La circulación cerebral en condiciones normales y patológicas VI: el caso del vasoespasmo

the basal brain arteries are a system of high flow velocity and high shear stress and energy dissipation, with collateral vessels that get profit from those facts, with a low pressure, that could have some influence in the ischemic pathology at this level, and a distal zone where the flow arrives with lower energy, comparatively with extracranial vessels of the same calibre. it is possible that the increase of flow velocity at the basal arteries after sah be a consequence of a diminished peripheral resistance due to autoregulation abolition. because of the principle of energy preservation, the increase in velocity diminishes the lateral pressure producing a passive diameter decrease of the artery, increasing the width of the wall, that increases the vascular tone, and tends to decrease the diameter, closing a noid hemorrhage using a transient hyperemic response test of vicious circle. other factors are the extraluminal pressure and the presence of clots outside the vessel wall. with abolished autorregulation, ischemia is impending, facilitated by the increased resistance opposed by the diminished diameter of the vessels. the intracranial hypertension can be explained by the spotaneous or iatrogenic hyperemia. the microcirculatory trouble proposed can be assessed by the cerebral circulatory time, the transient hyperemia test, the test of acetazolamide and the reactivity to the increase in pco2. the abolition of autorregulation so displayed, precedes vasospasm for days. this mechanical physiopathological process is presented hypothetically, with its eventual therapeutic consequences.