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✓ The real pathogenetic role of no-reflow phenomenon in clinical situations such as the acute stage of subarachnoid hemorrhage (SAH) is not yet known. To study this problem, we carried out the following experiment in dogs: SAH was induced 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), electroencephalogram (EEG), and sensory evoked response were monitored under controlled ventilation for 3 hours 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 two basic patterns of ICP changes which simulated those previously reported with human SAH. In the first 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 second 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. From the results, the pathogenetic role of the no-reflow phenomenon in the acute stage of SAH as influencing the prognosis is strongly suspected.
Asano et al. (Fri,) studied this question.