Anesthetic methods in rats determine outcome after experimental focal cerebral ischemia: mechanical ventilation is required to obtain controlled experimental conditions.

The effects of hypercapnia on enhancement of reduced cerebral perfusion were re-evaluated in areas of ischemia produced by occlusion of the canine middle cerebral artery. Perfusion was measured by 85Kr (beta-ray) and 133Xe (gamma-ray) clearances, fluorescein angiography and diameter measurement of arteries. Between 45 and 55 mm Hg of PaCO2 rCBF measured with both isotopes increased significantly. When PaCO2 was elevated above 55 mm Hg, there was a remarkable dissociation in the rCBF measured by both isotopes. Cortical blood flow measured by 85Kr clearance decreased and, conversely, rCBF measured by 133Xe continued to increase. Arteries of less than 50 mu in diameter in areas of ischemia dilated significantly during hypercapnia. At PaCO2 above 65 mm Hg, progressive sub-pial hemorrhage and extravasation of dye were observed as side effects of hypercapnia. The use of mannitol combined with hypercapnia appeared to be harmful. A PaCO2 level between 45 and 55 mm Hg increases perfusion in areas of mildly reduced rCBF.

Effects of hypercapnia on enhancement of decreased perfusion flow in non-infarcted brain tissues.

In terms of increase of perfusion flow into an area of ischemia, carbon dioxide must be one of the most promising candidates, even though complete agreement has still not been obtained. A controversial, but attractive point in this field is that there is a discrepancy between experimental results obtained by beta-emitting 85Kr and gamma-emitting 133Xe clearance techniques. To resolve this discrepancy in the results from the two isotopes, the experiment of this series were undertaken and our first report clarified that between 45 and 55 mmHg of arterial carbon dioxide pressure (PaCO2), microregional cerebral blood flow (rCBF), measured with both the 85Kr and 133Xe clearance techniques, increased significantly. However, in the same study, as PaCO2 was elevated above this level, there was a remarkable dissociation in rCBF change as measured by each isotope. The cortical blood flow measured with 85Kr clearance method decreased and conversely, global miniregional cerebral blood flow measured by 133Xe continued to increase steadily. In our first report, occurrence of subpial hemorrhage, extravasation of dye and increase of brain volume were considered as possible factors contributing to decrease in cortical blood flow by 85Kr clearance following a stage of its definite increase. In that report, the former two factors were analyzed in detail. Since cerebrovascular occlusive disease in humans tends to produce intracranial hypertension of varying degrees, depending upon secondary brain edema, the elevation of intracranial pressure by inhalation of carbon dioxide must be carefully investigated. If two methods of management, increase of perfusion flow by inhalation of carbon dioxide and reduction of increased brain volume by infusion of hypertonic solution are compatible on treatment and are capable of extending the range of PaCO2 which permits an increase of cortical blood flow measured with 85Kr clearance, an application of carbon dioxide to humans will be much safer and its therapeutic indication will be much wider. Therefore, Part 2 of our experiments was done with administration of 20% mannitol solution, using the same materials and methods as in the previous experiment and a comparison of the results with and without mannitol was made. In results, between 45 and 55 mmHg of PaCO2, cortical blood flow measured with the 85Kr clearance method, increased significantly with a gradual decline at PaCO2 higher than this level, which was very similar to the previous work done without mannitol. With the combined use of these two agents, subpial hemorrhage of more marked degree was observed at a PaCO2 above 65 mmHg with extravasation of dye appearing at lower PaCO2 level than with hypercapnia alone. The use of mannitol combined with hypercapnia appeared to be harmful.

A Study of Method for Enhancement of Perfusion Flow in Experimental Cerebral Ischemia

The Cerebral Vascular Response to Hypercapnia in Stroke

Cerebral autoregulation is one of the main factors controlling cerebral circulation. It permits a fluctuation in blood pressure over a wide range without an appreciable change in cerebral blood flow. Recently several studies in animals (1, 2) and in man (3–6) have shown that under certain circumstances cerebral autoregulation may be impaired or lost and that cerebral blood flow will become passively dependent on changes in arterial blood pressure. The purpose of this study was to determine the frequency of the loss or presence of total and regional cerebral autoregulation following induced hypertension.

Cerebral Autoregulation. Regional Cerebral Blood Flow and Cardiohemodynamic Measurements

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The Cerebral Vascular Response to Hypercapnia in Stroke

Cerebral Autoregulation. Regional Cerebral Blood Flow and Cardiohemodynamic Measurements