OBJECTIVES: To determine whether alterations in intracranial volume occurred following cross-clamping of the descending thoracic aorta in pigs. DESIGN AND SETTING: Laboratory animal study. MATERIALS: Eight pigs undergoing cross-clamping of the descending thoracic aorta for 30 min. CHIEF OUTCOME MEASURES: A Philips Gyroscan T5-II Release 3 (0.5 T) was used to obtain intracranial images before cross-clamping, during cross-clamping and after declamping. The ventricular volume was measured on Spin Echo T1-weighted images. The signal intensity of the cerebral tissue was measured on Spin Echo T2-weighted images. Increased signal intensity of the cerebral tissue relative to an external reference was used as an indicator of cerebral oedema. MAIN RESULTS: The ventricular volume decreased to 89% (p < 0.01) of the baseline value after 5 min of cross-clamping. At 5 min after declamping the ventricular volume decreased further to 71% (p < 0.01). At 25 min after declamping the ventricular volume had returned to the baseline value. The signal intensity of the cerebral tissue did not differ from baseline values following aortic cross-clamping. CONCLUSIONS: In this study, ventricular volume decreased following cross-clamping of the descending thoracic aorta. Since no cerebral oedema was observed, the decrease of ventricular volume was most likely due to increased intracranial blood volume.
OBJECTIVES: To determine whether alterations in intracranial volume occurred following cross-clamping of the descending thoracic aorta in pigs. DESIGN AND SETTING: Laboratory animal study. MATERIALS: Eight pigs undergoing cross-clamping of the descending thoracic aorta for 30 min. CHIEF OUTCOME MEASURES: A Philips Gyroscan T5-II Release 3 (0.5 T) was used to obtain intracranial images before cross-clamping, during cross-clamping and after declamping. The ventricular volume was measured on Spin Echo T1-weighted images. The signal intensity of the cerebral tissue was measured on Spin Echo T2-weighted images. Increased signal intensity of the cerebral tissue relative to an external reference was used as an indicator of cerebral oedema. MAIN RESULTS: The ventricular volume decreased to 89% (p < 0.01) of the baseline value after 5 min of cross-clamping. At 5 min after declamping the ventricular volume decreased further to 71% (p < 0.01). At 25 min after declamping the ventricular volume had returned to the baseline value. The signal intensity of the cerebral tissue did not differ from baseline values following aortic cross-clamping. CONCLUSIONS: In this study, ventricular volume decreased following cross-clamping of the descending thoracic aorta. Since no cerebral oedema was observed, the decrease of ventricular volume was most likely due to increased intracranial blood volume.