Effect of induced hypertension on cerebral blood flow following middle cerebral occlusion in rats
The following is in response: To the Editor: The additional information provided by Drs. Arboix and Martf-Vilalta is very helpful and the reference to their published article appreciated since there is so little other data available on the onset times for different stroke subtypes. Dr. Koltringer's letter summarizes data from 423 patients showing that viscoelasticity of whole blood is higher in the morning and lower in the afternoon. Although the inciting mechanism of ischemic stroke has not
... c stroke has not yet been established, the correlation observed does offer an additional mechanism to consider. He does not mention whether there could be a corresponding practical, low-risk medical intervention that might reduce the incidence or severity of stroke if his findings in fact prove to be significant. Drummond et al 1 have recently reported that induced hypertension increased regional cerebral blood flow in the aftermath of middle cerebral artery occlusion in the rat. They were unable to conclude that this represented a therapeutic effect since no metabolic studies were performed, but they claim that this was a reasonable inference. Using the same model and a comparable moderate increase in arterial pressure, we found that both cerebral lactate and water content were significantly reduced at 2 hours postocclusion. 2 The mechanism of this apparently beneficial effect is not proven. A return to aerobic metabolism and restoration of membrane transport systems could be a direct effect of better tissue oxygenation, but it is also possible that the washout of lactate, etc., plays a role. Once the blood-brain barrier is breached and vasogenic edema occurs, induced hypertension will cause aggravated edema and an increased risk of hemorrhage. 3 The duration of both the "therapeutic window," when reoxygenation can save ischemic cerebral tissue, and the "safety window," before reperfusion at high pressure has adverse effects, needs to be precisely identified before these experimental data can be used as rationale for a clinical trial.