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

• Published in: Stroke (1970) 1974-03, Vol.5 (2), p.230-246
• Main Authors: Petruk, K C, Weir, B K, Overton, T R, Marriott, M R, Grace, M G
• Format: Article
• Language: English
• Subjects: Animals; Blood Pressure; Carbon Dioxide - blood; Carbon Dioxide - pharmacology; Carotid Artery Diseases - physiopathology; Carotid Artery, Internal - diagnostic imaging; Carotid Artery, Internal - drug effects; Carotid Artery, Internal - physiopathology; Cerebral Angiography; Cerebrovascular Circulation; Disease Models, Animal; Electrocardiography; Haplorhini; Heart Rate; Hydrogen-Ion Concentration; Hypercapnia - physiopathology; Intracranial Pressure; Ischemic Attack, Transient - diagnostic imaging; Ischemic Attack, Transient - physiopathology; Macaca; Partial Pressure; Subarachnoid Hemorrhage - diagnostic imaging; Subarachnoid Hemorrhage - physiopathology; Vascular Resistance - drug effects
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.STR.5.2.230

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 Pa CO CO2 values of 30 mm Hg and 60 mm Hg. An increase in Pa CO CO2 from 40 mm Hg to 62 mm Hg produced a mean CBF increase of 74% while a reduction of Pa CO CO2 to 25 mm Hg resulted in a decrease of 40%. Cerebral gray matter was more responsive to Pa CO CO2 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 Pa CO CO2 . However, when Pa CO CO2 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 Pa CO CO2 change, although diminished, were not abolished in the acute period after SAH, (3) hypercapnia (Pa CO CO2 > 60 mm Hg) significantly increased cerebral perfusion whether or not vasospasm was alleviated, and (4) the small distal cerebral vessels were more reactive to Pa CO CO2 change and were more intimately associated with regulation of cerebral perfusion.