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  • Title: Chronic nonpulsatile blood flow. I. Cerebral autoregulation in chronic nonpulsatile biventricular bypass: carotid blood flow response to hypercapnia.
    Author: Tominaga R, Smith WA, Massiello A, Harasaki H, Golding LA.
    Journal: J Thorac Cardiovasc Surg; 1994 Nov; 108(5):907-12. PubMed ID: 7967674.
    Abstract:
    To investigate the response of the carotid blood flow and general circulation to hypercapnia in chronic nonpulsatile blood flow, we performed 18 carbon dioxide gas inhalation studies on three calves undergoing a centrifugal biventricular bypass with ventricular fibrillation. An ultrasonic flow probe was put on the carotid artery during biventricular bypass pump implantation, and pump flows were maintained at 90, 100, and 120 ml/kg per minute for 1 week each. The carbon dioxide inhalation studies were performed twice a week. Hypercapnia was induced by administering pure carbon dioxide gas through a nasal tube at flow rates of 0, 5, 7.5, 10, 12.5, and 15 L/min for 5 minutes each at three different nominal pump flow rates, and the resultant arterial blood gas and hemodynamic changes were recorded. No significant correlation existed between the carotid blood flow and mean aortic pressure, which varied from 70 to 140 mm Hg, but the carotid blood flow correlated significantly (p < 0.01) with the systemic pump flow rate. A significant (p < 0.01) linear relationship was found between the carotid blood flow and arterial carbon dioxide tension. For each 1 mm Hg change in arterial carbon dioxide tension, there was a 2.8 % change in the carotid blood flow. The percent changes in the carotid blood flow in response to arterial carbon dioxide tension were calculated as 2.9%, 3.7%, and 2.5% for each 1 mm Hg change in arterial carbon dioxide tension at pump flows of 90, 100 and 120 ml/kg per minute. No significant differences in the carotid blood flow response to hypercapnia were detected among the three systemic pump flow rates. These results thus suggested that chronic nonpulsatile blood flow had no detrimental effects on cerebral autoregulation.
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