposed by transpharyngeal approach in rats. The anterior lobe was removed and the posterior lobe was incubated in situ, that is in conditions of anatomical integrity of the hypothalamus with the posterior pituitary lobe. The 15-min samples of the medium incubating the posterior pituitary lobe in situ were collected. Vasopressin (AVP) content in the incubation medium was determined by radioimmunoassay. The stimulation of preganglionic fibers of the superior cervical ganglion (SCG) with alternate short (5 s) bursts of electric pulses with short (5 s) breaks did not change A VP release. However, stimulation of preganglionic fibres with alternate long (30 s) bursts of electric pulses with long (30 s) breaks evoked an increase in AVP release after some latency . Probably, at the hypothalamic or posterior pituitary level temporal summation should occur affecting vasopressinergic neurons or their endings and evoking AVP release.
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The aim of this experiment was to compare the role of renin-angiotensin and sympathetic nervous system in post-haemorrhagic mechanism of oxytocin release. Oxytocin content in venous dialysates was determined by radioimmunoassay. In control rats the release of oxytocin into dialysates did not change during whole experiment. The injection of captopril induced 2-fold higher oxytocin release, but caused no change in oxytocin release after bleeding. Superior cervical ganglionectomy (SCGx) 20 days before, caused 5-fold higher increase in oxytocin release than in control group. Injection of captopril in rats after SCGx, did not decrease the high level of oxytocin in dialysate. However, bleeding increased oxytocin release and 1 hour after bleeding the highest - 14-fold increase, took place. In the contrary to 14-fold increase in oxytocin release in animals with superior cervical ganglia (SCG), bleeding after SCGx caused only 2-fold higher oxytocin release. When SCGx, bleeding and injection of captopril were done simultaneously, oxytocin release remained on the control concentration level. We assumed that blockade of renin angiotensin system and sympathetic dennervation prevent the increase in oxytocin release after bleeding. On basis of our present experiments, it can be assumed that, in posthaemorrhagic oxytocin release into the blood, sympathetic innervation derived from SCGx, as well as, renin-angiotensin system are involved.
Various investigators have shown that unilateral ganglionectomy or transection of the internal and external carotid nerves leads to a regenerative response in the ipsilateral superior cervical ganglion and to uninjured mature sympathetic neurons sprouting into bilaterally innervated shared target organs. In this study changes in the supraependymal neuronal network following unilateral and bilateral cervical sympathectomy on the infundibular floor of the third ventricle were studied by scanning electron microscopy in comparison with normal and sham-operated control animals. After unilateral cervical sympathectomy there was a great increase in the number of varicose nerve fibres on the infundibular floor as compared to the normal and sham-operated control animals. Not only was there an increase in the number of nerve fibres, but also their varicosities were substantially larger than those normally present on the ependymal surface. This study indicates the possible sympathetic projections from the superior cervical ganglia to the ependymal surface of the third cerebral ventricle.
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