1 Divisions of Neurosurgery and Biomedical Engineering, University of Alberta Faculty of Medicine, Edmonton, Alberta, Canada
Address reprint requests to: Bryce Weir, M.D., Division of Neurosurgery, University of Alberta Faculty of Medicine, Edmonton, Alberta, Canada
Correlative cerebral blood flow (CBF) and vessel diameter studies were performed during graded Paco, change in control monkeys and in monkeys subjected to subarachnoid hemorrhage and internal carotid artery spasm. In the control series CBF increased linearly between PaCOCO2 values of 30 mm Hg and 60 mm Hg. An increase in PaCOCO2 from 40 mm Hg to 62 mm Hg produced a mean CBF increase of 74% while a reduction of PaCOCO2 to 25 mm Hg resulted in a decrease of 40%. Cerebral gray matter was more responsive to PaCOCO2 change than white matter. Caliber of the larger capacitance vessels did not provide an adequate index of the status of cerebral circulation. In the experimental series both SAH and traumatic internal carotid artery spasm caused a decreased hemodynamic responsiveness to PaCOCO2. However, when PaCOCO2 was raised to 60 to 65 mm Hg, marked increases in cerebral perfusion occurred (breakthrough phenomenon). In general, a poor correlation between CBF and vessel diameter studies was found in the postinsult period. The studies indicated: (1) SAH caused an increase in cerebrovascular resistance and a decrease in CBF, (2) hemodynamic responses to PaCOCO2 change, although diminished, were not abolished in the acute period after SAH, (3) hypercapnia (PaCOCO2 > 60 mm Hg) significantly increased cerebral perfusion whether or not vasospasm was alleviated, and (4) the small distal cerebral vessels were more reactive to PaCOCO2 change and were more intimately associated with regulation of cerebral perfusion.
Note:
Medical Research Council of Canada Fellow.
© 1974 American Heart Association, Inc.
The Effect of Graded Hypocapnia and Hypercapnia on Regional Cerebral Blood Flow and Cerebral Vessel Caliber in the Rhesus Monkey: Study of Cerebral Hemodynamics Following Subarachnoid Hemorrhage and Traumatic Internal Carotid Spasm
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