Time-Course of Cerebral Perfusion and Tissue Oxygenation in the First 6 h after Experimental Subarachnoid Hemorrhage in Rats

Present knowledge about hemodynamic and metabolic changes after subarachnoid hemorrhage (SAH) originates from neuromonitoring usually starting with aneurysm surgery and animal studies that have been focusing on the first 1 to 3 h after SAH. Most patients, however, are referred to treatment several hours after the insult. We examined the course of hemodynamic parameters, cerebral blood flow, and tissue oxygenation (ptiO2) in the first 6 h after experimental SAH. Sixteen Sprague–Dawley rats were subjected to SAH using the endovascular filament model or served as controls ( n = 8). Bilateral local cortical blood flow, intracranial pressure, cerebral perfusion pressure, and ptiO2 were followed for 6 h after SAH. After induction of SAH, local cortical blood flow rapidly declined to 22% of baseline and returned to 80% after 6 h. The decline of local cortical blood flow markedly exceeded the decline of cerebral perfusion pressure. ptiO2 declined to 57%, recovered after 2 h, and reached ≥140% of baseline after 6 h. Acute vasoconstriction after SAH is indicated by the marked discrepancy of cerebral perfusion pressure and local cortical blood flow. The excess tissue oxygenation several hours after SAH suggests disturbed oxygen utilization and cerebral metabolic depression. Aside from the sudden increase of intracranial pressure at the time of hemorrhage and delayed cerebral vasospasm, the occurrence of acute vasoconstriction and disturbed oxygen utilization may be additional factors contributing to secondary brain damage after SAH.

Vascular pressures and cortical blood flow in cavernous angioma of the brain

✓ This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (± standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 ± 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 ± 0.6 torr. Mean CO2 reactivity was 1.1 ± 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 ± 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.

Cerebral Circulation during Arteriovenous Malformation Operation

The circulatory changes in the cortex around a cerebral arteriovenous malformation (AVM) were studied in 18 patients. The AVMs had rapid circulation times with early draining veins on angiography. Local cortical blood flow (ICoBF) was measured with cortically applied thermister/Peltier stack arrays. The AVMs had a more pronounced effect on ICoBF at a 2- to 4-cm distance from the AVM margin than in the adjacent cortex. Mean preexcision ICoBF was 62.9 ± 6.7 (SE) ml/100 g/minute (i.e., similar to normal controls) near the AVM margin and 43.0 ± 4.2 ml/100 g/minute far (i.e., >2 cm) from the AVM. CO2 reactivity (COR) before excision was 1.1 ± 0.3 ml/100 g/minute/torr of CO2 (i.e., similar to normal controls) at near sites and 0.6 ± 0.3 ml/100 g/minute/torr of CO2 at far sites. The mean postexcision near ICoBF remained stable at 55.8 ± 5.1 ml/100 g/minute at near sites, but the far ICoBF significantly increased (P < 0.05) to 57.2 ± 6.8 ml/100 g/minute. The cortical feeding artery pressure was substantially below the normal cortical artery pressure in 50% of the cases studied. Pressure in these arteries normalized after occlusion and AVM excision, resulting in a rapid increase in cortical artery perfusion pressure. Draining red vein pressure, which was elevated before AVM excision, also dropped after excision, contributing to the increase in perfusion pressure. Two patients who developed the normal perfusion pressure breakthrough syndrome (PBS) after operation had low ICoBF and disturbed COR before AVM excision and marked increase of ICoBF after excision. Factors that contribute to the development of PBS include: (a) low ICoBF around an AVM; (b) impaired COR; (c) low cortical artery pressure before AVM excision; (d) normalization in cortical artery pressure after AVM removal; and (e) substantial increase in ICoBF after AVM removal. Maintenance of a low systemic arterial blood pressure during the early postoperative period is essential in reducing the risk of severe cerebral edema.