The endogenous ouabain-like sodium pump inhibitor in cold injury-induced brain edema.

An endogenous ouabain-like factor (EOLF) was measured in brain tissue of cats 12 and 24 hrs after cold injury-induced edema. EOLF was assayed via its inhibition of 86Rb+ uptake in human red blood cells in a fraction which was obtained from brain tissue by methanol extraction, chloroform treatment and purification of the water phase by C-18 HPLC. As compared to the contralateral hemispheres with an EOLF concentration of 605 +/- 71 pmol ouabain equivalents per g wet weight, the edematous hemisphere had significantly higher concentrations: 12 hours after cold injury it was 2600 +/- 1762 pmol (p < 0.03) and fell to 857 +/- 160 pmol ouabain equivalents/g wet weight after 24 hrs. Similar kinetics were evident for the EOLF concentrations in cerebrospinal fluid. It is suggested that the increase of EOLF in the edematous brain hemisphere may participate as a mediator in the development of vasogenic brain edema in the disturbance of the sodium metabolism.

Different types of postoperative diabetes insipidus and the relation to basal and stimulated serum prolactin levels in patients with hypothalamo-hypophyseal tumorous lesions.

To evaluate the interrelationships between anterior pituitary function and the antidiuretic system in patients harbouring hypothalamo-hypophyseal tumorous lesions, combined anterior pituitary stimulation tests were performed in the pre (n = 192 patients) and postoperative (n = 151 patients) state. Basal and stimulated plasma antidiuretic hormone, serum as well as urinary osmolality and diuresis were analyzed to determine the residual functional capacity of the antidiuretic system. In 106 patients with non-prolactin (PRL) secreting tumours basal and stimulated PRL secretion of the residual anterior pituitary was studied pre- and postoperatively. It was found that in the preoperative state latent (n = 12 patients) or manifest (n = 10 patients) types of diabetes insipidus (DI) were related to a significant decrease of maximal stimulated levels of thyroid stimulating hormone as well as basal and maximal stimulated levels of follicle stimulating hormone relative to patients without DI. In the postoperative state DI lasting longer than 10 days (n = 51 patients) was associated with decreased basal and maximal stimulated concentrations of cortisol, luteinizing and follicle stimulating hormone, whereas basal and maximal stimulated levels of PRL were significantly increased compared to those patients without DI (n = 61 patients). Decompression (n = 65 procedures) via the transnasal route was related with a lower frequency of the more severe types of DI (n = 7 patients) and a significant decrease of basal and maximal PRL levels in patients with non-PRL secreting tumours. The transcranial approach (n = 86 procedures) caused a higher rate of severe DI types (n = 33 patients) and an increase of PRL secretion from the residual anterior pituitary lobe. Patients without DI or DI of mild severity (n = 50), as a group, had a significant decrease of basal and maximal PRL levels compared with preoperative values (preoperative: basal = 14.3 +/- 1.5 ng/ml, max = 31.4 +/- 1.5 ng/ml, postoperative: basal = 9.6 +/- 1.1 ng/ml, max = 24.9 +/- 2.9 ng/ml). In patients with severer degrees of DI (n = 40) PRL levels were significantly increased, respectively (preoperative: basal = 15.3 +/- 3.1 ng/ml, max = 23.9 +/- 7.6 ng/ml, postoperative: basal = 19.7 +/- 3.4 ng/ml, max = 38.6 +/- 7.9 ng/ml). It was concluded that in the surgical treatment of non-PRL secreting hypothalamo-hypophyseal lesions the results of early postoperative assessment of basal and stimulated PRL levels may predict the type of postoperative DI.(ABSTRACT TRUNCATED AT 400 WORDS)

Relationship between plasma antidiuretic hormone and atrial natriuretic peptide during the triphasic diuresis response to experimentally induced acute intracranial hypertension.

Plasma antidiuretic hormone (pADH) and atrial natruiretic peptide (pANP) were determined during the triphasic diuresis response to acute cerebral compression in cats. The first, the polyuric phase, was accompanied by the cardiovascular response, characterized by a simultaneous increase of pADH and pANP. During the second, the oliguric phase and the third phase of diabetes insipidus pADH and pANP concentrations decreased to initial values. These changes were accompanied by symptoms of central vegetative dysregulation namely hypotension, respiratory arrest and EEG cessation. Thus, the results exhibited the same pattern of vasopressinergic and atriopeptinergic activities after induction of an acute intracranial hypertension and suggest that the mutual interaction of both systems may modify the type of diuresis response.

Dissociation between activation of the hypothalamo-hypophyseal antidiuretic system and the type of diuresis during acute intracranial hypertension. Experimental observation.

Acute cerebral compression by a supra- and infratentorial balloon produced a triphasic pattern of diuresis. The 1st phase was characterized by polyuria associated with five fold increase of plasma (p) antidiuretic hormone (ADH) concentration, decreased urine osmolality in spite of natriuresis and blood pressure elevation. The 2nd phase was characterized by oliguria, a decrease of pADH and reduced urine Na+ concentration, whereas urine osmolality transiently increased. At this stage there was respiratory arrest and fall of blood pressure. The final stage was diabetes insipidus (DI), when EEG activity had disappeared. An increase of serum osmolality mainly occurred during the last DI phase. Serum Na+ concentration fluctuated slightly during the whole period of diuresis. These results present evidence, that the diuresis pattern reflects the hypothalamo-hypophyseal antidiuretic system (HHAS) reaction to acute intracranial pressure (ICP) increase with the vegetative symptoms of cerebral shock.

Effect of increased intracranial pressure on the blink reflex in cats.

During an acute increase in ICP produced by balloon inflation three different phases could be observed. In the first phase (ICP 40-50 mm Hg) the latencies of R 1 and R 2 showed an initial decrease followed by increase in latency. In the second phase (ICP 50-70 mm Hg) R 2 disappeared, whereas R 1 showed marked alterations, prolongation of the latency and duration, and a decreasing amplitude. In the third phase no response could be evoked. The pathophysiological observations correlated with the morphological alterations. Two ischaemic zones with BBB damage which "transsected" the mesodiencephalic and pontomesencephalic border were found. The results suggest that the disappearance of R 2 depends on rostral damage, whereas alteration of R 1 is caused by a pontomesencephalic lesion.

Influence of damage of hypothalamo-hypophysial neurosecretory system and adrenalectomy on the blood-brain barrier alteration during intracranial hypertension.

Short-term intermittent cerebral compression following the lesion of NSO, NPV or ME alone or with adrenalectomy, caused disturbances in cerebrovascular system. It was characterized by congestion of blood vessels or vasoparalysis with the damage of BBB. These symptoms were much more pronounced in animals in which ME lesion was combined with adrenalectomy. It seems that the decreased level of vasopressor peptides (VSP, Ox) and catecholamines(A, NA) in the blood could be related to the increased activity of cholinergic system and other substances which are responsible for the dilatation of vessels. It is quite possible that the mutual relation of the above mentioned neuro-humoral factors determine the threshold for cardiovascular and cerebrovascular response to cerebral shock. The breakdown of this threshold could occur at the last stage of intracranial hypertension, being expressed by insufficient control of cardiovascular system with the fall of blood pressure and paralysis of cerebral blood vessels, BBB damage, that eventually might lead to brain death.

Effect of prostaglandin E2 and of indomethacin upon cerebral and pulmonary consequences of exposure to hyperbaric oxygen in rats.

There are few data in the literature suggesting that endogenous prostaglandins (PGs) might be involved in the pathomechanism of seizures. Since the mechanism of seizures inducted by exposure to oxygen high pressure (OHP) is not fully elucidated, this study was designed to investigate the effect of exogenous PG s and of indomethacin (a Pg synthesis inhibitor) upon the development and consequences of seizures in rats exposed to OHP (5 ata). In the animals pretreated with PGE2 (1 ng/kg s.c.) pre-seizure time was shortened, lung weight : body weight index increased and symptoms of respiratory failure potentiated, as compared with the control group. Indomethacin (5 mg/kg i.p) prevented the development of seizures and of pulmonary consequences of OHP exposure. Biochemical examination of brains has shown that velocity of free radical oxidation of lipids (reactions manifested by the breakdown of phospholipid fatty acids, mainly unsaturated ones) enhanced by OHP exposure, is further potentiated in rats pretreated with PGE2. Electron microscopic study has shown the alterations similar to those seen in brain ischemia and/or hypoxia, and the magnitude of changes was related to the intensity of symptoms evoked by OHP. The results show that cerebral and pulmonary consequences of OHP exposure are potentiated by exogenous PGE2 and prevented by inhibition of endogenous PG synthesis. This suggests that PGs and/or their active metabolites might be involved in the mechanism of oxygen toxicity during exposure to hyperbaric oxygen.