Cerebral Blood Flow and Metabolic Responses to Sustained Hypercapnia in Awake Sheep

Abstract

Summary: This investigation determined the effects of sustained hypercapnia on cerebral blood flow (CBF; ra diolabeled microspheres), cerebral metabolic rates for O2 and glucose (CMR02 and CMRg1c), and brain water con tent in conscious sheep instrumented with aortic, left ven tricular, vena cava, and brain sagittal sinus catheters. PaC02 was elevated from 38 ± 3 to 53 ± 3 (mean ± SD) mm Hg and Pa02 from 109 ± 7 to 131 ± 4 mm Hg for 96 h in an environmental chamber. Hypercapnia did not alter sheep behavior, food and water intake, arterial pressures, core temperature, or brain lactate release. Total and re gional CBF and CBF/CMR02 reached peak values at 1 h and then readjusted, to stabilize at lower, but still ele vated levels at 24 h and thereafter. CMR02 and CMRglc CO2 retention is commonly observed in patients with chronic pulmonary disease and this can be as sociated with impairment of integrated brain func tion (Sieker and Hickam, 1956; Woodbury and Received September \, 1993; final revision received Novem ber 18, 1993; accepted December 13, 1993. Abbreviations used: bpm, beats per minute; Ca g le and CV gle , cerebral arterial and venous blood glucose content, respectively; CaOZ and CvOz, cerebral arterial and venous blood oxygen con tent, respectively; CMRlaco cerebral metabolic rate for lactate; CPP, cerebral perfusion pressure; CVR, cerebral vascular resis tance; FE g i c and FEOz, cerebral glucose and oxygen extraction fraction, respectively; F\COz, inspired fraction of carbon diox ide; GD, cerebral glucose delivery; GOI, glucose-oxygen index; Hba and Hbv, arterial and venous hemoglobin, respectively; Hcta and Hctv, arterial and venous hematocrit, respectively; HR, heart rate; 10, inner diameter; OD ' cerebral oxygen delivery; 00, outer diameter; Pa and P s a s' arterial and sagittal sinus pres sure, respectively; pHa' arterial pH; PRU, peripheral resistance units; rCBF, regional CBF; SaOZ% and SvOz%, arterial and ve nous oxygen saturation, respectively. 115increased at 6 h and thereafter during hypercapnia. PaC02, CBF, CMR02, and CMRglc remained elevated at 3 h after restoration to room air, while CBF/CMR02 re turned to the control value. Frontal and occipital lobe wet-to-dry weight ratios increased modestly but signifi cantly after hypercapnic exposure. It is concluded that sustained hypercapnia induces stable and nonadapting in creases in both CBF and brain metabolism that persist for at least 3 h after restoration to room air in association with hypoventilization and modest elevations of brain wa ter. Key Words: Brain bicarbonate-Brain edema-Brain glucose metabolism-Brain lactate-Brain O2 uptake Cerebral fluid shifts-C02 retention-Hyperventilation. Karler, 1960; Krnjevic et aI. , 1965). Most studies have attributed the increase in cerebral blood flow (CBF) during hypercapnia to an increase in the [H+] in brain interstitial fluid (Kontos et aI. , 1977). More recently, evidence indicates that nitric oxide related mechanisms may contribute to hypercapnic brain vasodilation also (ladecola, 1992; Wang ...

Dynamics of Changes in Blood Flow, Volume, and Oxygenation: Implications for Dynamic Functional Magnetic Resonance Imaging Calibration

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The Contribution of Arterial Blood Gases in Cerebral Blood Flow Regulation and Fuel Utilization in Man at High Altitude

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