Arterial spin labeling (ASL) uses magnetic resonance imaging methods to measure cerebral blood flow (CBF) non-invasively. ASL CBF validly localizes brain function and may be especially useful for studies where the time frame of behavioral change is more than a few minutes, such as in longitudinal and treatment studies. ASL measures of cerebral perfusion are highly accurate in detecting lesion laterality in temporal lobe epilepsy, stenotic-occlusive disease, and brain tumors. Among lesioned patients, ASL CBF has excellent concurrent validity when correlated with CBF measured by Positron Emission Tomography or with dynamic susceptibility-weighted magnetic resonance. ASL CBF can predict tumor grading in vivo and can predict six-month response to the surgical treatment of brain tumors. ASL's capability to selectively and non-invasively tag flow in major vessels may refine the monitoring of treatment of cerebrovascular disease and brain tumors. Conclusions about the utility of ASL are limited by the small sample sizes of the studies currently in the literature and by the uncertainty caused by the effect of brain disease on transit times of the magnetic tag. As the method evolves, ASL techniques will likely become more widely used in clinical research and practice. (JINS, 2007, 13, 526–538.)

Arterial spin labeling (ASL) is a magnetic resonance imaging (MRI) method that provides a highly repeatable quantitative measure of cerebral blood flow (CBF). As compared to the more commonly used blood oxygenation level dependent (BOLD) contrast-based methods, ASL techniques measure a more biologically specific correlate of neural activity, with the potential for more accurate estimation of the location and magnitude of neural function. Recent advances in acquisition and analysis methods have improved the somewhat limited sensitivity of ASL to perfusion changes associated with neural activity. In addition, ASL perfusion measures are insensitive to the low-frequency fluctuations commonly observed in BOLD experiments and can make use of imaging sequences that are less sensitive than BOLD contrast to signal loss caused by magnetic susceptibility effects. ASL measures of perfusion can aid in the interpretation of the BOLD signal change and, when combined with BOLD, can measure the change in oxygen utilization accompanying changes in behavioral state. Whether used alone to probe neural activity or in combination with BOLD techniques, ASL methods are contributing to the field's understanding of healthy and disordered brain function. (JINS, 2007, 13, 517–525.)

Background and objective: The safety of hypotension induced by sevoflurane and splanchnic organ blood flow remains to be clarified. The aim was to investigate the effects of sevoflurane-induced hypotension on systemic haemodynamics and splanchnic organ blood flows in dogs.

Methods: Mean arterial pressure was maintained at 60 mmHg by increasing sevoflurane concentrations. The renal, hepatic and pancreatic blood flows were measured by using the hydrogen clearance method.

Results: Hypotension induced by sevoflurane resulted in a 50% decrease of mean arterial pressure due to a 30% reduction in systemic vascular resistance associated with a 30% decrease in cardiac index. The mechanisms causing the lower cardiac index were produced by the decreases in heart rate and left ventricular dP/dtmax. Renal, hepatic and pancreatic blood flow were reduced, but the whole-body oxygen consumption did not change during the hypotensive period.

Conclusions: The haemodynamic changes induced by sevoflurane were caused by the suppression of arterial baroreflexes and myocardial depression, but splanchnic organ blood flows, though reduced, could provide adequate peripheral perfusion to meet the decrease in oxygen supply.

A small decrease in cerebral blood flow (approximately 10%) in response to 100% oxygen (O2) administration is well recognized. This observation was based on human volunteer studies, which employed a nitrous oxide washout method for the measurement of cerebral blood flow. Because this method is now appreciated to be subject to potential errors we have examined the cerebral blood flow response to 100% oxygen using a magnetic resonance imaging technique to quantify changes in carotid and basilar artery flow. The study, was performed in 12 normal male subjects aged 23–42 years. We report decreases in cerebral blood flow ranging from 9 to 31% with a mean value of over 20%. The decrease in cerebral blood flow was greater in seven young subjects (aged 23–26 years) with decreases in cerebral blood flow of 19.3–31.4% (mean 26.8%). In five older subjects (aged 32–42 years), decreases in CBF were smaller (mean 16.2%). The administration of 100% O2 was accompanied by a small decrease in end-tidal CO2 (3.7–7.1%), insufficient to explain the changes in cerebral blood flow. We conclude that the decrease in cerebral blood flow in response to O2 administration is greater than previously described and appears to be greater in young adults.

This study was designed to examine the effect of volume loading on haemodynamic responses and regional cardiac function in dogs subjected to two infusion rates of propofol. Instrumentation was established to measure aortic and left ventricular pressures, cardiac output and myocardial segmental lengths. Measurements were taken during two successive infusion rates of propofol: 0.2 (P0.2) and 0.4 (P0.4) mg kg−1 min−1. One group (VL+) (n=6) received volume loading (dextran 40, 10 mL kg−1 h−1), the other group (VL−) (n=6) received only basal perfusion (Ringer solution, 2 mL kg−1.h−1). Regional blood flows were measured by radio-labelled microspheres. P0.4 induced a decrease in cardiac output and in dP/dtmax. End-diastolic length decreased with propofol without any difference between groups. Regional contractility was not modified by propofol or by volume loading. P0.4 decreased endocardial and epicardial blood flow in the VL-group only. Renal, small intestine and large intestine blood flows decreased in both groups with P0.4. P0.2 did not alter regional blood flows significantly. It was concluded that in this model, propofol infusion at 0.4 mg kg−1 min−1 induced splanchnic, renal and myocardial hypoperfusion in animals not submitted to a mild fluid loading. Fluid loading allowed myocardial perfusion to be maintained but could not prevent a marked decrease in splanchnic and renal perfusion.