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.
D000311:Adrenal Glands / Q000502:physiology*; D000818:Animals; D001812:Blood-Brain Barrier; D002415:Cats; D004837:Epinephrine / Q000097:blood; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology*; D007427:Intracranial Pressure; D008473:Median Eminence / Q000502:physiology; D009489:Neurosecretion; D009638:Norepinephrine / Q000097:blood; D010120:Oxytocics / Q000097:blood; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology; D013495:Supraoptic Nucleus / Q000502:physiology; D014667:Vasopressins / Q000097:blood
D010120:Oxytocics; D014667:Vasopressins; D009638:Norepinephrine; D004837:Epinephrine