Effects of dihydroergotamine on intracranial pressure, cerebral blood flow, and cerebral metabolism in patients undergoing craniotomy for brain tumors.

In a search for a nonsurgical intervention to control intracranial hypertension during craniotomy, the authors studied the effects of dihydroergotamine on mean arterial blood pressure (MABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and cerebral metabolism in patients who underwent craniotomy for supratentorial brain tumors. Twenty patients were randomized to receive either dihydroergotamine 0.25 mg intravenously or placebo as a bolus dose during craniotomy. Anesthesia was induced with thiopental/fentanyl/atracurium, and maintained with isoflurane/N2O/fentanyl at normocapnia. After removal of the bone flap and exposure of intact dura, ICP was measured subdurally and dihydroergotamine/placebo was administered. Intracranial pressure and MABP were measured continuously. Cerebral blood flow (after intravenous administration of 133Xe) and arteriojugular venous difference of oxygen (AVDO2) were measured before, and 30 minutes after, dihydroergotamine/placebo administration. Cerebral metabolic rate of oxygen (CMRO2) was calculated. After administration of dihydroergotamine, a significant increase in MABP from 74 to 87 mm Hg (median) and CPP from 65 to 72 mm Hg (median) were found. Simultaneously to the increase in MABP, a significant increase in ICP from 9.5 to 11.5 mm Hg (median) was disclosed, whereas no significant differences in CBF, AVDO2, or CMRO2 were found. Intracranial pressure was significantly higher after dihydroergotamine than after placebo. In conclusion, no ICP decreasing effect of a bolus dose of dihydroergotamine was found when administered to patients with brain tumors during isoflurane/N2O anesthesia. Corresponding increases in MABP and ICP suggest that abolished cerebral autoregulation might explain why dihydroergotamine was associated with an ICP increase.

Biomechanical properties of porcine cerebral bridging veins with reference to the zero-stress state.

Passive mechanical and morphometric properties of porcine cerebral bridging veins were studied. Fifteen cerebral bridging veins were obtained from 7 pigs. The superior sagittal sinus, bridging veins and the meninges were excised and placed in aerated calcium-free Krebs solution. The outflow cuff segment is a narrow region at the junction of the cerebral bridging veins and superior sagittal sinus. The principal direction of collagen fibres was longitudinal in the bridging vein and circumferential in the cuff region. The diameter was smaller in the outflow cuff segment than in the cerebral bridging veins in the pressure range studied (0-23 mm Hg) whereas the thickness was highest in the outflow cuff segment (p < 0.01). The circumferential stress-strain analysis showed that the outflow cuff segment was extensible up to a strain of 0.25. At higher strains the outflow cuff segment was progressively stiffer than the cerebral bridging vein (p < 0.05). The longitudinal stress-strain relation for the cerebral bridging vein was shifted to the left compared to the outflow cuff segment (p < 0.05). When compared to the stress-strain properties in the circumferential direction, the outflow cuff segment was more extensible and the cerebral bridging vein stiffer in longitudinal direction (p < 0.05). The opening angle of the outflow cuff segment and the cerebral bridging vein was 115 +/- 4 and 120 +/- 4 (means +/- SE) without statistical difference between the two regions. In conclusion the difference in biomechanical properties between the outflow cuff segment and the cerebral bridging vein was associated to their difference in histology and fibre arrangement. This indicates that the function of the outflow cuff segment is to act as a flow-limiting resistance to the outflow from the cerebral circulation.

Xenon CT cerebral blood flow in patients with head injury: influence of pulmonary trauma on the input function.

The noninvasive xenon-enhanced CT (Xe CT) cerebral blood flow (CBF) method has been used in patients with severe traumatic brain injury (TBI) to identify the blood-flow thresholds for the development of irreversible ischaemia or infarction following severe TBI. Quantitative regional CBF (rCBF) estimates are based on the assumption of identity between the end-tidal xenon concentration curve, used as the input function, and the arterial xenon concentration curve, being the true input function to the brain. Accordingly, rCBF data addressing the issue of ischaemia should be viewed in relation to possible deviations between the end-tidal and arterial xenon concentration curves. To evaluate this possible source of error, we studied five patients with severe TBI (Glasgow coma score < or =7) who also had pulmonary trauma. CBF was studied with the Xe CT CBF method and flow rates were determined by fitting the Kety equation to each CT voxel using either the end-tidal or the arterial xenon curve as input function. In all patients rCBF estimates were lower using the end-tidal xenon curve than with the arterial xenon curve; the mean underestimation was 20.3% in gray metter and 17.3 % in white matter. The deviation between the end-tidal and arterial xenon concentration curves should be considered as a source of error when defining critical flow values according to the flow thresholds of tissue viability.

The influence of the input function on quantitative rCBF by the Xe/CT method.

Measurements of rCBF by the Xe/CT method are based on the assumption of identity between the end-tidal xenon curve which is applied as input function, and the arterial xenon curve being the true input function to the brain. In this study corresponding end-tidal and arterial xenon curves were measured in an experimental animal model (part 1) and in 5 patients with traumatic brain injury (part 2) and used for rCBF calculation. In both studies rCBF was underestimated by using the end-tidal xenon concentration curve as brain input function. In part 1 rCBF underestimation was depended on pulmonary gas exchange; high or low levels of rCBF; tissue type; and xenon inhalation protocols. In part 2 the mean rCBF underestimation was 18.8 +/- 8.3%. In conclusion, non-invasive estimate of the input function should be considered as a source of error when defining quantitative blood flow values e.g. the flow thresholds of ischaemic infarction.

Cerebral blood flow in volunteers measured by PET and Xe CT/CBF. A comparison.

Aim of this study was to compare two quantitative CBF methods. Seven young, healthy volunteers were studied with PET (15-0 labelled water) and afterwards with Xe CT/CBF (30% xenon in oxygen, 3 minutes wash-in, 5 minutes washout protocol). Xe CT/CBF showed greater differences between high and low flow areas than PET CBF. Correlation was found within subjects between ROI's, but no agreement or correlation between the methods could be demonstrated. The disagreement in this study could be due to changes in PCO2.

Pulmonary function affects the quantification of rCBF by non-invasive xenon methods.

Estimates of regional cerebral blood flow (rCBF) by non-invasive xenon methods (133-xenon inhalation, xenon-enhanced computed tomography (Xe/CT) and 133-xenon iv injection) are frequently applied in the diagnosis and evaluation of patients suffering from diseases which cause disturbances in the cerebrovascular circulation. These methods all depend on an estimate of the arterial xenon concentration curve derived non-invasively from measurements of the end-tidal xenon concentration curve and used as brain input function in the Kety equation. We have studied the influence of impaired pulmonary gas exchange on the end-tidal and arterial xenon concentration curves in nine anaesthetized pigs by simultaneously measurements of both the end-tidal xenon and arterial xenon concentration curves. Computer simulations were performed to determine the deviations in the calculated rCBF values when using the end-tidal as compared to the arterial xenon concentration curve as brain input function. The results indicated that impairment of the pulmonary gas exchange caused a significant further 'delay' in the arterial xenon concentration curve in comparison to the end-tidal xenon concentration curve. The time constants of arterial curve delay were 11.9 s in the normal pulmonary group, 21 s in the right lung atelectasis group, and 19.7 s in the left pulmonary artery occlusion group. Accordingly, computer simulations indicated a statistically significant 'underestimation' of rCBF due to: (1) pulmonary gas exchange; (2) high or low levels of rCBF; (3) partition coefficient (lambda) of gray and white matter; and (4) xenon inhalation protocols. Our results indicate that quantitative measurements of rCBF by non-invasive xenon methods are markedly affected by deviations between the end-tidal and arterial xenon concentration curve, so that estimates of flow thresholds for infarction are problematic under conditions of impaired pulmonary gas exchange.

ICP during anaesthesia with sevoflurane: a dose-response study. Effect of hypocapnia.

In patients with a supratentorial cerebral tumor, an increase in sevoflurane concentration from 1.5% (0.7 MAC) to 2.5% (1.3 MAC) did not change the intracranial pressure (ICP) significantly (12 to 14 mm Hg (medians)). However, a significant increase in cerebral blood flow (CBF) from 29 to 39 ml/100 g/min (medians) was disclosed. During administration of sevoflurane 1.5% and 2.5%, a significant decrease in ICP (3.5 and 3.0 mm Hg (median) respectively) was found when PaCO2 was decreased by 0.8 kPa.

Effects of sevoflurane on intracranial pressure, cerebral blood flow and cerebral metabolism. A dose-response study in patients subjected to craniotomy for cerebral tumours.

BACKGROUND: Studies concerning the cerebrovascular effects of sevoflurane in patients with space-occupying lesions are few. This study was carried out as a dose-response study comparing the effects of increasing sevoflurane concentration (1.5% (0.7 MAC) to 2.5% (1.3 MAC)) on cerebral blood flow (CBF), intracranial pressure (ICP), cerebrovascular resistance (CVR), metabolic rate of oxygen (CMRO2) and CO2-reactivity in patients subjected to craniotomy for supratentorial brain tumours. METHODS: Anaesthesia was induced with propofol/fentanyl/atracurium and maintained with 1.5% sevoflurane in air/oxygen at normocapnia. Blood pressure was maintained constant by ephedrine. In group 1 (n = 10), the patients received continuously 1.5% sevoflurane. Subdural ICP, CBF and CMRO2 were measured twice at 30-min intervals. In group 2 (n = 10), sevoflurane concentration was increased from 1.5% to 2.5% after CBF1. CBF2 was measured after 20 min during 2.5% sevoflurane. Finally, CO2-reactivity was studied in both groups. RESULTS: In group 1, no time-dependent alterations in CBF, CVR, ICP and CMRO2 were found. In group 2, an increase in sevoflurane from 1.5% to 2.5% resulted in an increase in CBF from 29 +/- 10 to 34 +/- 12 ml 100 g-1 min-1 and a decrease in CVR from 2.7 +/- 0.9 to 2.3 +/- 1.2 mmHg ml-1 min 100 g (P < 0.05), while ICP and CMRO2 were unchanged. CO2-reactivity was maintained at 1.5% and 2.5% sevoflurane. CONCLUSION: Sevoflurane is a cerebral vasodilator in patients with cerebral tumours. Sevoflurane increases CBF and decreases CVR in a dose-dependent manner. CO2-reactivity is preserved during 1.5% and 2.5% sevoflurane.