Pathogenetic role of no-reflow phenomenon in experimental subarachnoid hemorrhage in dogs

Abstract

The real pathogenetic role of no-reflow phenomenon in clinical situations such as the acute stage of subarachnoid hemorrhage (SAH) is not yet known. SAH was induced in dogs by withdrawing a needle previously inserted into the internal carotid artery through a small craniectomy in the lateral base of the skull. Complete dural repair and cranioplasty was done to avoid cerebrospinal fluid leakage. Cortical cerebral blood flow (CBF) changes, measured by a double-needle type thermocouple, intracranial pressure (ICP), EEG, and sensory evoked response were monitored under controlled ventilation for 3 h after SAH. At the end of the experiment, the brain was perfused with carbon black solution at a pressure of 120 mm Hg. The 32 episodes of SAH thus induced yielded 2 basic patterns of ICP changes which simulated those previously reported with human SAH. In the 1st pattern, reactive hyperemia was always observed, followed by complete or incomplete recovery of cerebral function. Perfusion defects were frequently seen in the thalamus, basal ganglia, and parietooccipital cortex symmetrically. In the 2nd pattern, prolonged elevation of ICP resulted in failure of recovery of both CBF and EEG. Carbon black filled only the pial arteries and the rest of the brain was totally unperfused. The pathogenetic role of the no-reflow phenomenon in the acute stage of SAH as influencing the prognosis is strongly suspected.