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The original well-mixed tissue model for the arterial spin tagging techniques is extended to a two-compartment model of restricted water exchange between microvascular (blood) and extravascular (tissue) space in the parenchyma. The microvascular compartment consists of arterioles, capillaries, and venules, with the blood/tissue water exchange taking place in the capillaries. It is shown that, in the case of limited water exchange, the individual FAIR (Flow-sensitive Alternating Inversion Recovery) signal intensities of the two compartments are comparable in magnitude, but are not overlapped in time. It is shown that when the limited water exchange is assumed to be fast, flows quantified from the signal-intensity difference are underestimated, an effect that becomes more significant for larger flows and higher magnetic field strengths. Experimental results on cat brain at 4.7 T comparing flow data from the FAIR signal-intensity difference with those from microspheres over a cerebral blood flow range from 15 to 150 mL 100 g(-1) min(-1) confirm these theoretic predictions. FAIR flow values with correction for restricted exchange, however, correlate well with the radioactive microsphere flow values. The limitations of the approach in terms of choice of the intercompartmental exchange rates are discussed.

The ability of the magnetic resonance imaging transverse relaxation time, R2 = 1/T2, to quantify cerebral blood volume (CBV) without the need for an exogenous contrast agent was studied in cats (n = 7) under pentobarbital anesthesia. This approach is possible because R2 is directly affected by changes in CBF, CBV, CMRO2, and hematocrit (Hct), a phenomena better known as the blood-oxygenation-level-dependent (BOLD) effect. Changes in CBF and CBV were accomplished by altering the carbon dioxide pressure, PaCO2, over a range from 20 to 140 mm Hg. For each PaCO2 value, R2 in gray and white matter were determined using MRI, and the whole-brain oxygen extraction ratio was obtained from arteriovenous differences (sagittal sinus catheter). Assuming a constant CMRO2, the microvascular CBV was obtained from an exact fit to the BOLD theory for the spin-echo effect. The resulting CBV values at normal PaCO2 and normalized to a common total hemoglobin concentration of 6.88 mmol/L were 42+/-18 microL/g (n = 7) and 29+/-19 microL/g (n = 5) for gray and white matter, respectively, in good agreement with the range of literature values published using independent methodologies. The present study confirms the validity of the spin-echo BOLD theory and, in addition, shows that blood volume can be quantified from the magnetic resonance imaging spin relaxation rate R2 using a regulated carbon dioxide experiment.

The hypothesis was tested that hypoperfused brain regions, such as the ischemic penumbra, are detectable by reductions in absolute transverse relaxation time constant (T2) using magnetic resonance imaging (MRI). To accomplish this, temporal evolution of T2 was measured in several models of hypoperfusion and focal cerebral ischemia in the rat at 9.4 T. Occurrence of acute ischemia was determined through the absolute diffusion constant D(av) = 1/3 TraceD, while perfusion was assessed by dynamic contrast imaging. Three types of regions at risk of infarction could be distinguished: (1) areas with reduced T2 (4% to 15%, all figures relative to contralateral hemisphere) and normal D(av), corresponding to hypoperfusion without ischemia; (2) areas with both reduced T2 (4% to 12%) and D(av) (22% to 49%), corresponding to early hypoperfusion with ischemia; (3) areas with increased T2 (2% to 9%) and reduced D(av) (28% to 45%), corresponding to irreversible ischemia. In the first two groups, perfusion-deficient regions detected by bolus tracking were similar to those with initially reduced T2. In the third group, bolus tracking showed barely detectable arrival of the tracer in the region where D(av) was reduced. We conclude that T2 reduction in acute ischemia can unambiguously identify regions at risk and potentially discriminate between reversible and irreversible hypoperfusion and ischemia.